digoxin and Myocardial-Infarction

Heart failure (HF) is a syndrome characterized by upregulation of the sympathetic nervous system and abnormal responsiveness of the parasympathetic nervous system. Studies in the 1980s and 1990s demonstrated that inhibition of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitors improved symptoms and mortality in HF resulting from systolic dysfunction, thus providing a framework to consider the use of β-blockers for HF therapy, contrary to the prevailing wisdom of the time. Against this backdrop, this article reviews the contemporary understanding of the sympathetic nervous system and the failing heart.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Afferent Pathways; Angiotensin Receptor Antagonists; Autonomic Nervous System Diseases; Brain; Cardiac Imaging Techniques; Cardiotonic Agents; Digoxin; Efferent Pathways; Exercise Therapy; Exercise Tolerance; Forecasting; Heart Failure; Humans; Kidney Failure, Chronic; Muscle, Skeletal; Myocardial Infarction; Norepinephrine; Oxidative Stress; Polymorphism, Genetic; Receptors, Adrenergic; Receptors, Adrenergic, beta; Reflex; Renin-Angiotensin System; Sleep Apnea, Obstructive; Sympathetic Nervous System

beta-Blockers are currently being evaluated more intensively to define their role in clinical use as antiarrhythmic agents. beta-Adrenergic blockade has been studied in relation to atrial fibrillation, ventricular arrhythmias, and sudden death; however, it is apparent from a number of studies that not all beta-blockers are equally effective. Randomized clinical trial data, both in heart failure and post-myocardial infarction (MI) patients, have shown differences in mortality benefits in addition to a variable effect on arrhythmias and sudden death. Carvedilol, a third-generation beta-blocker with proven clinical benefit in the management of heart failure and post-MI patients, has properties that may make it an effective antiarrhythmic agent. This paper reviews the current clinical arrhythmia data available for carvedilol from large-scale clinical trials and small studies. The trial evidence demonstrates that carvedilol therapy can be an effective adjunctive rate-control therapy in patients with atrial fibrillation, prevent mortality in patients with heart failure or post-MI with left ventricular dysfunction, with or without atrial fibrillation, and reduce its onset and the incidence of ventricular arrhythmia and sudden death.

Topics: Adrenergic beta-Antagonists; Amiodarone; Anti-Arrhythmia Agents; Atrial Fibrillation; Bisoprolol; Carbazoles; Carvedilol; Death, Sudden, Cardiac; Digoxin; Heart Failure; Humans; Metoprolol; Myocardial Infarction; Propanolamines; Randomized Controlled Trials as Topic

Aldosterone blockade has been shown to be effective in reducing total mortality as well as hospitalization for heart failure in patients with systolic left ventricular dysfunction (SLVD) due to chronic heart failure and in patients with SLVD post acute myocardial infarction. The evidence for the effectiveness of aldosterone blockade in chronic heart failure comes from the randomized aldactone evaluation study (RALES) while that for patients post infarction from the eplerenone post acute myocardial infarction efficacy and survival study (EPHESUS). These studies suggest that mineralocorticoid receptor activation remains important despite the use of an angiotensin converting enzyme-inhibitor/angiotensin receptor blocking (ARB) agent and a beta blocker. Increasing evidence suggest that aldosterone blockade has important effects not only on the kidney but on ventricular remodeling, myocardial fibrosis, autonomic balance, fibrinolysis, oxidative stress, and activation of the NF-kappaB and AP-1 signaling pathways. The results of these studies in patients with SLVD has important implications not only for patients with chronic heart failure and post infarction but also for the therapy of patients with essential hypertension and other cardiovascular diseases.

Topics: Aldosterone; Angiotensin Receptor Antagonists; Digoxin; Enzyme Inhibitors; Eplerenone; Female; Humans; Male; Mineralocorticoid Receptor Antagonists; Myocardial Infarction; Randomized Controlled Trials as Topic; Spironolactone; Systole; Ventricular Dysfunction, Left

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a frequently prescribed group of highly effective drugs of which the most well-known side effect is gastrointestinal peptic ulcer. However, NSAIDs have additional renal, cardiovascular, hematological, dermatological, and neurological side effects. Although the spectrum of side effects is slightly different between the conventional NSAIDs and the recently developed cyclooxygenase 2 (COX-2) inhibitors, their overall spectrum is quite similar. Aim of this review is to summarize the current knowledge about NSAIDs and their effects on patients with cardio- or cerebrovascular disorders. NSAIDs interact with many drugs which are used in patients with cardio- or cerebrovascular disorders: They attenuate the effects of diuretics, betablockers, ACE inhibitors and AT-2 blockers, thus leading to uncontrolled hypertension or aggravation of heart failure. They increase digoxin levels, potentiate the effect of oral anticoagulants and interact with platelet inhibitors, thus leading to a higher bleeding risk. There are indications that NSAIDs may induce hypertension in normotensives and that COX-2 inhibitors may lead to an increased rate of myocardial infarction and strokes. Based on these data it is recommended that NSAIDs should be avoided in patients with cardio- or cerebrovascular disorders and alternative pharmaceutical, physical or surgical therapy should be applied. If NSAIDs are inevitable, their side effects should be well monitored; they should be prescribed with caution when given in combination with diuretics, betablockers, ACE inhibitors, AT-2 blockers, digitalis, oral anticoagulants and platelet inhibitors. COX- 2 inhibitors should be avoided in patients with known coronary or cerebrovascular disorders. In patients with uncontrolled hypertension or worsening of heart failure, unreported NSAID-use should be considered. Generally, there is a need to develop further analgetic drugs without the described side effects for patients with cardio- and cerebrovascular disorders.

Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Anti-Inflammatory Agents, Non-Steroidal; Cardiovascular Diseases; Cerebrovascular Disorders; Digoxin; Diuretics; Drug Interactions; Heart Failure; Humans; Hypertension; Myocardial Infarction; Pain

Endoxin is a factor with a digitalis-like biological activity. It is a Na+ pump inhibitor and may be an endogenous medium of digitalis receptor. There are abnormal plasma levels of endoxin in some pathophysiologic states such as hypertension, acute myocardial infarction, arrhythmia, heart failure, etc. Some studies have demonstrated that the abnormal endoxin levels may be implicated in pathogenesis of these diseases or pathophysiologic process involved. Therefore, to clarify the effects of endoxin has much significance in understanding pathogenesis, prevention and treatment of hypertension and other cardiovascular diseases.

Topics: Animals; Cardenolides; Cardiomegaly; Cardiovascular System; Diabetes Mellitus; Digoxin; Enzyme Inhibitors; Heart Diseases; Heart Failure; Humans; Hypertension; Myocardial Infarction; Pulmonary Heart Disease; Saponins; Sodium-Potassium-Exchanging ATPase

Topics: Adrenergic beta-Antagonists; Adult; Age Factors; Aged; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Digoxin; Diuretics; Heart Failure; Humans; Middle Aged; Myocardial Infarction; Prognosis

Neurohumoral activation refers to increased activity of the sympathetic nervous system, renin-angiotensin system, vasopressin and atrial natriuretic peptide. It is now known that neurohumoral activation contributes to the transition from ventricular dysfunction to clinical heart failure, and is an independent predictor of poor prognosis in heart failure. Although the treatment of heart failure has traditionally focused on drugs to improve ventricular function, there is increasing evidence that therapeutic modulation of neurohumoral activation is a key to successful treatment of heart failure. For example, there is mounting evidence that angiotensin converting enzyme inhibitors (the unquestioned cornerstone for treatment of heart failure), beta receptor blockers, digitalis, and endurance exercise training exert their benefit in heart failure in large part through neurohumoral modulation. This observation--discussed in this brief review--highlights the concept that compensatory neurohumoral activation to decreased cardiac function may itself contribute to the development of heart failure and its poor prognosis.

Topics: Adrenergic beta-Antagonists; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Clinical Trials as Topic; Digoxin; Exercise Therapy; Heart Failure; Humans; Myocardial Infarction; Neurotransmitter Agents; Sympathetic Nervous System; Ventricular Dysfunction, Left

Even at rest, blood pressure and heart fluctuate continuously around their mean values. Considerable interest has recently focused on the assessment of spontaneous in fluctuations in heart rate and blood pressure, i.e., heart rate and blood pressure variability, using time or frequency domain indexes. Heart rate variability has been extensively studied in cardiovascular disease and has emerged as a valuable parameter for detecting abnormalities in autonomic cardiovascular control, evaluating the prognosis and assessing the impact of drug therapy on the autonomic nervous system in patients with myocardial infarction, congestive heart failure or a heart transplant. In contrast, until the recent development of noninvasive methods for continuous blood pressure recording, blood pressure variability received little attention, and this parameter remains to be evaluated in cardiovascular disease.

Topics: Adrenergic beta-Antagonists; Animals; Autonomic Nervous System; Blood Pressure; Cardiotonic Agents; Digoxin; Dogs; Heart Failure; Heart Rate; Heart Transplantation; Humans; Myocardial Infarction; Signal Processing, Computer-Assisted; Vagus Nerve

Topics: Aged; Anti-Arrhythmia Agents; Atrial Fibrillation; Digoxin; Electric Countershock; Female; Humans; Myocardial Infarction; Quinidine

Topics: Animals; Cardiac Output, Low; Cardiotonic Agents; Cause of Death; Contraindications; Digoxin; Humans; Myocardial Infarction; Practice Patterns, Physicians'

Monoclonal antibody technology has resulted in an entirely new class of agents, which have been applied to a variety of problems in cardiology and which hold great promise for future diagnostic, as well as therapeutic, applications. The four antibodies, which have been most widely used in clinical cardiology, are Digibind, OKT3, Myoscint, and 7E3. Each demonstrates the unique potential for the use of antibodies in clinical cardiology.

Topics: Antibodies; Antibodies, Monoclonal; Blood Platelets; Digoxin; Graft Rejection; Heart Diseases; Heart Transplantation; Humans; Muromonab-CD3; Myocardial Infarction; Myocarditis; Myosins; Radionuclide Imaging; Receptors, Antigen, T-Cell

Although digitalis preparations have been in use for greater than 200 years, it is only within the last 2 decades that the central hemodynamic and neurohumoral effects occurring over several hours following intravenous administration of digoxin have been investigated in patients with congestive heart failure (CHF). Although digoxin has been shown to stimulate myocardial contractility in tissue preparations, its positive inotropic activity does not consistently translate into improvements in hemodynamic measurements in humans. Digoxin given intravenously results in increased cardiac index and decreased heart rate, left ventricular filling pressure, and right atrial pressure, as well as in acute attenuation of neurohumoral abnormalities, in patients with chronic CHF who have abnormal baseline hemodynamic measurements. Unlike other drugs with positive inotropic activity, however, digoxin does not influence hemodynamics in normal volunteers or in CHF patients in whom hemodynamics have been normalized with other therapies. These differing effects may be related to the drug's diverse peripheral vascular effects in CHF patients in whom vasodilation may occur in comparison with those that occur in normal subjects in whom the peripheral vasoconstrictor effects may prevent the inotropic effects of the drug from being translated into an increase in cardiac output. The hemodynamic effects of digoxin in patients with chronic CHF due primarily to diastolic dysfunction have not been fully investigated. Intravenous digoxin produces hemodynamic effects in patients with CHF associated with acute myocardial infarction, but these changes are small compared with those resulting from the administration of dobutamine. Digoxin does not appear to influence hemodynamic measurements in patients with right ventricular dysfunction unless concomitant left ventricular failure is present. In patients with chronic left ventricular dysfunction, the hemodynamic effects of intravenous digoxin and vasodilators are enhanced when these agents are given in combination.

Topics: Cardiotonic Agents; Digoxin; Drug Therapy, Combination; Heart Failure; Hemodynamics; Humans; Myocardial Infarction; Vasodilator Agents; Ventricular Function, Right

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Calcium Channel Blockers; Digoxin; Fibrinolytic Agents; Humans; Myocardial Infarction; Nitroglycerin; Nitroprusside; Platelet Aggregation Inhibitors; Recurrence

Topics: Animals; Digoxin; Humans; Myocardial Infarction; Time Factors

Topics: Animals; Atrial Fibrillation; Digitalis Glycosides; Digoxin; Heart Failure; Hemodynamics; Humans; Myocardial Infarction

Antibodies, long used as discriminating tools in immunoassay, are now being used in vivo, both in diagnosis and therapy. In cardiovascular medicine, applications that have reached the stage of clinical trial include the reversal of digitalis intoxication by digoxin-specific antibodies and the imaging of cardiac necrosis with monoclonal myosin-specific antibodies. An exciting future prospect, still in an early experimental stage, is the application of fibrin-specific monoclonal antibodies to both the visualization of thrombi and emboli and the targeting of fibrinolytic agents.

Topics: Adolescent; Adult; Animals; Antibodies, Monoclonal; Cells, Cultured; Child; Child, Preschool; Clinical Trials as Topic; Digoxin; Dogs; Fibrinolytic Agents; Heart Diseases; Humans; Immunoglobulin Fab Fragments; Infant; Male; Myocardial Infarction; Myocardium; Myosins; Necrosis; Rabbits; Thrombosis

Topics: Animals; Arrhythmias, Cardiac; Digitalis Glycosides; Digoxin; Drug Interactions; Drug Tolerance; Electric Countershock; Heart; Humans; Immunoglobulin Fab Fragments; Immunoglobulin G; Kinetics; Myocardial Infarction; Phenytoin; Potassium Chloride

Digitalis glycosides continue to place high on the list of prescribed drugs. Digoxin is 8th on prescriptions written in the United States in 1980, digitoxin 16th, and digitalis leaf 23rd. There is little doubt that most physicians continue to believe these drugs are useful. The application of more definite indications, smaller doses, and the recognition of the role of pharmacokinetics and drug interactions make use of the glycosides more challenging than ever before in 1985.

Topics: Administration, Oral; Adrenergic beta-Antagonists; Age Factors; Anti-Arrhythmia Agents; Antihypertensive Agents; Arrhythmias, Cardiac; Biological Availability; Bretylium Tosylate; Deslanoside; Digitalis Glycosides; Digitoxin; Digoxin; Dose-Response Relationship, Drug; Drug Interactions; Heart Failure; Humans; Injections, Intramuscular; Injections, Intravenous; Intestinal Absorption; Kidney Failure, Chronic; Lidocaine; Metabolic Clearance Rate; Myocardial Infarction; Obesity; Phenytoin; Potassium; Pulmonary Heart Disease; Thyroid Diseases

The principal causes of digitalis toxicity are overdose, reduced volume of distribution, reduced renal elimination, and increased myocardial sensitivity. The metabolic mechanism of digitalis toxicity is intense inhibition of sarcolemma Na-K ATPase, which leads to increases of intracellular Na+ and Ca2+ and arrhythmogenic membrane ionic currents. A variety of cellular electrophysiologic effects and effects on the nervous system are responsible for the array of clinical arrhythmias seen during digitalis toxicity, i.e., sinus bradycardia, atrioventricular block, nonparoxysmal atrioventricular junctional tachycardia, and ventricular tachycardia.

Topics: Arrhythmias, Cardiac; Digitalis Glycosides; Digoxin; Drug Interactions; Humans; Myocardial Infarction; Quinidine

Since the initial introduction of digitalis 200 years ago by Withering, its low therapeutic ratio has limited the use of this agent. The utility of digitalis in patients with congestive heart failure and a recent myocardial infarction has been questioned recently. Findings of rigorously controlled clinical studies suggest a small but definite hemodynamic and clinical improvement in patients administered digitalis. Congestive heart failure can be effectively treated without cardiac glycosides. However, when used judiciously, digitalis provides an additional agent in our therapeutic armamentarium. The inotropic, dormotropic, and vagomimetic properties are uniquely suited for the patient with supraventricular arrhythmias and compromised left ventricular function.

Topics: Digitalis Glycosides; Digoxin; Heart Failure; Humans; Myocardial Contraction; Myocardial Infarction

Topics: Acute Disease; Blood Pressure; Cardiac Complexes, Premature; Cardiotonic Agents; Chronic Disease; Digoxin; Diuretics; Dobutamine; Heart Failure; Hemodynamics; Humans; Isoproterenol; Myocardial Infarction

Topics: Animals; Anti-Mullerian Hormone; Antibodies, Monoclonal; Antibody Affinity; Antibody Specificity; Cardiac Glycosides; Digoxin; Epitopes; Glycoproteins; Growth Inhibitors; Humans; Hybridomas; Male; Myocardial Infarction; Myosins; Radioimmunoassay; Testicular Hormones; Testis; Thyrotropin

Topics: Animals; Antibodies; Antibody Specificity; Chemistry, Pharmaceutical; Digoxin; Forecasting; Humans; Immune Sera; Immunization, Passive; Myocardial Infarction; Radionuclide Imaging; Receptors, Drug; Renin; Structure-Activity Relationship

Topics: Arrhythmias, Cardiac; Blood Pressure; Creatine Kinase; Digitalis Glycosides; Digitoxin; Digoxin; Diuretics; Heart Failure; Humans; Myocardial Contraction; Myocardial Infarction; Oxygen Consumption

Topics: Catecholamines; Digoxin; Dobutamine; Dopamine; Drug Therapy, Combination; Heart Failure; Hemodynamics; Humans; Myocardial Contraction; Myocardial Infarction; Nitroprusside; Oxygen Consumption

The more recent antiarrhythmic drugs sometimes with more complex action extend the therapeutic possibilities. In addition, numerous other substances are in clinical trial. An ideal antiarrhythmic agent with a reliable action, persistent effective levels, easily absorbable and with few side effects is not found among them. The indication for therapy in ventricular extrasystole is made on the grounds of an ominous ECG criteria and a presumed clinical threat. Controversial results of lidocaine therapy of acute mayocardial infarction are possibly due to pharmacokinetic factors. For "inhomogeneous repolarization" with increased tendency to ventricular fibrillation inducing drugs should be avoided. Malignant cardiac rhythm irregularities possible leading to sudden death require systemic therapeutical testing. In this case, combinations of antiarrhythmic drugs have the highest effectiveness.

Topics: Action Potentials; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Bretylium Compounds; Calcium; Cardiac Complexes, Premature; Digoxin; Disopyramide; Electrophysiology; Humans; Lidocaine; Mexiletine; Myocardial Infarction; Phenytoin; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Verapamil

Topics: Acute Disease; Digoxin; Diuretics; Heart; Hemodynamics; Humans; Hyaluronoglucosaminidase; Methylprednisolone; Myocardial Infarction; Propranolol; Vasodilator Agents

Topics: Angina Pectoris; Arrhythmias, Cardiac; Biological Availability; Cardiac Glycosides; Central Nervous System Diseases; Digitoxin; Digoxin; Endocrine System Diseases; Gastrointestinal Diseases; Heart Failure; Humans; Hypersensitivity; Hypertension; Intestinal Absorption; Myocardial Infarction; Preoperative Care

Topics: Adult; Cell Membrane Permeability; Digitalis Glycosides; Digoxin; Electrolytes; Heart; History, 19th Century; History, 20th Century; Humans; Kinetics; Magnesium; Middle Aged; Myocardial Infarction; Myocardium; Potassium; Preoperative Care; Sodium; Tritium

Topics: Cardiac Output; Catecholamines; Digitalis Glycosides; Digitoxin; Digoxin; Dopamine; Glucagon; Heart; Heart Failure; Humans; Isoproterenol; Myocardial Infarction; Norepinephrine

Topics: Anemia, Macrocytic; Anti-Arrhythmia Agents; Anticoagulants; Azathioprine; Chemical and Drug Induced Liver Injury; Cholelithiasis; Clofibrate; Colitis, Ulcerative; Dextrans; Digoxin; Drug Therapy; Fibrinolytic Agents; Halothane; Heparin; Hepatitis B Antigens; Humans; Hyperthyroidism; Iodine Isotopes; Leukemia; Myocardial Infarction; Platelet Adhesiveness; Pulmonary Embolism; Thrombosis; Venoms

For out-of-hospital cardiac arrest (OHCA) to be predicted and prevented, it is imperative the healthcare system has access to those vulnerable before the event occurs. We aimed to determine the extent of contact to the healthcare system before OHCA.. All patients in Denmark with a registered OHCA June 1, 2001-December 31, 2005 were matched on age and sex with 10 random controls from the entire Danish population. We estimated the association with OHCA by conditional logistic regression analyses, and we determined the proportion of patients in contact with the healthcare system before OHCA from hospital admissions or claimed prescriptions.. We identified 12,089 patients with an OHCA. Of these, 62% (7548) and 85% (10,312) were in contact with the healthcare system up to 30 days and 1 year before OHCA, respectively. Association with OHCA up to 30 days before the event pertained to myocardial infarction (odds ratio (OR)=6.4, 95% confidence interval (CI): 4.7-8.6)); heart failure (OR=5.1, CI: 4.1-6.3); ischemic heart disease (OR=1.9, CI: 1.6-2.4); and cardiac dysrhythmia (OR=1.8, CI: 1.4-2.2). Concomitant pharmacotherapy up to 30 days before OHCA with the strongest association was: corticosteroids (systemic) (OR=2.7, CI: 2.5-3.0), bronchial dilators (OR=2.5, CI: 2.3-2.7), anti-psychotic medication (OR=2.1, CI: 1.9-2.3), and digoxin (OR=2.1, CI: 2.0-2.3). Similar results were found for associations up to 1 year before OHCA.. Contrary to general belief, the majority of OHCA patients are in contact with the healthcare system shortly before OHCA.

Topics: Adrenal Cortex Hormones; Aged; Antipsychotic Agents; Arrhythmias, Cardiac; Bronchodilator Agents; Denmark; Digoxin; Female; Health Behavior; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Myocardial Ischemia; Out-of-Hospital Cardiac Arrest; Patient Admission; Regression Analysis

A comparative randomized clinical study was conducted to evaluate the diagnostic and prognostic value of the activation of proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1alpha, IL-2, IL-6, IL-8)] and the increased production of autoimmune complexes in the pathogenesis of chronic heart failure (CHF) in patients with coronary heart disease (CHD). The study included 47 patients with CHD who had a more than 6-month history of Q-forming myocardial infarction. The patients were randomized into 3 groups: 1) 21 patients with NYHA Functional Class (FC) II heart failure (HF); 2) 16 patients with FC III HF; and 3) 10 with FC IV HF. Basic therapy involved angiotensin-converting enzyme (ACE) inhibitors, nitrates, diuretics, beta-adrenoblockers; 27.6% received digoxin, disaggregatory agents. A study protocol involved the estimation of the parameters of EchCG, paired bicycle ergometric tests, 6-min walking test, ECG daily monitoring, the levels of proinflammatory cytokines in the serum and IgG autoantibodies to cardiolipin. The findings suggest that with the higher expression of autoimmune complexes, the activation of cytokines (primarily TNF-alpha, IL-1alpha, IL-2) plays an important role in the pathogenesis of CHF in patients with postinfarct cardiac dysfunction: the high activation of cytokines and the elevated level of autoimmune complexes are associated with moderate or severe NYHA FC II-IV HF, depressed left ventricular contractility (ejection fraction, 23-38%), low exercise tolerance, and cardiac remodeling.

Topics: Adrenergic beta-Antagonists; Adult; Angiotensin-Converting Enzyme Inhibitors; Antigen-Antibody Complex; Coronary Disease; Cytokines; Digoxin; Diuretics; Heart Failure; Humans; Middle Aged; Myocardial Infarction; Nitrates; Platelet Aggregation Inhibitors; Stroke Volume

Previous reports have yielded contradictory conclusions regarding the safety of digoxin therapy in patients with acute myocardial infarction. The purpose of our study was to determine whether digoxin therapy is associated with increased mortality in patients with chronic coronary artery disease. We analyzed data from 8173 patients who were screened for participation in the Bezafibrate Infarction Prevention (BIP) trial and who survived an acute myocardial infarction at least 6 months prior to the study. Three-year overall mortality of the 451 (15.5%) patients receiving digoxin (according to the judgement of their treating physician) at the time of screening for BIP participation, was 22.4% compared to 8.3% in the patients who did not receive digoxin. Cardiac mortality was 16.2% in the digoxin-treated group, compared to 4.9% in the non-treated patients. The increased risk associated with digoxin remained statistically significant when patients were stratified according to sex, age groups, functional capacity and the presence of hypertension, diabetes or angina. The administration of digoxin to survivors of an acute myocardial infarction in the chronic phase of their disease, is statistically associated with a 30-50% increase in the risk of overall and cardiac mortality during long-term follow-up. A propensity of increased risk of arrhythmias in ischemic coronary patients may explain this finding.

Topics: Cardiotonic Agents; Chronic Disease; Digoxin; Female; Follow-Up Studies; Humans; Israel; Male; Middle Aged; Myocardial Infarction; Odds Ratio; Retrospective Studies; Risk Factors; Survival Rate

We examined clinical outcomes associated with non-randomised digoxin therapy in a postmyocardial infarction population with clinical heart failure (AIRE study). Our results raise concern about the safety of digoxin in this population.

Topics: Adult; Cardiotonic Agents; Digoxin; Female; Follow-Up Studies; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Product Surveillance, Postmarketing; Tachycardia, Ventricular; Treatment Outcome

Controversy surrounds the safety of digoxin use in patients recovering from acute myocardial infarction. Previous observations yielded contradictory conclusions. To determine whether digoxin therapy is associated with increased mortality in patients recovering from acute myocardial infarction, we analyzed data from 1731 survivors of acute myocardial infarction enrolled in the Secondary Prevention Reinfarction Israeli Nifedipine Trial (SPRINT), from which patients with severe heart failure were excluded. At the time of hospital discharge, 175 patients (10%) were taking digoxin. Mortality over 1 year after infarction was significantly higher in patients treated with digoxin than in patients who were not receiving digoxin [27 of 175 (15%) vs. 60 of 1556 (4%); p < 0.0001]. Digoxin administration was associated with increased mortality in several subsets of patients. Since patients treated with digoxin had baseline characteristics predictive of mortality more frequently than their counterparts, we adjusted for these differences. Multivariate analysis performed by the Cox proportional hazards model identified treatment with digoxin as an independent determinant associated with increased death during the first year after myocardial infarction [relative risk (RR) 2.8; 90% confidence interval (CI) 1.8-4.2]. Subgroup multivariate analysis indicated digoxin as an independent predictor of first year death in 464 patients who developed heart failure during their hospital stay (RR 2.3; 90% CI 1.3-4.0), as well as among 1267 patients who did not (RR 3.4; 90% CI 1.7-6.9). The present study suggests a significant excess mortality associated with digoxin therapy after myocardial infarction. The increased mortality risk may be related to unidentified variables associated with the severity of disease in patients treated with digoxin. However, our findings raise concern that the administration of digoxin may contribute to increased mortality in survivors of acute myocardial infarction.

Topics: Acute Disease; Adrenergic beta-Antagonists; Aged; Arrhythmias, Cardiac; Cardiotonic Agents; Digoxin; Double-Blind Method; Electrocardiography, Ambulatory; Female; Humans; Israel; Male; Middle Aged; Myocardial Infarction; Regression Analysis; Risk; Survivors

We conducted a prospective, double-blind, placebo-controlled multicenter trial in order to evaluate the long-term effects of captopril (50 mg/day), digoxin (0.25 mg/day) and placebo on quality of life, cardiovascular events, clinical symptoms and exercise tolerance in patients with documented myocardial infarction, resulting in regional wall motion abnormalities, and with mild heart failure (NYHA class II to III without treatment) and exercise not limited by angina. 222 patients were studied, 63 were randomized to captopril, 66 to digoxin, 67 to placebo. Follow-up was conducted for two years. Base line characteristics in the three treatment groups were similar. After one year of therapy, digoxin had significantly improved general well-being (p < 0.01 vs captopril), symptom score (p < 0.05 vs captopril and placebo), and vitality (p < 0.05 vs captopril). Digoxin improved NYHA class in 45% as compared to placebo (28%, p < 0.05). Worsening of angina was more frequent with captopril as compared to digoxin (p < 0.05). However, cardiovascular events during follow-up were lower in the captopril group as compared to placebo and digoxin (p < 0.01 captopril vs placebo). No differences between groups were observed in baseline and follow-up exercise tolerance between the three groups. Dizziness during upright tilt and cough were more frequent with captopril as compared to digoxin or placebo. After two years of follow-up (captopril n = 32, digoxin n = 29, placebo n = 27) general well-being was improved with both digoxin and captopril (p < 0.004 and p < 0.03 vs placebo).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Angina Pectoris; Captopril; Coronary Disease; Digoxin; Double-Blind Method; Drug Therapy, Combination; Exercise Test; Female; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Nitroglycerin; Prospective Studies; Quality of Life; Survival Rate

The efficacy of captopril (capoten) and digoxin was comparatively studied in long-term randomized, double blind trials of 22 male patients with postinfarction cardiosclerosis, functional classes I-III and preserved sinus rhythm. The optimal doses of the drugs proved to be small (0.31 and 35 mg/day of digoxin and capoten, respectively). No adverse effects were noted. The mortality rate was 10 and 16.7% with digoxin and captopril, respectively. The drugs equally improved the functional class by 0.51 and 0.45 and VO2 max by 1.5 and 1.7 ml/min. Digoxin had a mild effect on heart rate (-8.4%) and ejection fraction (+5.7%) and deteriorated diastolic relaxation, by slowing down the early peak of transmitral Doppler spectrum by 16.2%. Captopril significantly improved diastolic function by increasing the early peak by 17.2%. No significant changes in left ventricular sizes were recorded. The clinical efficacy of captopril was explained by a significant decrease in angiotension II (70%) and norepinephrine (40%) levels and by associated normalization of baroreflex regulation. Digoxin insignificantly affected the levels of angiotensin II and norepinephrine, but improved the baroreceptor regulation of sympathetic control impaired in chronic heart failure. It is concluded that extracardiac mechanisms play a major role in the action of not only captopril, but digoxin in the treatment of patients with postinfarct cardiosclerosis and chronic heart failure with sinus rhythm.

Topics: Adult; Aged; Angiotensin II; Baroreflex; Captopril; Cardiac Output, Low; Chronic Disease; Digoxin; Double-Blind Method; Heart Rate; Humans; Male; Middle Aged; Myocardial Infarction; Myocardium; Norepinephrine; Sclerosis; Stroke Volume; Time Factors

The effects of captopril and digoxin treatment on left ventricular remodeling and function after anterior myocardial infarction were evaluated in a randomized unblinded trial. Fifty-two patients with a first transmural anterior myocardial infarction and a radionuclide left ventricular ejection fraction less than 40% were randomly assigned to treatment with captopril (Group A) or digoxin (Group B). The two groups had similar baseline hemodynamic, coronary angiographic, echocardiographic and radionuclide angiographic variables. Among the 40 patients (20 in each group) who were followed up for 1 year, echocardiographic end-diastolic and end-systolic volumes were unmodified in Group A and global wall motion index was improved (p less than 0.01); in Group B, end-diastolic and end-systolic volumes increased (p less than 0.001 for both) and global wall motion index was unchanged. Rest radionuclide ejection fraction increased significantly in both groups (p less than 0.001, Group A; p less than 0.005, Group B). A comparison of the changes in the considered variables between the two groups after 1 year of treatment showed a difference in end-diastolic (p less than 0.005) end-systolic volumes (p less than 0.001) and global wall motion index (p less than 0.005) without differences in radionuclide ejection fraction, which improved to a similar degree in both groups. The results of this study suggest that captopril therapy, started 7 to 10 days after symptom onset in patients with anterior myocardial infarction and an ejection fraction less than 40%, improves both left ventricular remodeling and function and prevents left ventricular enlargement and in these patients performs better than digitalis.

Topics: Captopril; Cardiomegaly; Digoxin; Echocardiography; Female; Follow-Up Studies; Gated Blood-Pool Imaging; Humans; Male; Middle Aged; Myocardial Infarction; Stroke Volume; Time Factors; Ventricular Function, Left

Topics: Amiodarone; Atrial Fibrillation; Benzofurans; Digoxin; Humans; Myocardial Infarction

Recent studies have led to controversy about whether long-term digoxin therapy after confirmed or suspected myocardial infarction increases mortality. We analyzed the mortality experience in 903 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size (MILIS). As in previous studies, the decision to treat or not to treat with digoxin was made by the patient's personal physician on the basis of the usual clinical indications. Cumulative mortality was 28 percent for the 281 digoxin-treated patients as compared with 11 percent for the 622 patients who did not receive digoxin (P less than 0.001; follow-up interval, six days to 36 months; mean, 25.1 months). However, patients treated with digoxin had more base-line characteristics predictive of mortality than did their counterparts. Adjustment for these differences with two separate applications of the Cox method yielded P values of 0.14 and 0.34 for tests of difference in mortality, providing no evidence for a significant excess mortality associated with digoxin. Thus, the findings in the MILIS population do not support the assertion that digoxin therapy is excessively hazardous after infarction, but the existence of an undetected harmful effect can only be excluded with a randomized study. Until the results of such a study are available, we recommend careful consideration of whether any treatment of ventricular dysfunction is actually needed, consideration of alternatives to digoxin therapy, and restriction of digoxin use to the subgroup of patients (with severe chronic congestive failure and a dilated left ventricle) previously shown to have a beneficial clinical response.

Topics: Clinical Trials as Topic; Digoxin; Humans; Myocardial Infarction; Regression Analysis; Risk; Tachycardia

Antibodies, long used as discriminating tools in immunoassay, are now being used in vivo, both in diagnosis and therapy. In cardiovascular medicine, applications that have reached the stage of clinical trial include the reversal of digitalis intoxication by digoxin-specific antibodies and the imaging of cardiac necrosis with monoclonal myosin-specific antibodies. An exciting future prospect, still in an early experimental stage, is the application of fibrin-specific monoclonal antibodies to both the visualization of thrombi and emboli and the targeting of fibrinolytic agents.

Topics: Adolescent; Adult; Animals; Antibodies, Monoclonal; Cells, Cultured; Child; Child, Preschool; Clinical Trials as Topic; Digoxin; Dogs; Fibrinolytic Agents; Heart Diseases; Humans; Immunoglobulin Fab Fragments; Infant; Male; Myocardial Infarction; Myocardium; Myosins; Necrosis; Rabbits; Thrombosis

This study compares the effects of digoxin, placebo and ibopamine (SB-7505), the orally active 3,4-diisobutyryl ester of N-methyl-dopamine, on exercise tolerance and cardiac rhythm of 14 patients whose left ventricular heart failure (end-diastolic pressure, 26.3 +/- 5.9 mmHg; ejection fraction, 0.42 +/- 0.10%) depended on a previous myocardial infarction. Patients were admitted to the study while on chronic oral digoxin treatment (serum levels between 1.1 and 1.9 ng/ml). Placebo instead of digoxin was given for the following month. Thereafter ibopamine 50 mg t.i.d. for one month was given. A sequence of one-month treatments with digoxin, placebo and ibopamine was repeated, then ibopamine was administered continuously for the next two months. The concurrent treatment (diuretics in all patients, nitroderivates in twelve, calcium antagonists in two) remained unchanged during the observation period. Symptoms-limited exercise tests and 24-h Holter recordings were obtained at admission, at the end of each one-month treatment and at the end of the observation period. Two patients developed unstable angina without increase of serum creatine phosphokinase while on ibopamine and were withdrawn. Out of the 12 patients that concluded the trial, one required supplementary doses of diuretic at the end of the second period on placebo. The results obtained during the trial suggest that: a) therapeutic plasma levels of digoxin have no deleterious effect on cardiac rhythm nor significantly increase exercise tolerance as compared with placebo; b) diuretics and nitrates appear to sustain the clinical stability of these patients as a group.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Arrhythmias, Cardiac; Cardiotonic Agents; Deoxyepinephrine; Digoxin; Dopamine; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Myocardial Infarction; Physical Exertion

Hemodynamic effects of digoxin in acute myocardial infarction (AMI) have been acknowledged to depend on the basal cardiocirculatory state. In the present study, the effects of digoxin in patients with AMI were evaluated in four hemodynamic subsets, based on the relationship between mean pulmonary capillary wedge pressure (PCWP, in mm Hg) and left ventricular stroke work index (LVSWI, in g-m/m2): subset 1: normal (less than or equal to 15 mm Hg) PCWP and normal (greater than or equal to 35 g-m/m2) LVSWI; subset 2: elevated (greater than 15 mm Hg) PCWP and normal LVSWI; subset 3: reduced (less than 35 g-m/m2) LVSWI and normal PCWP; and subset 4: elevated PCWP and LVSWI moderately reduced to a range between 16 and 34 g-m/m2. Forty patients were admitted to the study and were randomly assigned to one of two groups in each subset: control group (19 patients) and treated group (21 patients). Five patients were randomized into each of the subsets 2, 3, and 4 in both the control and treated groups, while in subset 1 there were four control and six digoxin-treated patients. Control patients were administered a placebo saline solution and digoxin-treated patients received 0.50 mg of the drug intravenously in 20 minutes. The effects of the placebo and of the drug were evaluated at 30, 60, and 90 minutes from the end of the infusion. Hemodynamic data did not vary in the control group, and digoxin did not exert any relevant effect in subsets 1 and 2. After drug infusion, cardiac index (Cl, in L/min/m2) significantly increased in subset 3 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Clinical Trials as Topic; Digoxin; Electrocardiography; Female; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Pulmonary Wedge Pressure; Random Allocation; Stroke Volume; Vascular Resistance

In order to verify the usefulness of long-term digitalis therapy during physical rehabilitation in patients with recent myocardial infarction (MI) and left ventricular disfunction during exercise, 24 consecutive pts with PAedP greater than or equal to 25 mmHg (Swan-Ganz cath.) at maximal work load were selected. Pts with angina, ST depression (greater than or equal to 2 mm), complex ventricular arrhythmias (Lown 4-5), symptoms of left ventricular failure were excluded. At random 12 pts were assigned to group A (digoxin therapy) and 12 to group B (no therapy). Serum digoxin level was on average 1.48 ng/ml (range 1-2.85 ng/ml). Both groups performed over 4 weeks the same controlled training program. Before and soon after the end of the training period all pts underwent to an exercise test, standard chest x-ray films, 24 hour ambulatory ECG and two-dimensional echocardiography. No complication was observed during exercise test and training period. Age, myocardial infarction location, cardiac volume and hemodynamic behaviour during the first exercise test were similar in both groups. After training, maximal work capacity was increased in group A by 14% and in group B by 16% without significant changes in PAedP and Cl; at the same work load PAedP was lower in group B (-12%, p less than .02) while LVSWI was increased in both groups (14% and 17% respectively, p less than .05). No significant changes in cardiac volume, left ventricular asynergy, EF, and ventricular premature beats were observed. QT interval at rest decreased significantly only in group A 408 +/- 31 msec vs 371 +/- 34 msec (p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Digoxin; Echocardiography; Exercise Test; Hemodynamics; Humans; Male; Myocardial Infarction; Physical Education and Training

Topics: Administration, Oral; Aged; Alprenolol; Arrhythmias, Cardiac; Blood Pressure; Clinical Trials as Topic; Digoxin; Diuretics; Drug Therapy, Combination; Heart Failure; Heart Rate; Humans; Injections, Intravenous; Middle Aged; Myocardial Infarction; Random Allocation; Time Factors

Topics: Adolescent; Adult; Coronary Disease; Digoxin; Female; Heart Aneurysm; Heart Failure; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Nitroglycerin; Propranolol; Radionuclide Imaging; Technetium; Theophylline; Verapamil

In order to compare the effectiveness of different therapeutic regimens in reducing infarct size serial determinations of CPK activity (at 4 hourly intervals in the first 48 hours from the admission to CCU, at the 72th and at 120th hours) were performed in 100 patients with transmural AMI (53 anterior and 47 inferior) with no obvious evidence of LV failure and basal CPK levels lower than 50 U/L. 20 patients (control group) have been treated with glucose-insulin-potassium (GIK). 20 patients have been treated with GIK plus Verapamil (GIK + V). Verapamil was administered at the dose of 50 mg in continuous drip. 20 patients received GIK plus digoxin at the dose of 0.25 mg b.i.d. (GIK + D). 40 patients received GIK, Verapamil and digoxin at the above doses (GIK + V + D). Different values of CKr and infarct size (IS.) show a statistically significant difference between the various regimens, which is more evident if we consider the whole series. Infarct size was greater in patients treated with digoxin with respect to controls, while it was smaller in patients treated with Verapamil. Combined Verapamil-digoxin therapy is associated to an enzymatic behaviour not different from controls. Authors emphasize that in uncomplicated AMI digoxin causes an increase in infarct size while Verapamil reduces significantly it. Association of Verapamil allows the use of digoxin, if clinically justified, without increase in infarct size.

Topics: Adult; Aged; Clinical Enzyme Tests; Creatine Kinase; Digoxin; Female; Glucose; Humans; Insulin; Male; Middle Aged; Myocardial Infarction; Myocardium; Necrosis; Potassium; Verapamil

Discontinuation of digoxin in 56 patients with sinus rhythm who had been taking it for a long time did not produce clinical deterioration in 33 of 34 patients whose pre-withdrawal steady-state plasma-digoxin concentration was less than 0.8 ng/ml; fast atrial fibrillation developed in the other patient. 22 patients had plasma-digoxin levels between 0.8 and 2.0 ng/ml before withdrawal--of these, 7 deteriorated without digoxin (5 had atrial fibrillation, which was associated with congestive heart-failure, measurement of the pre-injection period/left-ventricular ejection time (P.E.P./L.V.E.T.) ratio suggested that digoxin did exert a sustained positive inotropic effect. Thus, successful discontinuation of digoxin was possible in 86% of the total group and was more likely when the plasma-digoxin concentration was below 0.8 ng/ml. Unexpected atrial fibrillation was the commonest development inthe 8 patients in whom digoxin withdrawal was unsuccessful.

Topics: Adult; Aged; Atrial Fibrillation; Clinical Trials as Topic; Digoxin; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Stimulation, Chemical; Substance Withdrawal Syndrome; Tachycardia

The effect of nitroglycerin, digoxin and inderal on myocardial asynergy was studied in 108 patients with ischemic heart disease by means of echocardiography. The effect of nitroglycerin was studied in 32 patients; myocardial contractions were restored in the areas of asynergy in 15 patients, in 17 the character of myocardial asynergy did not change. The effect of digoxin was studied in 42 patients; intensification of myocardial contractions in the asynergic areas was noted in 18 patients in 16 the character of asynergy of the myocardium did not change, and in 8 paradoxical protrusion of the cardiac wall increased. Prescription of inderal for 34 patients did not lead to the development of additional areas of myocardial asynergy; proportionate decrease of the amplitude of the systolic myocardial movement in healthy areas and in areas with hypo-and dyskinesia was noted in such cases. The study showed changeability of the character of myocardial asynergy under the effect of the drugs investigated, which should be taken into account when these drugs are given to patients with ischemic heart disease.

Topics: Adult; Aged; Angina Pectoris; Clinical Trials as Topic; Coronary Disease; Digoxin; Drug Evaluation; Echocardiography; Female; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Nitroglycerin; Propranolol

The effects of maintenance oral digoxin therapy on segmental left ventricular wall motion (wall motion videotracking) and left heart size (radiographic left heart dimension) were evaluated in 14 patients with a prior myocardial infarction but without clinical signs or symptoms of congestive heart failure. The left heart dimension decreased in all six patients with cardiomegaly from an average of 55.0 +/- 1.6 (standard deviation) to 52.2 +/- 2.7 mm/m2 body surface area (P less than 0.01) during digoxin therapy. However, there was no significant change in the eight patients with normal heart size. In the resting state, the average extent of shortening in normal segments increased significantly from 3.1 +/- 0.8 to 4.2 +/- 1.2 mm during digoxin therapy. During submaximal handgrip exercise, the extent of shortening averaged 4.0 +/- 1.3 mm and increased further with digoxin therapy to 5.1 +/- 2.1 mm. The effects of digoxin therapy on the maximal velocity of shortening in normal segments at rest and during handgrip exercise were similar. In all 14 patients, there was a decrease in the number of segments with abnormal wall motion at rest or with handgrip exercise during digoxin therapy. With therapy, the number of abnormal sites decreased from 52 to 35 in the resting state and from 84 to 49 during handgrip exercise. Thus, in patients 6 or more months after transmural myocardial infarction, orally administered digoxin decreases cardiomegaly, increases the extent and maximal velocity of shortening in normal left ventricular segments and often reduces the extent of abnormal wall motion at rest or during isometric exercise.

Topics: Administration, Oral; Adult; Aged; Blood Pressure; Cardiomegaly; Clinical Trials as Topic; Digoxin; Female; Heart; Heart Rate; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Physical Exertion

Patients with acute myocardial infarction were allocated to two groups according to a double blind-system of radomization. The patients (n = 18) in one of the groups received digoxin intravenously as an injection of 0.01 mg. per kilogram of body weight during 10 minutes. The patients in the other group (n = 15) received saline and served as controls. A continuous ECG record was obtained from each patient during 1 hour preceding the administration of digoxin or saline and was continued for 3 hours following the injection. No antiarrhythmic treatment was given during the time of the study. Based on the continuous ECG, calculations were made of the relative incidence of patients with different types of ventricular tachyarrhythmias during the period of observation as well as the percentage of arrhythmia-containing 1 minute intervals observed during this period. There was no statistical difference between the incidence of ventricular tachyarrhythmias in the two groups in the 1 hour period preceding drug injection. The administration of digoxin and saline did not change the incidence of ventricular tachyarrhythmias and there was also no statistically significant difference between the two groups as regards the incidence of patients showing different types of ventricular tachyarrhythmias during the 3 hour period following drug administration, Considering the 1-minute intervals, those without any ventricular premature contractions were less in the digoxin group (92 per cent) than in the saline group (88 per cent; p less than 0.001). Serum levels of digoxin at the end of the observation period were well above what is considered the minimum therapeutic level and in three patients the level approached or reached the toxic range. In these three patients there was still no increased incidence of ventricular tachyarrhythmias. It is concluded that patients with acute myocardial infarction complicated by incipient left ventricular failure do not show an increased sensitivity to an ordinary dose of digoxin as measured by the occurrence of ventricular tachyarrhythmia.

Topics: Acute Disease; Adult; Aged; Blood Pressure; Clinical Trials as Topic; Digoxin; Dose-Response Relationship, Drug; Electrocardiography; Female; Heart Failure; Heart Rate; Humans; Infusions, Parenteral; Male; Middle Aged; Myocardial Infarction; Tachycardia

Intramuscular injections of digoxin, bumetanide, pentazocine or isotonic sodium chloride have been given to 39 patients. We followed the serum concentrations of creatine kinase (CK), aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH) and LDH isoenzymes for 4 days. Ten patients receiving 500 mug digoxin showed a significant rise in CK, which lasted for 48 hours, and 6 of them had CK values exceeding the upper normal limit. Pentazocine in a dose of 30 mg given to 9 patients caused a significant rise in CK and LDH isoenzyme 1, but in no case did the level exceed the upper normal limit. No rise in ASAT or total LDH was found after digoxin and pentazocine injections. No changes in enzymes were discovered after bumetanide or isotonic sodium chloride. In the diagnostic evaluation of acute myocardial infarction, a moderate rise in CK must be assessed with caution when the patients have received i.m. injections of drugs with osmolarity and pH outside the physiological limits.

Topics: Aspartate Aminotransferases; Bumetanide; Creatine Kinase; Digoxin; Diuretics; Humans; Injections, Intramuscular; Isoenzymes; L-Lactate Dehydrogenase; Myocardial Infarction; Pentazocine; Sodium Chloride

Left ventricular function was investigated at rest and during exercise by heart catheterization in 15 patients 3-5 months after acute myocardial infarction. The effect of 1 mg digoxin i.v. in ten patients was correlated to placebo (saline solution) in five patients. A significant decrease of the left ventricular enddiastolic pressure, increase of left ventricular systolic ejection fraction and a shift of the left ventricular function curve to left upwards was found after digoxin with no changes in the placebo group. This beneficial effect of acute digitalization in patients convalescing from uncomplicated myocardial infarction without clinical signs of manifest heart failure could have therapeutic implication.

Topics: Acute Disease; Adult; Aged; Blood Pressure; Cardiac Output; Clinical Trials as Topic; Digoxin; Drug Evaluation; Heart Rate; Heart Ventricles; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Physical Exertion

Haemodynamic changes after intravenous administration of 0.4 mg beta-methyldigoxin or 0.4 mg digoxin daily were measured on the first to fourth day in 42 patients in heart failure after onset of transmural myocardial infarction. Regular reduction in filling pressure and increased stroke volume while arterial blood pressure remained unaltered pointed to improved contractility. Digitalization in the first few days after infarction achieved sustained tendency towards improved haemodynamics. It is concluded that early digitalization is indicated in patients with acute myocardial infarction if there are signs of heart failure.

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Time Factors

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Berlin; Digoxin; Heart Block; Heart Failure; Humans; Myocardial Infarction; Myocardium; Oxygen Consumption; Tachycardia; Ventricular Fibrillation

Topics: Adult; Aged; Angina Pectoris; Blood Pressure; Clinical Trials as Topic; Coronary Disease; Digoxin; Electrocardiography; Female; Heart Rate; Humans; Hypertension; Hypnotics and Sedatives; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Placebos; Respiration; Vasodilator Agents

Topics: Acute Disease; Adult; Aged; Blood Pressure; Blood Volume; Cardiac Output; Digoxin; Electrocardiography; Female; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Vascular Resistance

Topics: Aged; Bradycardia; Clinical Trials as Topic; Digoxin; Female; Heart Diseases; Heart Valve Diseases; Humans; Hypertension; Male; Middle Aged; Myocardial Infarction; Pulmonary Edema; Pulmonary Heart Disease; Sclerosis

Digoxin is used for rate control in atrial fibrillation (AF), but evidence for its efficacy and safety after myocardial infarction (MI) is scarce and mixed. We studied post-MI digoxin use effects on AF patient outcomes in a nationwide registry follow-up study in Finland. Digoxin was used by 18.6% of AF patients after MI, with a decreasing usage trend during 2004-2014. Baseline differences in digoxin users (n = 881) and controls (n = 3898) were balanced with inverse probability of treatment weight adjustment. The median follow-up was 7.4 years. Patients using digoxin after MI had a higher cumulative all-cause mortality (77.4% vs. 72.3%; hazard ratio [HR]: 1.19; confidence interval [CI]: 1.07-1.32; p = 0.001) during a 10-year follow-up. Mortality differences were detected in a subgroup analysis of patients without baseline heart failure (HF) (HR: 1.23; p = 0.019) but not in patients with baseline HF (HR: 1.05; p = 0.413). Cumulative incidences of HF hospitalizations, stroke and new MI were similar between digoxin group and controls. In conclusion, digoxin use after MI is associated with increased mortality but not with HF hospitalizations, new MI or stroke in AF patients. Increased mortality was detected in patients without baseline HF. Results suggest caution with digoxin after MI in AF patients, especially in the absence of HF.

Topics: Anti-Arrhythmia Agents; Atrial Fibrillation; Digoxin; Follow-Up Studies; Heart Failure; Humans; Myocardial Infarction; Risk Factors; Stroke

Topics: Digoxin; Disease Progression; Drug-Related Side Effects and Adverse Reactions; Humans; Myocardial Infarction; Phenytoin; Tachycardia

To determine the prognosis of Takayasu arteritis (TA) patients with moderate-to-severe aortic regurgitation treated with surgical vs conservative treatment and to identify independent prognostic factors of long-term outcomes.. Between January 2002 and January 2017, 101 consecutive TA patients with moderate-to-severe aortic regurgitation treated with either surgical (n = 38) or conservative (n = 63) treatments were investigated in this retrospective observational case-control study. The primary end point was all-cause mortality, and the secondary end point comprised the combined end points of death, non-fatal stroke and cardiac events (non-fatal myocardial infarction and congestive heart failure). Propensity score matching was used to reduce the bias of baseline risk factors.. The unadjusted all-cause 10-year mortality in the conservative group was increased compared with the surgical group (28.2% vs 7.4%; log-rank P = 0.036), and the combined end points showed the same trend (52.1% vs 25.3%; log-rank P = 0.005). After an adjustment of baseline risk factors, the conservative treatment was associated with reduced survival rates of both all-cause mortality [hazard ratio (HR): 8.243; 95% CI: 1.069, 63.552; P = 0.007] and combined end points (HR: 6.341; 95% CI: 1.469, 27.375; P = 0.002). Conservative treatment (HR: 3.838, 95% CI: 1.333, 11.053; P = 0.013) and left ventricular end-diastolic diameter (HR: 1.036, 95% CI: 1.001, 1.071; P = 0.042) were risk factors for increased combined end points.. Surgical treatment improves the outcomes of patients with moderate-to-severe aortic regurgitation due to TA. The dilated left ventricle indicated a worse prognosis.

Topics: Adrenergic beta-Antagonists; Adult; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Aorta; Aortic Valve Insufficiency; Calcium Channel Blockers; Cardiotonic Agents; Case-Control Studies; Cause of Death; Conservative Treatment; Digoxin; Female; Glucocorticoids; Heart Failure; Heart Valve Prosthesis Implantation; Humans; Immunosuppressive Agents; Male; Middle Aged; Mortality; Myocardial Infarction; Platelet Aggregation Inhibitors; Prednisone; Propensity Score; Retrospective Studies; Severity of Illness Index; Stroke; Takayasu Arteritis; Treatment Outcome

Ouabain preconditioning (OPC) initiated by low concentrations of the cardiac glycoside (CG) ouabain binding to Na/K-ATPase is relayed by a unique intracellular signaling and protects cardiac myocytes against ischemia/reperfusion injury. To explore more clinically applicable protocols based on CG properties, we tested whether the FDA-approved CG digoxin could trigger cardioprotective effects comparable with those of ouabain using PC, preconditioning and PostC, postconditioning protocols in the Langendorff-perfused mouse heart subjected to global ischemia and reperfusion. Ouabain or digoxin at 10 μmol/L inhibited Na/K-ATPase activity by approximately 30% and activated PKCε translocation by approximately 50%. Digoxin-induced PC (DigPC), initiated by a transient exposure before 40 minutes of ischemia, was as effective as OPC as suggested by the recovery of left ventricular developed pressure, end-diastolic pressure, and cardiac Na/K-ATPase activity after 30 minutes of reperfusion. DigPC also significantly decreased lactate dehydrogenase release and reduced infarct size, comparable with OPC. PostC protocols consisting of a single bolus injection of 100 nmoles of ouabain or digoxin in the coronary tree at the beginning of reperfusion both improved significantly the recovery of left ventricular developed pressure and decreased lactate dehydrogenase release, demonstrating a functional and structural protection comparable with the one provided by OPC. Given the unique signaling triggered by OPC, these results suggest that DigPostC could be considered for patients with risk factors and/or concurrent treatments that may limit effectiveness of ischemic PostC.

Topics: Animals; Cardiotonic Agents; Cell Death; Digoxin; Disease Models, Animal; Enzyme Inhibitors; Isolated Heart Preparation; Male; Mice, Inbred C57BL; Myocardial Contraction; Myocardial Infarction; Myocardial Reperfusion Injury; Myocytes, Cardiac; Ouabain; Protein Kinase C-epsilon; Recovery of Function; Signal Transduction; Sodium-Potassium-Exchanging ATPase; Ventricular Function, Left; Ventricular Pressure

The treatment of elderly multimorbid patients according to clinical guidelines often results in polypharmacy. An individual risk assessment is required to consider the possibility of deprescribing especially potentially inappropriate medication in the elderly. This exemplary case report describes a medication review of a patient with multiple chronic cardiovascular diseases taking into account the impact on renal function.

Topics: Aged, 80 and over; Atrial Fibrillation; Carbazoles; Carvedilol; Diclofenac; Digoxin; Drug Interactions; Drug Therapy, Combination; Female; Heart Failure; Humans; Hypertension; Kidney Failure, Chronic; Myocardial Infarction; Potassium; Potentially Inappropriate Medication List; Propanolamines; Ramipril; Risk Factors; Spironolactone

Ischemic-reperfusion (I/R) is a major event in the pathogenesis of ischemic heart disease that leads to higher rate of mortality. The study has been designed to investigate the therapeutic potential and molecular mechanism of vitamin P and digoxin in I/R-induced myocardial infarction in isolated rat heart preparation by using Langendorff apparatus. The animals were treated with vitamin P (50 and 100 mg/kg; p.o.) and digoxin (500 μg/kg) for 5 consecutive days. Digoxin served as a positive control in the present study. On the sixth day, the heart was harvested and induced to 30 min of global ischemia followed by 120 min of reperfusion using Langendorff apparatus. The coronary effluent was collected at different time intervals (i.e. basal, 1, 15, 30, 45, 60 and 120 min.) for the assessment of myocardial contractility function. In addition, creatine kinase-M and B subunits (CK-MB), lactate dehydrogenase (LDH1) and Na(+)-K(+)-ATPase activity along with oxidative tissue biomarkers (i.e. thio-barbituric acid reactive substances (TBARS) and reduced glutathione (GSH)) changes were estimated. The I/R of myocardium produced decrease in coronary flow rate; increase in CK-MB, LDH1 and Na(+)-K(+)-ATPase activity along with increase in TBARS and decrease in GSH levels as compared to normal group. The treatment with vitamin P (100 mg/kg) and digoxin (500 μg/kg) have produced a significant (p < 0.05) ameliorative effect against I/R induced above functional, metabolic and tissue biomarkers changes. Vitamin P has an ameliorative potential against I/R induced myocardial functional changes. It may be due to its free radical scavenging and anti-infarct property via inhibition of Na(+)-K(+)-ATPase activity. Therefore, it can be used as a potential therapeutic medicine for the management of cardiovascular disorders.

Topics: Animals; Cardiotonic Agents; Coronary Circulation; Digoxin; Disease Models, Animal; Dose-Response Relationship, Drug; Isolated Heart Preparation; Male; Myocardial Contraction; Myocardial Infarction; Myocardial Reperfusion Injury; Oxidative Stress; Rats, Sprague-Dawley; Rutin

Topics: Aged; Angiography; Anti-Arrhythmia Agents; Diagnostic Errors; Digoxin; Electrocardiography; Female; Humans; Myocardial Infarction

The commonly used cardiac glycoside, digoxin (DIG), has a narrow therapeutic window. Although some investigations were made to counteract its toxic effects, no alternate phytochemical is available till date that is more potent and safer than DIG.. Our main aim was to isolate a novel cardenolide from the seeds of Trigonella foenum graceium and to evaluate its relative potential in comparison to that of DIG.. In one experiment effects of the isolated compound at 2.5, 5.0, and 10 mg/kg (p.o.) were evaluated in isoproterenol (ISO)-induced cardiovascular problems in rats. As the test drug (TDR) reversed most of the ISO-induced changes, it was subjected to the phytochemical analyses and was identified as digoxigenin-3-O-rutin. In another experiment effects of DIG and rutin (Rtn) were compared with those of TDR or DIG alone. The hydroxyl radical scavenging activity was also measured by electron spin resonance (EPR).. digoxigenin-3-O-rutin at 10 mg/kg markedly reduced the ISO-induced increase in cardiac lipid peroxidation and in the levels of serum creatinine phosphokinase-MB, glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, and creatinine. It also reversed the ISO-induced changes in the cardiac histomorphology. Interestingly TDR appeared to be more effective than DIG alone or DIG and Rtn in combination.. The newly isolated digoxigenin-3-O-rutin appears to be more potent and safe than digoxin. Its higher efficacy could be due to its structural specificity and might have been mediated through its better free radical scavenging action.

Topics: Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Biomarkers; Cardiotonic Agents; Creatine; Creatine Kinase, MB Form; Digoxigenin; Digoxin; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Free Radical Scavengers; Hydroxyl Radical; Isoproterenol; L-Lactate Dehydrogenase; Lipid Peroxidation; Myocardial Infarction; Myocardium; Rats; Rats, Wistar; Rutin; Seeds; Trigonella

Oxidative damage and impaired cytosolic Ca(2+) concentration ([Ca(2+)](cyto)) handling are associated with mitochondrial [Ca(2+)] ([Ca(2+)](mito)) overload and depressed functional recovery after cardiac ischemia-reperfusion (I/R) injury. We hypothesized that hearts from old guinea pigs would demonstrate impaired [Ca(2+)](mito) handling, poor functional recovery, and a more oxidized state after I/R injury compared with hearts from young guinea pigs. Hearts from young (∼4 wk) and old (>52 wk) guinea pigs were isolated and perfused with Krebs-Ringer solution (2.1 mM Ca(2+) concentration at 37°C). Left ventricular pressure (LVP, mmHg) was measured with a balloon, and NADH, [Ca(2+)](mito) (nM), and [Ca(2+)](cyto) (nM) were measured by fluorescence with a fiber optic probe placed against the left ventricular free wall. After baseline (BL) measurements, hearts were subjected to 30 min global ischemia and 120 min reperfusion (REP). In old vs. young hearts we found: 1) percent infarct size was lower (27 ± 9 vs. 57 ± 2); 2) developed LVP (systolic-diastolic) was higher at 10 min (57 ± 11 vs. 29 ± 2) and 60 min (55 ± 10 vs. 32 ± 2) REP; 3) diastolic LVP was lower at 10 and 60 min REP (6 ± 3 vs. 29 ± 4 and 3 ± 3 vs. 21 ± 4 mmHg); 4) mean [Ca(2+)](cyto) was higher during ischemia (837 ± 39 vs. 541 ± 39), but [Ca(2+)](mito) was lower (545 ± 62 vs. 975 ± 38); 5) [Ca(2+)](mito) was lower at 10 and 60 min REP (129 ± 2 vs. 293 ± 23 and 122 ± 2 vs. 234 ± 15); 6) reduced inotropic responses to dopamine and digoxin; and 7) NADH was elevated during ischemia in both groups and lower than BL during REP. Contrary to our stated hypotheses, old hearts showed reduced [Ca(2+)](mito), decreased infarction, and improved basal mechanical function after I/R injury compared with young hearts; no differences were noted in redox state due to age. In this model, aging-associated protection may be linked to limited [Ca(2+)](mito) loading after I/R injury despite higher [Ca(2+)](cyto) load during ischemia in old vs. young hearts.

Topics: Aging; Animals; Calcium; Cardiotonic Agents; Coronary Circulation; Cytosol; Digoxin; Dopamine; Guinea Pigs; Mitochondria; Myocardial Contraction; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; NAD; Recovery of Function

We assessed, in patients with a first hospitalization for heart failure (HF), the temporal relationship of the incidence of cardiovascular events, all-cause mortality, and cardiovascular drug treatment.. Data were obtained from the PHARMO Record Linkage System, a population-based registry of pharmacy records linked with hospital discharge records in The Netherlands. Patients were selected based on a first hospital discharge diagnosis of documented HF. Two time-periods were compared: 1998-2002 and 2003-07. In each time-period, we analysed all prescribed cardiovascular medications, all-cause mortality, and cardiovascular events (rehospitalization for HF and ischaemic events) within the first year after hospitalization, and the occurrence of ischaemic events separately (myocardial infarction and ischaemic stroke). Cox-regression analysis was performed to calculate hazard ratios (HR) with 95% confidence intervals (CI). We identified 8276 patients in 1998-2002 and 9548 patients from 2003-07. There was an increase in almost all cardiovascular medication prescriptions in the second period: in particular, beta-blocker prescriptions rose from 36% in 1998-2002 to 55% in 2003-07. In the first year after hospitalization, there was no difference in all-cause mortality or any cardiovascular event (HR 1.00, 95%CI: 0.95-1.05), as a composite endpoint or when analysed separately. The incidence of ischaemic events decreased from 2.7 to 1.9% in the first and second time-period, respectively (HR 0.74, 95%CI: 0.61-0.90).. Prescription of cardiovascular medications in patients with a first hospitalization for HF has increased in recent years, particularly for beta-blockers, and the incidence of ischaemic events may have decreased. There was no decrease in all-cause mortality or cardiovascular events.

Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angina Pectoris; Angiotensin-Converting Enzyme Inhibitors; Cardiotonic Agents; Digoxin; Diuretics; Female; Heart Failure; Hospitalization; Humans; Male; Myocardial Infarction; Myocardial Ischemia; Practice Patterns, Physicians'; Prognosis; Spironolactone; Stroke

Cardiac electric therapies effectively terminate tachyarrhythmias. Recent data suggest a possible increase in long-term mortality associated with implantable cardioverter-defibrillator shocks. Little is known about the association between external cardioversion episodes (ECVe) and long-term mortality. We sought to assess the safety of repeated ECVe with regard to cardiovascular mortality and morbidity.. We analyzed the data of the 4060 patients from the AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial. In particular, associations of ECVe with all-cause mortality, cardiovascular mortality, and hospitalizations after ECVe were studied. Over an average follow-up of 3.5 years, 660 (16.3%) patients died, 331 (8.2%) from cardiovascular causes. A total of 207 (5.1%) and 1697 (41.8%) patients had low ejection fraction and nonparoxysmal atrial fibrillation, respectively; 2460 patients received no ECVe, whereas 1600 experienced ≥ 1 ECVe. Death occurred in 412 (16.7%), 196 (16.5%), 39 (13.5%), and 13 (10.4%) of patients with 0, 1, 2, and ≥ 3 ECVe, respectively. There was no significant association between ECVe and mortality within any of the 4 subgroups defined by ejection fraction and atrial fibrillation type, although myocardial infarction, coronary artery bypass graft, and digoxin were significantly associated with death (estimated hazard ratios, 1.65, 1.59, and 1.62, respectively; P < 0.0001). ECVe were associated with increased cardiac hospitalization reported at the next follow-up visit (39.3% versus 5.8%; estimated odds ratio, 1.39; P < 0.0001).. In the AFFIRM study, there was no significant association between ECVe and long-term mortality, even though ECVe were associated with increased hospitalizations from cardiac causes. Digoxin, myocardial infarction, and coronary artery bypass graft were significantly associated with mortality.

Topics: Anti-Arrhythmia Agents; Atrial Fibrillation; Coronary Artery Bypass; Defibrillators, Implantable; Digoxin; Electric Countershock; Follow-Up Studies; Hospitalization; Humans; Myocardial Infarction; Survival Rate

Topics: Adrenergic beta-Antagonists; Aged; Amiodarone; Atrial Fibrillation; Bisoprolol; Bradycardia; Calcium Channel Blockers; Cardiovascular Agents; Combined Modality Therapy; Digoxin; Diltiazem; Female; Humans; Hypothyroidism; Kidney Failure, Chronic; Myocardial Infarction; Pacemaker, Artificial; Renal Dialysis

Topics: Benzazepines; Cardiac Resynchronization Therapy; Cardiac Resynchronization Therapy Devices; Cardiovascular Agents; Digoxin; Diuretics; Echocardiography; Electrocardiography; Furosemide; Heart Atria; Heart Failure; Heart Rate; Heart Ventricles; Humans; Ivabradine; Male; Middle Aged; Myocardial Infarction; Spironolactone; Treatment Outcome

D.G. was a 59-year-old male patient who was retired and married, and had 3 children. He reported no psychopathology prior to a myocardial infarction he had in 1996. Following bypass surgery he had erectile dysfunction. Subsequently, gynecomastia developed as a side effect of spironolactone and digoxin treatment. After a long period of depression he claimed was caused by non-adaptation to the changes in his body, he realized differences about himself; he began to feel like a woman. Upon referral to our clinic, he said that he had decided to continue his life as a woman and wished to get pink colored (as opposed to blue for male) identity card issued by the Turkish Government for female Turkish citizens. He reported that his wish was to learn how to become a woman. This is the first case in the medical literature defined as sexual identity disorder secondary to a general medical condition. The case is discussed in terms of pathological grief reaction.

Topics: Bereavement; Depression; Digoxin; Erectile Dysfunction; Female; Gender Identity; Gynecomastia; Humans; Male; Middle Aged; Mineralocorticoid Receptor Antagonists; Myocardial Infarction; Spironolactone

Clinical autopsy rate have been declining since the 1950s, but it remains a useful investigation tool.. Through six examples of our experience, we underline its interest for clinical, didactic and public health purposes.. We try to understand the reasons for its decline and, as demonstrated, it can be attributed to a number of factors. These need to be addressed in order to reassert the status of the autopsy as an investigation and audit tool which is crucial to the future effectiveness of modern medicine.

Topics: Adult; Aged; Atherosclerosis; Atrial Fibrillation; Autopsy; Cardiotonic Agents; Casuistry; Cause of Death; Coronary Artery Disease; Coronary Thrombosis; Diagnosis, Differential; Digoxin; Education, Medical; Female; France; Hallucinations; Hospitals, University; Humans; Male; Marfan Syndrome; Meningitis, Listeria; Meningitis, Pneumococcal; Middle Aged; Myocardial Infarction

Little is presently known regarding whether a rhythm-control or a rate-control strategy is more frequently used in patients hospitalized for atrial fibrillation (AF). This study was conducted to assess patient and physician characteristics associated with each treatment strategy and with the use of anticoagulants. Hospitalizations for primary diagnoses of AF were examined using hospital claims from January 2000 to December 2004. Patients who received antiarrhythmic drugs, ablation, or cardioversion for AF were categorized as receiving rhythm control. Patients managed only with beta blockers, calcium channel blockers, or digoxin were categorized as receiving rate control. Characteristics associated with rhythm compared with rate control and anticoagulant use with CHADS(2) score were determined. The study cohort included 155,731 hospitalizations from 464 hospitals. Of these, 75,397 (48%) were categorized as involving rhythm control and 80,334 (52%) as involving rate control. Care by a noncardiologist (adjusted odds ratio [OR] 0.33, 95% confidence interval [CI] 0.31 to 0.36) and increasing age >65 years (adjusted OR 0.87, 95% CI 0.86 to 0.88) were associated with lower odds of rhythm versus rate control; hypertrophic cardiomyopathy was associated with greater odds (adjusted OR 2.3, 95% CI 1.81 to 2.84) of rhythm control. Warfarin use was greater in the rhythm-control group compared with the rate-control group (adjusted OR 1.56, 95% CI 1.52 to 1.60), and warfarin use was greater with a CHADS(2) score > or =2 (unadjusted OR 1.21, 95% CI 1.19 to 1.24). In conclusion, rhythm- and rate-control strategies were used equally in patients hospitalized for AF. Some observations, such as greater use of the rate-control strategy with increasing age, were consistent with recommendations, but others, such as lower use of warfarin in the rate-control group, were not.

Topics: Adrenergic beta-Antagonists; Age Factors; Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Anticoagulants; Aspirin; Atrial Fibrillation; Calcium Channel Blockers; Cardiomyopathy, Hypertrophic; Catheter Ablation; Digoxin; Drug Utilization; Electric Countershock; Female; Hospitalization; Humans; Male; Medicine; Middle Aged; Myocardial Infarction; Platelet Aggregation Inhibitors; Retrospective Studies; Severity of Illness Index; Specialization; United States; Warfarin; Wolff-Parkinson-White Syndrome

The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study showed that rhythm-control treatment of patients with atrial fibrillation (AF) offered no survival advantage over a rate-control strategy. In a subgroup analysis of that study, it was found that digoxin increased the death rate [relative risk (RR) = 1.42), but it was suggested that this may have been attributable to prescription of digoxin for patients at greater risk of death, such as those with congestive heart failure (CHF). No study has investigated a priori the effect of digoxin on mortality in patients with AF. This study aimed to address this question.. Using data from the Registry of Information and Knowledge about Swedish Heart Intensive care Admissions (RIKS-HIA), we studied the 1-year mortality among patients admitted to coronary care units with AF, CHF, or AF+CHF with or without digoxin (n = 60,764) during 1995-2003. Adjustment for differences in background characteristics and other medications and treatments was made by propensity scoring.. Twenty percent of patients with AF without CHF in this cohort were discharged with digoxin. This group had a higher mortality rate than the corresponding group not given digoxin [adjusted RR 1.42 (95% CI 1.29-1.56)], whereas no such difference was seen among patients with CHF with or without AF, although these patients had a nearly three-times higher mortality.. The results suggest that long-term therapy with digoxin is an independent risk factor for death in patients with AF without CHF.

Topics: Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Atrial Fibrillation; Creatinine; Digoxin; Female; Heart Failure; Humans; Male; Myocardial Infarction; Proportional Hazards Models; Prospective Studies; Registries; Research Design; Risk Assessment; Risk Factors; Stroke Volume; Sweden; Time Factors; Treatment Outcome; Ventricular Function, Left

Internationally, research indicates that pharmacotherapy for chronic heart failure (CHF) is sub-optimal. Traditionally, assessment of drug use in heart failure has focused on the use of individual agents irrespective of CHF severity. This study investigates drug use for CHF patients in general practice with respect to the available evidence, incorporating both disease severity and the use of combination drug regimes.. A cross-sectional survey of 769 Dutch CHF patients was performed as part of IMPROVEMENT of HF study. For each New York Heart Association severity classification the minimum treatment appropriate for the heart failure severity according to the scientific evidence available at the time of the study (1999) was defined. The proportion of patients treated with each drug increased with increasing severity, with the exception of the beta-blockers. Patients with less severe heart failure were approximately four to eight times more likely to receive evidence-based treatment than those with more severe heart failure.. To assess pharmacological treatment of heart failure, in relation to the available evidence, it is important to take severity into account. While the number of drugs prescribed increased with increasing severity, the use of evidence-based regimes was lower in patients with more severe heart failure.

Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Atrial Fibrillation; Comorbidity; Cross-Sectional Studies; Digoxin; Diuretics; Drug Therapy; Drug Therapy, Combination; Evidence-Based Medicine; Family Practice; Female; Heart Failure; Humans; Hypertension; Male; Middle Aged; Myocardial Infarction; Severity of Illness Index; Treatment Outcome

Atrial fibrillation (AF) is a common complication of acute myocardial infarction (AMI) with a reported incidence of 7-18%. Recently, P-wave signal-averaged electrocardiogram (P-SAECG) has been used to assess the risk of paroxysmal AF attacks in some diseases. The aim of this study was to determine prospectively whether patients with AMI at risk for paroxysmal AF would be identified by P-SAECG and other clinical variables.. A total of 100 patients (mean age: 59+/-12, 77 male, 23 female) with ST segment elevation AMI were enrolled in this study. Patients with chronic AF were excluded. At entry, all patients underwent standard 12-lead ECG and in the first 24 hours, P-SAECG was taken, and echocardiography and coronary angiography were performed on the patients. Patients are followed for a month in terms of paroxysmal AF attacks and mortality.. AF was determined in 19 patients (19%). In patients with AF, abnormal P-SAECG more frequently occurred than in patients without AF (37% vs 15%, P<0.05). Patients with AF were older (70+/-14 vs 56+/-10, P<0.001) and had lower left ventricular ejection fraction (42%+/-8 vs 49%+/-11, P<0.05). AF was less common in thrombolysis-treated patients (47% vs 74%, P<0.05). Thirty-day mortality was higher in patients with AF (16% vs 2%, P=0.05).. An abnormal P-SAECG may be a predictor of paroxysmal AF in patients with AMI. Advanced age and systolic heart failure were detected as two important clinical risk factors for the development of AF.

Topics: Adrenergic beta-Antagonists; Aged; Aged, 80 and over; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Anticoagulants; Atrial Fibrillation; Coronary Angiography; Digoxin; Echocardiography; Electric Countershock; Electrocardiography; Female; Fibrinolytic Agents; Humans; Male; Middle Aged; Myocardial Infarction; Predictive Value of Tests; Prospective Studies; Risk Factors; Stroke Volume; Treatment Outcome; Ventricular Dysfunction, Left

5-Fluorouracil, a widely used drug in cancer treatment, is known to have cardiotoxic effects: chest pain with ECG changes, arrhythmias, arterial hypertension or hypotension, myocardial infarction, cardiogenic shock and sudden death have been described in the literature. Coronary artery vasospasm is the pathogenetic mechanism hypothesized in most cases, but mechanisms other than myocardial ischemia had been advocated in some patients. The approach to the patient with persistent chest pain, despite therapy and persistent ST-segment elevation mimicking an acute myocardial infarction, has not been well addressed, and the appropriate diagnostic and therapeutic pathways have not yet been defined. We present our experience regarding 2 patients treated with 5-fluorouracil and referred to our coronary care unit because of prolonged chest pain (in one case with clinical evidence of hemodynamic impairment) and persistent ST-segment elevation, in whom an acute myocardial infarction was suspected. One patient was treated with systemic fibrinolysis, and coronary angiography was performed 6 days later; the other was submitted to urgent coronary angiography shortly after admission. In both cases the ECG and echocardiographic abnormalities were transient and normalized within a few days, the serum markers of myocardial necrosis were persistently in the normal range and the coronary artery trees were normal. The diagnostic and therapeutic approach to patients with this unusual clinical presentation is also discussed.

Topics: Aged; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Antimetabolites, Antineoplastic; Atrial Fibrillation; Captopril; Chest Pain; Colorectal Neoplasms; Coronary Angiography; Digoxin; Disease Management; Echocardiography; Electrocardiography; Fluorouracil; Humans; Laryngeal Neoplasms; Middle Aged; Myocardial Infarction; Nitrates; Verapamil

The novel Na(+)/K(+)-ATPase inhibitor (E,Z)-3-((2-aminoethoxy)imino)androstane-6,17-dione hydrochloride (PST2744) was characterized for its inotropic and toxic properties. Inhibition potency on dog kidney Na(+)/K(+)-ATPase was comparable (0.43 microM) to that of digoxin (0.45 microM). PST2744 concentration-dependently increased force of contraction in guinea pig atria and twitch amplitude in isolated guinea pig myocytes; in the latter, aftercontractions developed significantly less than with digoxin. Intravenous infusion of 0.2 mg/kg/min PST2744 in anesthetized guinea pigs exerted an immediate and long-lasting inotropic effect (ED(80) of 1.89 +/- 0.37 mg/kg) without causing lethal arrhythmias up to a cumulative dose of 18 mg/kg. Conversely, an equieffective infusion of digoxin (0.016 mg/kg/min; ED(80) of 0.32 mg/kg) caused lethal arrhythmias at a cumulative dose of 0.81 mg/kg. At a higher rate (0.4 mg/kg/min), PST2744 induced lethal arrhythmias, with a lethal dose/ED(80) ratio significantly greater than digoxin (20.2 +/- 6.3 versus 3.23 +/- 0.55, p < 0.05). Decay of the inotropic effect (t(1/2), min) was significantly faster for PST2744 (6.0 +/- 0.39) than for digoxin (18.3 +/- 4.5, p < 0.05). In anesthetized dogs, PST2744 dose-dependently increased maximum velocity of pressure rise (+dP/dt(max)) in the range 32 to 500 microg/kg i.v. and was safer than digoxin. In conscious dogs with a healed myocardial infarction, PST2744 significantly increased resting values of +dP/dt(max), left ventricular pressure, and SPB, and increased +dP/dt(max) throughout treadmill exercise while reverting the increase in left ventricular end diastolic pressure seen in control animals. Digoxin significantly decreased basal heart rate, while not affecting the hemodynamic response to exercise. Thus, PST2744 represents a new class of Na(+)/K(+)-ATPase inhibitors endowed with inotropic activity comparable with that of digitalis but having greater safety.

Topics: Animals; Cardiotonic Agents; Digoxin; Dogs; Dose-Response Relationship, Drug; Etiocholanolone; Guinea Pigs; Heart Atria; In Vitro Techniques; Myocardial Contraction; Myocardial Infarction; Myocardium; Physical Exertion; Radioligand Assay; Sodium-Potassium-Exchanging ATPase; Ventricular Function, Left

Atrial fibrillation (AF) is a fairly common complication of acute myocardial infarction (AMI). The aim of this study was to examine the safety and efficacy of intravenous amiodarone in converting AF associated with AMI.. Seventy patients with AMI complicated with AF were prospectively divided into 3 groups: a) In group D (n = 26), 0.75 mg digoxin was administered intravenously and thereafter as needed, b) In group AM (n = 16), 300 mg of amiodarone was infused over 2 hours followed by 44 mg/hour for up to 60 hours or until sinus rhythm was restored, c) In group D + AM (n = 28), 0.75 mg of digoxin was administered (as in group D) for the initial 2 hours followed by amiodarone infusion as in group AM.. Sinus rhythm was restored: a) by the end of the 2nd hour in 9/26 patients from group D, 4/16 from group AM, and 10/28 from group D + AM (p = NS), b) by the end of the 96th hour, in 18/26 patients from group D, and in all patients from group AM and groupd D + AM. The corresponding duration of AF was 51 +/- 34 hours, 17 +/- 15 hours and 9 +/- 13 hours, respectively (F = 15.4, p < 0.001). AF recurred in 9/26, 5/16 and 1/28 patients of groups D, AM and D + AM, respectively (p = 0.026). The required dosage of amiodarone was lower in the D + AM group than in the AM group (603 +/- 563 mg versus 1058 +/- 680 mg, p = 0.037).. Intravenous amiodarone was well tolerated in patients with AMI complicated by AF and was effective in decreasing the duration of AF. However, the combination of amiodarone and digoxin was superior to amiodarone alone in restoring sinus rhythm faster, maintaining sinus rhythm longer, and allowing the use of a lower cumulative amount of amiodarone.

Topics: Aged; Amiodarone; Anti-Arrhythmia Agents; Atrial Fibrillation; Digoxin; Female; Hemodynamics; Humans; Infusions, Intravenous; Male; Middle Aged; Myocardial Infarction; Treatment Outcome

We conducted this study to evaluate whether there is an association between preoperative drug therapy and in-hospital mortality in patients undergoing coronary artery graft surgery. We collected data on 1593 consecutive patients undergoing coronary artery surgery. The relative risk of in-hospital mortality was determined by logistic regression with in-hospital mortality as the dependent variable, and independent variables that included known risk factors and preoperative cardioactive or antithrombotic drug treatment, i.e., age; left ventricular function; left main coronary artery disease; urgent priority; gender; previous cardiac surgery; concurrent cardiovascular surgery; chronic lung disease; creatinine concentration; hemoglobin concentration; diabetes; hypertension; cerebrovascular disease; recent myocardial infarction; prior vascular surgery; number of arteries bypassed; and regular daily treatment with beta-blockers, aspirin within 5 days, calcium antagonists, angiotensin converting enzyme (ACE) inhibitors, digoxin, or warfarin. In-hospital mortality was 3.3%. The relative risk of in-hospital mortality (with 95% confidence intervals of the relative risk) associated with the following drug treatments was: nitrates 3.8 (1.5-9.6), beta-blockers 0.4 (0.2-0.8), aspirin within 5 days 1.0 (0.5-1.9), calcium antagonists 1.1 (0.6-2.1), ACE inhibitors 0.8 (0.4-1.5), digoxin 0.7 (0.2-1.8), and warfarin 0.3 (0.1-1.6). We conclude that in-hospital mortality is positively associated with preoperative nitrate therapy and negatively associated with beta-adrenergic blocker therapy. A significant association between in-hospital mortality and the preoperative use of calcium antagonists, ACE inhibitors, aspirin, digoxin, and warfarin was not confirmed.. We examined the association between common drug treatments for ischemic heart disease and short-term survival after cardiac surgery using a statistical method to adjust for patients' preoperative medical condition. Death after surgery was more likely after nitrate therapy and less likely after beta-blocker therapy.

Topics: Adrenergic beta-Antagonists; Age Factors; Aged; Angiotensin-Converting Enzyme Inhibitors; Anticoagulants; Aspirin; Cardiotonic Agents; Cerebrovascular Disorders; Chronic Disease; Coronary Artery Bypass; Coronary Disease; Creatinine; Diabetes Complications; Digoxin; Female; Fibrinolytic Agents; Forecasting; Hemoglobins; Hospital Mortality; Humans; Hypertension; Logistic Models; Lung Diseases; Male; Middle Aged; Myocardial Infarction; Nitrates; Reoperation; Risk Factors; Sex Factors; Survival Rate; Ventricular Function, Left; Warfarin

Cardiac involvement rarely occurs in classic hemolytic uremic syndrome (HUS); it is often fatal.. The first patient, a 21-month-old boy, developed classic HUS with acute renal failure. Peritoneal dialysis was performed for 20 days. On the 10th day of dialysis, myocardial infarction occurred, probably related to coronary thrombus. The patient was given heparin and antibiotics because of an unexplained fever. The outcome was favorable despite antero-apical cardiac necrosis, and moderated chronic renal failure. The second patient, a 24-month-old girl, also showed a classic HUS, which required peritoneal dialysis for 10 days. Dilated cardiomyopathy with cardiac failure appeared on the 4th day of dialysis, not related to the volume overload and metabolic consequences of the acute renal failure, such as systemic hypertension or ineffective dialysis. On the 5th day of dialysis neurological involvement appeared. Neurological, cardiac and renal outcome was favorable. The third patient, a 25-month-old girl, developed a classical HUS, requiring peritoneal dialysis for 25 days. No cardiac insult appeared during the acute phase of the disease. After dialysis, the child had chronic renal failure (creatinine clearance: 15 mL/min/1.73 m2). Dilated cardiomyopathy appeared 3 months later, without definite etiology. The outcome was favorable with digoxin treatment.. A cardiac involvement should also be searched for in the acute phase of HUS and several months later.

Topics: Acute Kidney Injury; Cardiac Output, Low; Cardiomyopathy, Dilated; Cardiotonic Agents; Creatinine; Digoxin; Female; Follow-Up Studies; Hemolytic-Uremic Syndrome; Humans; Infant; Kidney Failure, Chronic; Male; Myocardial Infarction; Peritoneal Dialysis; Psychomotor Agitation; Sleep Stages; Treatment Outcome

To assess whether implementation of guidelines increases the prescription of drugs, particularly beta blockers, recommended for secondary prevention after acute myocardial infarction.. Prescription patterns among 355 patients discharged from a public teaching hospital after recovery from myocardial infarction were prospectively monitored in a before-after trial. The implementation strategies included educational interventions (large group meetings), placement of guidelines in patients' records, and bimonthly general reminders sent to physicians.. Beta blockers were prescribed in 93 (38%) of 243 survivors of acute myocardial infarction before guideline implementation (12-month control period), as compared with 71 (63%) of 112 patients (P <0.001) after their implementation (6-month period). During the entire study period, the prescription of beta blockers at a neighboring public teaching hospital, used as a comparison, was unchanged. After adjusting for potential confounders, implementation of the guidelines remained significantly associated with prescription of beta blockers at discharge [odds ratio (OR) = 10; 95% confidence interval (CI), 3.2 to 33; P <0.001]. Other independent predictors of prescription of beta blockers were previous coronary artery bypass grafting (OR = 8.7; 95% CI, 2.5 to 31; P = 0.001), hypertension (OR = 2.5; 95% CI, 1.4 to 4.5; P = 0.003), age per 10-year increase (OR = 0.82; 95% CI, 0.67 to 0.99; P = 0.04), secular trend in prescription patterns expressed in months (OR = 0.9; 95% CI, 0.8 to 1.0; P = 0.02), a left ventricular ejection fraction < or = 40% (OR = 0.2; 95% CI, 0.1 to 0.4; P <0.001), the presence of atrioventricular block (OR = 0.1; 95% CI, 0.02 to 0.7; P = 0.02), and concomitant prescription of digoxin (OR = 0.2; 95% CI, 0.05 to 0.8; P = 0.02) or calcium antagonists (OR = 0.06; 95% CI, 0.01 to 0.3; P = 0.001).. When appropriately developed and implemented by local experts, literature-based guidelines may be effective in modifying use of recommended drugs for secondary prevention of coronary artery disease, such as prescription of beta blockers.

Topics: Adrenergic beta-Antagonists; Aged; Angiotensin-Converting Enzyme Inhibitors; Calcium Channel Blockers; Cardiotonic Agents; Coronary Artery Bypass; Digoxin; Drug Prescriptions; Female; Heart Block; Humans; Hypertension; Male; Myocardial Infarction; Odds Ratio; Practice Guidelines as Topic; Severity of Illness Index; Stroke Volume; Switzerland; Ventricular Dysfunction, Left

This prospective hospital-based, case-control study compares the outcome of unstable angina in non-insulin dependent diabetic patients and non-diabetic control subjects. One hundred and sixty-two diabetic patients and 162 non-diabetic control patients with unstable angina were entered into the study. The 3-month mortality was 8.6% (95% confidence interval, CI = 4.4-12.9%) in diabetic patients and 2.5% (CI = 0.1-4.9%) in control patients (p = 0.014). The 1-year mortality was 16.7% (CI = 10.9%-22.4%) in diabetic patients and 8.6% (CI = 4.4%-12.9%) in non-diabetic patients (p = 0.029). Diabetic patients received beta-blockade and underwent coronary angiography and angioplasty less frequently than controls; the frequency of unstable angina, of acute myocardial infarction, and coronary artery bypass grafting was similar in both groups at 1 year of follow-up. It is concluded that diabetic patients with unstable angina have a higher mortality than non-diabetic patients and that this difference is largely accounted for by early (first 3 months) mortality.

Topics: Adrenergic beta-Antagonists; Aged; Angina, Unstable; Angioplasty; Aspirin; Calcium Channel Blockers; Case-Control Studies; Confidence Intervals; Coronary Angiography; Coronary Artery Bypass; Coronary Disease; Diabetic Angiopathies; Digoxin; Female; Follow-Up Studies; Humans; Incidence; Male; Middle Aged; Myocardial Infarction; Nitrates; Prospective Studies; Risk Factors; Time Factors

To investigate the prevalence of and indications for digoxin use and the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension in an academic hospital-based geriatrics practice.. A retrospective analysis of charts from 528 unselected older patients, seen from June 1995 through July 1996 at an academic hospital-based geriatrics practice, was performed to investigate the prevalence of digoxin use and indications for digoxin use, the prevalence of beta blocker and calcium channel blocker use in older patients with previous myocardial infarction or coronary artery disease (CAD), and the prevalence of use of diuretics, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, and calcium channel blockers in older patients with hypertension.. An academic hospital-based, primary care geriatrics practice staffed by fellows in a geriatrics training program and full-time faculty geriatricians.. A total of 416 women and 112 men, mean age 81 +/- 8 years (range 58 to 101), were included in the study.. Ninety-two of the 528 patients (17%) were taking digoxin. Recorded indications for digoxin were atrial fibrillation with or without congestive heart failure (CHF) in 39% of patients, CHF with sinus rhythm and abnormal left ventricular ejection fraction (LVEF) in 18% of patients, a clinical assessment of CHF with sinus rhythm and no recorded measurement of LVEF in 20% of patients, paroxysmal atrial fibrillation in 14% of patients, and coronary artery disease (CAD) in 9% of patients. Of 121 patients with previous myocardial infarction, 23 (19%) were prescribed beta blockers, and 54 (45%) were taking calcium channel blockers. Of 173 patients with CAD, 41 (24%) were treated with beta blockers, and 79 (46%) were taking calcium channel blockers. LVEF was not recorded in the charts of 90 of 121 patients (74%) with prior myocardial infarction and of 125 of 173 patients (72%) with CAD. Of 480 older patients with hypertension, 154 (37%) were treated with diuretics, 55 (13%) were treated with beta blockers, 160 (38%) were treated with ACE inhibitors, and 197 (47%) were treated with calcium channel blockers.. In 528 older patients seen in an academic hospital-based geriatrics practice, the prevalence of digoxin use was 19%. Appropriate indications for digoxin were documented clearly in the charts of 53 of 92 patients (57%). Calcium channel blockers were used more often than beta blockers in patients with previous myocardial infarction or CAD. Calcium channel blockers were the most frequently used antihypertensive drugs.

Topics: Academic Medical Centers; Adrenergic beta-Antagonists; Age Factors; Aged; Aged, 80 and over; Ambulatory Care Facilities; Angiotensin-Converting Enzyme Inhibitors; Arrhythmias, Cardiac; Calcium Channel Blockers; Cardiovascular Agents; Coronary Disease; Digoxin; Diuretics; Drug Utilization; Female; Geriatrics; Heart Failure; Humans; Hypertension; Male; Middle Aged; Myocardial Infarction; Retrospective Studies

The inhibition of sarcolemmal Na+,K+-ATPase activity is closely related to ischemic myocardial cell injury. However, the involvement of this enzyme in preconditioning has not been determined.. We assessed the effect of ischemia on sarcolemmal Na+,K+-ATPase activity. Control and preconditioned rabbits were subjected to 0, 10, 20, 30, and 60 minutes of coronary occlusion. Ten to 60 minutes of ischemia reduced Na+,K+-ATPase activity, whereas preconditioning preserved the activity of this enzyme only during the first 20 minutes of ischemia. To determine whether the preservation of Na+,K+-ATPase activity in the early phase of ischemia contributed to limiting the infarct size, additional rabbits underwent 30 minutes of occlusion followed by 3 hours of reperfusion with or without pretreatment with digoxin, an inhibitor of Na+,K+-ATPase. Infarct size in animals pretreated with digoxin in the absence of preconditioning did not differ from that in controls. It was markedly reduced by preconditioning, whereas digoxin reduced the infarct size-limiting effect. Moreover, preconditioning increased sarcolemmal Na+-Ca2+ exchange activity in rabbits subjected to 20 minutes of ischemia, whereas digoxin diminished this increase.. Preconditioning preserves the ischemia-induced reduction in sarcolemmal Na+,K+-ATPase activity in the early phase of ischemia in rabbit hearts. Inhibition of Na+,K+-ATPase activity reduces the infarct size-limiting effect of preconditioning with a loss of increased Na+-Ca2+ exchange activity, implying that this preservation is responsible for the cardioprotective effect of preconditioning.

Topics: Animals; Digoxin; Enzyme Inhibitors; Hemodynamics; Ischemic Preconditioning, Myocardial; Myocardial Infarction; Myocardial Ischemia; Rabbits; Sarcoplasmic Reticulum; Sodium-Potassium-Exchanging ATPase

We hypothesized that positive inotropic stimulation during healing after myocardial infarction might increase contractile pull on the infarct segment, increase expansion and promote ventricular dilation.. The effect of prolonged inotropic stimulation on left ventricular remodeling during healing after myocardial infarction has not been studied.. The effects of 6 weeks of inotropic stimulation on in vivo changes in left ventricular topography, function and mass (serial two-dimensional echocardiograms), hemodynamic variables, postmortem topography (planimetry) and collagen (hydroxyproline content) were studied in 36 chronically instrumented dogs randomized, 2 days after small anterior infarction, to digoxin (0.125 mg daily) and no digoxin (control group).. Heart rate and arterial and left atrial pressures were similar in the two groups, but the first derivative of left ventricular pressure (peak dP/dt), systolic thickening of the noninfarct wall and systolic thinning of the infarct wall were higher in the digoxin group during the 6 weeks. At 6 weeks, infarct scar size and collagen content were similar in both groups, but the digoxin group had more infarct expansion and thinning. Between 2 days and 6 weeks, the digoxin group showed more in vivo diastolic infarct expansion, thinning and bulging; more aneurysm but less global dilation and increase in mass; and no change in ejection fraction. The effects of inotropic stimulation on remodeling were more marked in infarcts with 100% than 85% transmurality.. Prolonged inotropic stimulation with digoxin during healing after small anterior infarction increases infarct bulging without decreasing infarct collagen content and preserves global ventricular size, mass and systolic function.

Topics: Animals; Cardiotonic Agents; Diastole; Digoxin; Dogs; Echocardiography; Female; Heart Ventricles; Male; Myocardial Contraction; Myocardial Infarction; Myocardium; Systole

The authors report on a 47-years old woman with bacterial endocarditis involving both the mitral and aortic valves. At first echocardiographic examination, the mitral vegetation was small, while the aortic one was large highly mobile. Despite adequate antibiotic therapy, the aortic vegetation had become bigger and the valve regurgitation, initially mild to moderate, resulted severe and was associated with left heart failure. While awaiting surgery, the patient sustained an acute non Q wave myocardial infarction with ST segment elevation in inferior and anterolateral leads, complicated by ventricular arrhythmias. Thirty-six hours later, the patient received mitral and aortic valve replacement: at surgical view, the aortic vegetations was found to be very close to the right coronary orifice. After a period of further antibiotic therapy, the woman discharged and at a six months follow-up, she was fairly well. The authors review the mechanisms of acute coronary insufficiency in infective endocarditis and suggest an embolic pathogenesis in the case reported. Taking into account the possible life threatening embolic complications, it seems reasonable not to delay surgery when antibiotic therapy fails to reduce the size and mobility of valve vegetations.

Topics: Aortic Valve; Aortic Valve Insufficiency; Cardiotonic Agents; Digoxin; Diuretics; Echocardiography, Doppler, Color; Echocardiography, Transesophageal; Electrocardiography; Embolism; Endocarditis, Bacterial; Female; Follow-Up Studies; Furosemide; Heart Valve Prosthesis; Humans; Middle Aged; Mitral Valve; Mitral Valve Insufficiency; Myocardial Infarction; Penicillin G; Penicillins; Streptococcal Infections; Time Factors

The main aim of the study was to test the hypotheses that (a) concentrations of endogenous digoxin-like factor (EDLF) are increased in the initial period after acute myocardial infarction (AMI) and (b) may contribute to the onset of ventricular arrhythmias. 54 patients of both sexes with a first transmural AMI were included in a retrospective study. Plasma concentrations of EDLF were measured repeatedly during days 1-14 after AMI using DELFIA digoxin fluoroimmunoassay. 16 male patients with unstable angina pectoris and suspected AMI as well as 8 healthy subjects of both sexes served as controls. Plasma concentrations of EDLF in patients during the first day of AMI were increased (1.25 + (-)0.26 ng/ml, digoxin equivalents, p < 0.05) as compared with both healthy controls (0.34 + (-)0.08 ng/ml) and patients with unstable angina pectoris (0.4 + (-)0.06 ng/ml). First day after AMI plasma levels of EDLF in 7 patients with primary ventricular fibrillation were higher (2.54 + (-)0.67 ng/ml, p < 0.03) than in 47 patients without ventricular fibrillation (1.05 + (-)0.27 ng/ml). In 14 patients with AMI and congestive heart failure (class III, Killip) plasma concentrations of EDLF were significantly lower (0.32 + (-)0.09 ng/ml, p < 0.03) than in 40 patients with AMI without congestive heart failure (1.51 + (-)0.32 ng/ml). Starting from the second day of AMI plasma EDLF decreased to the level of control and did not change during two weeks of observation. These results, being in agreement with our previous experimental data, show an increase of plasma EDLF after AMI and suggest that EDLF may be involved in myocardial ischemia-induced arrhythmogenesis and participate in pathogenesis of congestive heart failure after AMI.

Topics: Adult; Aged; Angina, Unstable; Biomarkers; Cardenolides; Digoxin; Enzyme Inhibitors; Female; Fluoroimmunoassay; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Retrospective Studies; Saponins; Sodium-Potassium-Exchanging ATPase; Tachycardia, Ventricular

In congestive heart failure (CHF), endogenous compounds with ouabainlike activity (OLA) may contribute to the maintenance of the circulatory homeostasis by peripheral as well as central effects. In the present study, we assessed changes in peripheral (plasma and left ventricle) and central (pituitary, hypothalamus, pons, and cortex) OLA in two animal models of CHF and determined whether brain OLA mediates sympathetic hyperactivity in CHF. Cardiomyopathic hamsters with their controls were studied at 9 months of age for tissue OLA. Rats were studied 4 weeks after acute coronary artery ligation for tissue OLA and sympathetic activity. In both models, left ventricular end-diastolic pressure was markedly increased. CHF was associated with significant increases in both plasma and tissue OLA in both models. In the brain, the most marked (twofold to threefold) increases occurred in the hypothalamus. In vitro, all OLA measured could be blocked by antibody Fab fragments (Digibind). Conscious rats with CHF showed elevated plasma catecholamines and enhanced responses of mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) to air stress and to intracerebroventricular (ICV) injection of the alpha 2-adrenergic receptor agonist guanabenz compared with sham-operated rats. ICV administration of the Fab fragments did not change resting RSNA or responses to air stress at 1 hour. However, 18 hours after injection of the Fab fragments, resting RSNA levels had significantly decreased compared with the control values, and plasma catecholamine levels had decreased to control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Brain; Brain Chemistry; Cardiomyopathies; Catecholamines; Cricetinae; Digoxin; Guanabenz; Heart Failure; Hemodynamics; Immunoglobulin Fab Fragments; In Vitro Techniques; Male; Myocardial Infarction; Myocardium; Ouabain; Rats; Rats, Wistar; Stress, Physiological; Sympathetic Nervous System

A group of 65 patients with acute infarction of myocardium (IM) who were not treated with digitalis preparations were subdued to examination to the presence of digitalis-like substances in their urine by means of radioimmuno-analytic method with use of anti-digoxin antibodies. The control group was constituted of 69 healthy subjects. Patients afflicted with IM had significantly increased concentrations of DLS in serum in comparison with health subjects. No significant relations of DLS to the activity of creatinkinase, IM localisation, occurrence of dysrhythmias, heart insufficiency and IM mortality were discovered. An increase in DLS in the blood of patients with acute IM probably coincides with a decreased cardiac output, with the activation of the stress axis and retention of sodium and fluids. The second examined group of patients was constituted of 20 subjects with other severe cardiopathies (inborn and acquired heart defects, chronic ischemic heart disease, inflammatory and degenerative diseases of the heart, and hypertension), who were subdued to catheter examinations. The authors discovered no significant differences of DLS concentrations in the blood during catheterization of individual compartments of inferior vena cava, superior vena cava, and the right ventricle. They were not successful in defining the particular site of DLS secretion on the basis of this examination. The authors pay attention to interaction of DLS during the radioimmuno-analytic examination of the digoxin serum concentration.

Topics: Adult; Aged; Aged, 80 and over; Blood Proteins; Cardenolides; Digoxin; Female; Heart Diseases; Humans; Male; Middle Aged; Myocardial Infarction; Saponins; Sodium-Potassium-Exchanging ATPase

Digoxin therapy has been suggested to increase mortality risk in survivors of acute myocardial infarction. Since digoxin is a drug with a narrow therapeutic/toxic ratio, we raised the hypothesis that the association between digoxin and post myocardial infarction mortality may have a dose-dependent relationship. The purpose of this study was to evaluate this hypothesis. We retrospectively analyzed data from 1731 survivors of acute myocardial infarction. At the time of hospital discharge, 175 patients (10%) were taking digoxin. The exact dosage of digoxin was ascertained in 153 (87%) patients. Patients were divided into two groups based on the weekly dosage of digoxin at hospital discharge: The first group included 41 patients who were treated with a low dose (< or = 1.5 mg per week, usually 0.125 mg daily). The second group included 112 patients treated with a full dose (> 1.5 mg per week, usually 0.25 mg daily). Both groups were comparable with regard to mean age, gender, history of prior myocardial infarction, diabetes mellitus, hypertension, and prior angina. There were no significant differences in the incidence of in-hospital complications, such as heart failure, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, and postinfarction angina. One year mortality was significantly higher among patients treated with a full dose [19 of 112 (17%)] than patients treated with a low dose of digoxin [1 of 41 (2%); p < 0.02] Multivariate analysis performed by the Cox proportional hazards model identified treatment with a full dose of digoxin as an independent determinant associated with increased death during the first year after myocardial infarction (hazard ratio 10.7; 95% confidence interval 1.4-80.5). Thus, mortality among myocardial infarction survivors treated with digoxin was related to a full-dose therapy. Patients treated with a low dose experienced a low mortality rate. Our findings raise concern that digoxin may exert a dose-dependent deleterious effect upon the survival of patients recovering from acute myocardial infarction.

Topics: Adult; Aged; Analysis of Variance; Anti-Arrhythmia Agents; Cardiotonic Agents; Cohort Studies; Confounding Factors, Epidemiologic; Death, Sudden; Digoxin; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Multicenter Studies as Topic; Myocardial Infarction; Randomized Controlled Trials as Topic; Retrospective Studies

Heart failure is today one of the most serious health problems of modern industrialized societies. The increase in the mean age of the population is an additional factor which favours a high incidence of episodes of heart failure. Age is also a relevant factor in mortality linked with heart failure. On this basis more emphasis has been given by researchers and physicians to improve a preventive and therapeutic approach to heart failure. For many years the pharmacological treatment of heart failure patients was based on the increase in inotropism through the digitalis and on the reduction in sodium-water retention through diuretics, while less importance was given to the improvement of the afterload. We have had knowledge of vasodilatory drugs in chronic heart failure for at least 20 years but only 10 years ago with the Vasodilator-Heart Failure Trial (V-HeFTI), it was proved that the combination of hydralazine and nitrates in addition to the conventional treatment, improved the survival of patients affected by moderate-severe heart failure. With the advent of the ACE-inhibitors, in the '80s, the first studies concerning the role of such drugs in heart failure were carried out. In the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I) it was proved for the first time that an ACE-inhibitor (enalapril), added to the conventional heart failure therapy, improved the survival of patients with severe congestive heart failure (NYHA class IV). The result was so extraordinary that the study was interrupted for ethical reasons. However, it has raised a considerable interest in the study of the ACE-inhibitors in heart failure and now it has been proved that such drugs are a milestone in a correct pharmacological approach to heart failure.

Topics: Adult; Aged; Aged, 80 and over; Angina Pectoris; Angiotensin-Converting Enzyme Inhibitors; Clinical Trials as Topic; Clinical Trials, Phase I as Topic; Digoxin; Drug Therapy, Combination; Enalapril; Felodipine; Follow-Up Studies; Heart Failure; Humans; Middle Aged; Multicenter Studies as Topic; Myocardial Infarction; Randomized Controlled Trials as Topic; Time Factors; Vasodilator Agents; Ventricular Dysfunction

The safety of treatment with digoxin in patients with acute myocardial infarction (MI) was investigated in 584 hospital survivors of MI. All patients were examined by radionuclide ventriculography, with determination of left ventricular ejection fraction (LVEF), close to the time of discharge. Clinical data were collected on admission. All patients were followed up with regard to death (median 6.2 years, range 3.9-7.8 years). Patients treated with digoxin (N = 172 (29%) were older (median 66 vs 59 years; (P < 0.001), had a higher incidence of diabetes (13% vs 7%; P = 0.025), and a lower LVEF (0.33 vs 0.49; P < 0.001). As expected, clinical heart failure was more frequent among them (84% vs 14%; P < 0.001), than in patients not receiving digoxin. The 1- and 5-year mortality of patients treated with digoxin was 38% and 74% compared to 8% and 26% in patients not receiving digoxin (P < 0.001). The increased risk associated with digoxin therapy remained statistically significant when patients were stratified according to the presence or absence of heart failure or atrial fibrillation/flutter during hospitalization, or to LVEF above or below 0.45 at discharge. In a proportional hazard model including age, LVEF, diabetes mellitus, heart failure, atrial fibrillation or flutter, ventricular fibrillation, gender, dose of furosemide at discharge and calcium antagonists and digoxin treatment as covariates, digoxin was independently associated with an increased risk of death (relative risk 1.8 (95% confidence limit 1.2-2.5)). We conclude that administration of digoxin may be harmful in hospital survivors of MI.

Topics: Aged; Digoxin; Female; Gated Blood-Pool Imaging; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Proportional Hazards Models; Risk Factors; Stroke Volume; Survival Rate; Ventricular Function, Left

The aim of the study was to test the hypotheses that the concentrations of endogenous digoxin-like factor (EDLF) are (i) increased in the initial period after acute myocardial infarction (AMI) and (ii) may contribute to the genesis of ventricular arrhythmias.. Consecutive sample study.. An 800-bed city teaching hospital, primary hospitalized care centre.. Fifty-four consecutive patients of both sexes with a first transmural AMI, 16 male patients with unstable angina pectoris and eight healthy subjects.. None.. Time-course of the changes of plasma concentrations of EDLF (DELFIA digoxin fluoroimmunoassay) in patients during days 1-14 after uncomplicated AMI and AMI complicated with ventricular fibrillation and congestive heart failure.. Plasma concentrations of EDLF in patients on the 1st day after AMI were increased (1.25 +/- 0.26 ng ml-1 digoxin equivalents, P < 0.025) as compared with both healthy controls (0.34 +/- 0.06 ng ml-1) and patients with unstable angina pectoris (0.40 +/- 0.08 ng ml-1). On the 1st day after AMI the plasma levels of EDLF in seven patients with primary ventricular fibrillation were higher (2.54 +/- 0.67 ng ml-1, P < 0.05) than in 47 patients without ventricular fibrillation (1.05 +/- 0.27 ng ml-1). In 14 patients with AMI and congestive heart failure (class III, Killip), plasma concentrations of EDLF were significantly lower (0.32 +/- 0.09 ng ml-1, P < 0.01) than in 40 patients with AMI without congestive heart failure (1.51 +/- 0.32 ng ml-1). Starting from the 2nd day of AMI, plasma EDLF decreased to the level of the control values (0.35 +/- 0.04 ng ml-1) and did not change during a 2-week period of observation.. The results show an increase of plasma EDLF during the 1st day after AMI, and that higher plasma EDLF may be associated with the development of ventricular arrhythmias.

Topics: Adult; Aged; Arrhythmias, Cardiac; Blood Proteins; Cardenolides; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction; Saponins; Sodium-Potassium-Exchanging ATPase; Time Factors

The authors examined endogenous digitalis-like factor (DLF) concentrations in the serum and urine in 65 patients with acute myocardial infarction. Radioimmunoassay was used for the examination and patients' data were analyzed in detail in relation to sex, risk factors and acute myocardial infarction complications. The concentrations of digitalis-like factor found in the serum of men (0.317 +/- 0.026 micrograms/l) and women (0.256 +/- 0.057 micrograms/l) with acute myocardial infarction were much higher compared with values of healthy men (0.009 +/- 0.004 micrograms/l) and women (0.015 +/- 0.012 micrograms/l). This finding is in agreement with data published by others and suggests a role of DLF in the pathogenesis of myocardial infarction.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Blood Proteins; Cardenolides; Digoxin; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Reference Values; Risk Factors; Saponins; Sex Factors

Topics: Aspirin; Atrial Flutter; Digoxin; Electrocardiography; Furosemide; Humans; Isosorbide Dinitrate; Male; Middle Aged; Myocardial Infarction; Oxygen Inhalation Therapy

The aim was to look for the presence of circulating factor(s) with Na,K-ATPase inhibitory properties and digoxin like immunoreactivity in patients after acute myocardial infarction.. Venous blood samples were obtained when the patients were admitted and different methods were used to monitor the plasma concentrations of factor(s) with properties of digitalis. SUBJECTS - These were 26 patients of both sexes (mean age 57.7 years, range 40-72) during the first 24 h of a first transmural acute myocardial infarct, 11 male patients with unstable angina pectoris (52.5 years, 45-67), and 18 healthy male controls (25 to 50 years).. There was significant inhibition of ouabain sensitive Na,K-ATPase in intact erythrocytes in patients with myocardial infarction [1.4(SEM 0.15)mumol Pi.mg-1.h-1] compared with patients with unstable angina pectoris [3.1(0.4), p less than 0.01] and healthy controls [3.4(0.25), p less than 0.01]. In myocardial infarction complicated by ventricular fibrillation (n = 5) Na,K-ATPase activity was significantly lower than in the other 21 patients [0.95(0.2) and 1.55(0.11) mumol Pi.mg-1.h-1 respectively, p less than 0.05]. There was no change in erythrocyte Na,K-ATPase activity in myocardial infarction complicated by acute pulmonary oedema, nor was there any difference in activity in erythrocyte ghosts obtained from the patients with myocardial infarction v healthy controls, at 0.47(0.13) v 0.50(0.02) mumol Pi.mg-1.h-1. Boiled plasma supernatants obtained from the patients with myocardial infarction inhibited Na,K-ATPase in erythrocytes from healthy subjects. This inhibitory effect was antagonised by antidigoxin antibody. Plasma inhibitory potency was correlated with erythrocyte Na,K-ATPase activity in the patients with myocardial infarction (r = -0.65, p less than 0.001, n = 23). There was a 2.5-fold increase in plasma digoxin like immunoreactivity in the patients with myocardial infarction [1.65(0.5) ng.ml-1] using DELFIA fluoroimmunoassay as compared with five healthy controls [0.04(0.12), p less than 0.05] and nine patients with unstable angina [0.48(0.11), p less than 0.05]. There was no difference in plasma digoxin like immunoreactivity in myocardial infarction complicated or not by ventricular fibrillation, but there was very low digoxin like immunoreactivity in patients with myocardial infarction complicated by acute pulmonary oedema [0.26(0.08) ng.ml-1, n = 7]. There was no correlation between plasma digoxin like immunoreactivity and either plasma Na,K-ATPase inhibitory potency or erythrocyte Na,K-ATPase activity.. The results show that plasma factor(s) with some of the properties of digitalis are increased in acute myocardial infarction.

Topics: Adult; Aged; Angina, Unstable; Blood Proteins; Cardenolides; Digoxin; Erythrocytes; Female; Fluoroimmunoassay; Humans; Male; Middle Aged; Myocardial Infarction; Ouabain; Saponins; Sodium-Potassium-Exchanging ATPase

Suggesting endogenous digoxin-like factor (EDLF) to display arrhythmogenic activities in myocardial ischemia (MI), we studied the effect of anti-digoxin antiserum (ADS) on the ventricular fibrillation threshold (VFT) after the coronary ligation in cats and ventricular arrhythmias caused by MI in rats and chloroform-induced hypoxia in mice. Intravenous administration of ADS (5 mg/kg) enhanced VFT in cats with MI from 11.3 +/- 1.6 to 53.3 +/- 8.1 V (M +/- m; p less than 0.01) and significantly reduced ventricular arrhythmias in rats and mice. Our experiments on the isolated electro-stimulated rat atria demonstrated that EDLF is likely not to be an adrenergic cotransmitter in the heart. Possible mechanisms of the arrhythmogenic action of EDLF are discussed.

Topics: Animals; Antibodies; Arrhythmias, Cardiac; Blood Proteins; Cardenolides; Cats; Digoxin; Heart Ventricles; Immune Sera; Male; Mice; Myocardial Infarction; Rabbits; Rats; Rats, Inbred Strains; Saponins; Sodium-Potassium-Exchanging ATPase; Ventricular Fibrillation

The relationship between levels of potassium in the serum and the development of malignant arrhythmias was examined in a retrospective study involving 1011 patients presenting with acute myocardial infarction. Thirteen percent of the overall patients studied had significant hypokalemia (k less than 3.5 mmol/liter). The average initial level of potassium in patients who developed malignant arrhythmias was (4.10 mmol/liter) significantly lower (P less than 0.01) than those patients who did not develop such arrhythmias (4.19 mmol/liter). To determine whether the level of potassium was, in itself, the primary cause of malignant arrhythmias following myocardial infarction, a subgroup analysis of factors influencing these levels was performed. It was determined that diabetics have a higher level of potassium than nondiabetics (4.2 mmol/liter versus 4.11 mmol/liter - P = 0.01) and a lower incidence of malignant arrhythmias (50.5% versus 63.5% - P = 0.002). No correlation was found between treatment with either digitalis or diuretics and malignant arrhythmias. Size and location of infarcted areas was found to have a direct relationship with development of arrhythmias. Size and location of infarctions, however, were not found to be related to levels of potassium in the serum. Our findings support and clarify earlier suggestions establishing the levels of potassium in the serum as an important causative factor, together with size and location of infarctions, in the development of malignant arrhythmias.

Topics: Adrenergic beta-Antagonists; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Diabetes Mellitus; Digoxin; Diuretics; Female; Heart Block; Homeostasis; Humans; Hyperkalemia; Hypokalemia; Male; Middle Aged; Myocardial Infarction; Potassium; Retrospective Studies; Tachycardia; Ventricular Fibrillation

Because global T wave inversion has not been specifically characterized, 100 electrocardiograms (ECGs) with this pattern (frontal plane T vector -100 degrees to -170 degrees with precordial T inversion) were prospectively collected from approximately 30,000 consecutively interpreted ECGs and analyzed blindly. There was a striking female predominance (82 women vs. 18 men; p less than 0.0005) despite an essentially equal number of female and male hospital admissions. There was a single statistically significant ECG correlate: a more vertical QRS axis in women (+14.1 degrees +/- 45.3 degrees vs. -5.6 degrees +/- 31.3 degrees; p = 0.034). The T waves were basically symmetric (68%), the influence of this factor usually altering the characteristically asymmetric T wave inversions of right bundle branch block (4 of 5) and left ventricular hypertrophy (21 of 36). Asymmetry was mainly associated with digoxin therapy (21 of 32 patients taking digoxin; p less than or equal to 0.0005) and a corrected QT (QTc) interval (0.433 +/- 0.095) shorter than with symmetric T wave inversions (0.507 +/- 0.074; p less than or equal to 0.0005) though not reaching the degree of shortening expected for digitalization. Twenty-eight patients admitted for acute myocardial infarction and 23 for a central nervous system disorder accounted for the majority of patients with symmetric T wave inversion. Fifteen of 18 patients who had coronary angiography had some degree of coronary artery disease: 3 had angiographically normal coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Age Factors; Bundle-Branch Block; Cardiomegaly; Central Nervous System Diseases; Digoxin; Electrocardiography; Female; Gastrointestinal Diseases; Heart; Humans; Lung Diseases; Male; Metabolic Diseases; Myocardial Infarction; Sex Factors

As part of an ongoing community-wide study of time trends in the incidence and case-fatality rates of patients hospitalized with acute myocardial infarction (MI) in 16 Worcester, Mass., metropolitan hospitals during the calendar years 1975, 1978, 1981, and 1984, changes over time in the therapeutic management of 3,263 patients with validated acute MI were examined. Beta-blocker and nitrate therapy use increased consistently and dramatically. Use of antiplatelet agents was inconsistent, while use of digoxin remained stable. Use of antiarrhythmic medications other than lidocaine decreased consistently while lidocaine use increased between 1975 and 1978 and then leveled off to being used in approximately 45% of hospitalized patients with acute MI in 1981 and 1984. A variety of demographic (e.g. age, sex, teaching hospital) and clinical characteristics (e.g. MI order, MI type, MI location, peak CPK findings, occurrence of acute clinical complications) were also associated with the use of these therapies. The results of this community-wide study suggest changes over time in the therapeutic management of patients hospitalized with acute MI and of various patient demographic and clinical factors associated with the use of these agents.

Topics: Adrenergic beta-Antagonists; Aged; Anti-Arrhythmia Agents; Cohort Studies; Digoxin; Female; Humans; Longitudinal Studies; Male; Massachusetts; Middle Aged; Myocardial Infarction; Nitrates; Platelet Aggregation Inhibitors; Practice Patterns, Physicians'; Time Factors

In 105 patients at the age of 32-80 years after myocardial infarction the therapy with glycoside, diuretics and coronary pharmaca was analysed in dependence upon anamnesis, clinical treatment, ergometric and echocardiographic findings in the period from the discharge from the hospital to the first year. While glycosides, diuretics and nitrates were frequently prescribed unchanged, the intake of the beta-blockers increased from 19 to 28 per cent and that of the calcium antagonists from 21 to 39 per cent for the first year. In glycosides and diuretics the possible disadvantages of a withdrawal trial in clinically and paraclinically compensated patients were more taken into consideration than the side effects by uncritical administration. On the other hand, the advantages of the beta-receptor blockers and calcium antagonists were obviously not yet exhaustively used.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Calcium Channel Blockers; Digitoxin; Digoxin; Diuretics; Drug Therapy, Combination; Echocardiography; Exercise Test; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Pentaerythritol Tetranitrate

The potential interaction between certain antibiotics and digoxin has been discussed in the literature; however, few cases of actual erythromycin-induced digoxin toxicity have been reported. We present a case in which an 86-year-old woman who was taking digoxin 0.25 mg/d developed probably digoxin toxicity after the administration of erythromycin for the treatment of otitis media and streptococcal pharyngitis. Her digoxin concentration increased from a trough of 1.9 to 5.1 nmol/L six days after the erythromycin was started. Digoxin was discontinued and restarted approximately six weeks later when the patient's atrial fibrillation and congestive heart failure recurred. Her digoxin dose at this time was 0.125 mg/d and resulted in steady-state concentrations of 1.2, 1.4, and 1.2 nmol/L over the next year. Erythromycin inhibition of Eubacterium lentum, which converts digoxin into digoxin-reduction products in the gut, is the proposed mechanism of this interaction.

Topics: Aged; Aged, 80 and over; Atrial Fibrillation; Digoxin; Erythromycin; Female; Humans; Myocardial Infarction

As part of a community-wide study examining time trends in the incidence and case-fatality rates (CFR) of patients hospitalized with acute myocardial infarction (MI) in sixteen hospitals in the Worcester, Massachusetts metropolitan area, the association of age to the incidence rates of initial acute MI and to in-hospital and long-term survival among 2115 patients with validated acute MI was examined. After selected age-specific changes in the incidence rates of initial events of acute MI between 1975 and 1981, the incidence rates of acute MI markedly declined between 1981 and 1984, resulting in decreases in the age-specific incidence rates of initial acute MI between 1975 and 1984. For the combined study periods, the in-hospital CFR of acute MI increased from 5.0% in patients less than 55 years of age to 7.9% in those 55 to 64 years, to 16.1% in those 65 to 74 years and to 32.1% in patients 75 years of age and older. Among discharged hospital survivors, increasing age was related to poorer long-term survival over a 5-year follow-up period. The results of this population-based study reinforce the need for, and importance of, modification of coronary risk factors in both young and older individuals, and of focused therapeutic efforts to salvage jeopardized myocardium in elderly patients hospitalized with acute MI.

Topics: Adult; Age Factors; Aged; Creatine Kinase; Digoxin; Electrocardiography; Female; Heart Failure; Humans; Male; Massachusetts; Middle Aged; Myocardial Infarction; Prognosis; Risk Factors

Recently, this laboratory has demonstrated an enhanced susceptibility toward the development of lethal ventricular arrhythmias occurring in response to acute posterolateral ischemia in dogs with previous anterior myocardial infarction in the presence of therapeutic serum concentrations of digoxin. In the present study, acute posterolateral myocardial ischemia was produced in the absence of previous myocardial infarction in 15 digoxin-pretreated (1.19 +/- 0.21 ng/ml serum digoxin, 5-7 days pretreatment) and 11 vehicle-pretreated dogs. The incidences of sudden ventricular fibrillation and of 24 h arrhythmic mortality in response to posterolateral ischemia were 4/15 (27%) vs. 1/11 (9%) (p = 0.23) and 7/15 (47%) vs. 4/11 (36%) (p = 0.27) for digoxin- vs. vehicle-pretreated dogs, respectively. Ventricular ectopic activity at 24 and 48 h after the onset of posterolateral ischemia was reduced significantly by both intravenous lidocaine (1.0-5.0 mg/kg) and verapamil (50.0-500.0 micrograms/kg) in the vehicle-pretreated dogs, whereas neither antiarrhythmic agent significantly suppressed ventricular ectopy in the digoxin-pretreated dogs. The mean sizes for developing posterolateral myocardial infarctions (percentage of left ventricle) were greater for the digoxin-pretreatment group (31.9 +/- 2.8%) vs. vehicle-pretreatment group (14.8 +/- 2.0%, p less than 0.001). These findings suggest that uncomplicated acute myocardial ischemia in the presence of serum concentrations of digoxin that are considered clinically therapeutic may result in the development of larger areas of developing myocardial infarction and in the occurrence of ventricular arrhythmias that are less sensitive to suppression with conventional antiarrhythmic agents.

Topics: Animals; Arrhythmias, Cardiac; Coronary Disease; Digoxin; Dogs; Electrocardiography; Heart Rate; Heart Ventricles; Infusions, Intravenous; Lidocaine; Male; Myocardial Infarction; Verapamil

Recently, this laboratory has demonstrated an enhanced susceptibility toward the development of ischemia-related lethal ventricular arrhythmias in the presence of therapeutic serum concentrations of digoxin in conscious dogs after myocardial infarction. The present study was performed to assess the effect of the interruption of cardiac sympathetic influences, via subacute left stellate ganglionectomy (LSGX), on digitalis-mediated ischemic ventricular arrhythmias. Commencing 4-5 days after anterior myocardial infarction, 11 dogs with LSGX and 14 sham controls were administered digoxin (0.0125 mg/kg/day i.v.) for 5-7 consecutive days. At baseline testing, programmed ventricular stimulation failed to initiate ventricular tachycardia in any postinfarction dog entered into this evaluation. After treatment, 11/11 digoxin + LSGX (1.33 +/- 0.10 ng/ml serum digoxin) and 14/14 digoxin-treated sham (1.23 +/- 0.14 ng/ml serum digoxin) dogs remained nonresponsive to programmed stimulation testing. The incidence of arrhythmic mortality in response to subsequent ischemia at a site remote from the infarcted anterior region was greater in the digoxin-treated sham group (1.22 +/- 0.21 ng/ml serum digoxin) than in the digoxin + LSGX group (1.33 +/- 0.10 ng/ml serum digoxin); mortality was 6/10 (60%) digoxin sham vs. 1/10 (10%) digoxin + LSGX, p less than 0.005. The underlying anterior myocardial infarct sizes (% of left ventricle: 6.8 +/- 2.3 vs. 6.6 +/- 1.1) did not differ between the digoxin sham and digoxin + LSGX groups. However, the digoxin sham controls developed larger posterolateral myocardial infarctions than did the digoxin + LSGX animals (% of left ventricle: 27.4 +/- 3.0 vs. 16.7 +/- 2.7, p less than 0.05). Norepinephrine concentrations in posterolateral through posteroseptal ventricular sections were not altered by LSGX in a separate group of digoxin-treated postinfarct dogs. The results suggest that left stellate ganglionectomy may reduce the incidence of digitalis-mediated malignant ventricular arrhythmias during ischemia, possibly due to a reduction in the severity of ischemic injury.

Topics: Animals; Arrhythmias, Cardiac; Coronary Circulation; Denervation; Digoxin; Dogs; Ganglia, Sympathetic; Male; Myocardial Infarction; Myocardium; Norepinephrine; Stellate Ganglion; Sympathectomy

Topics: Angiotensin-Converting Enzyme Inhibitors; Digoxin; Diuretics; Drug Therapy, Combination; Heart Failure; Humans; Myocardial Infarction

Topics: Amrinone; Cardiotonic Agents; Digoxin; Diuretics; Dobutamine; Dopamine; Heart Failure; Humans; Myocardial Infarction; Vasodilator Agents

Previously, we have demonstrated an increased incidence of lethal ischemic arrhythmias in postinfarction dogs with clinically observable serum digoxin concentrations, and a significant reduction in digitalis-related lethal ischemic arrhythmias after subacute left stellectomy. In the present study, the protective actions of acute beta-adrenoceptor blockade with nadolol, 1.0 mg/kg administered intravenously immediately preceding the induction of posterolateral myocardial ischemia, were assessed in conscious dogs with recent, small anterior myocardial infarctions pretreated with digoxin, 0.0125 mg/kg/day intravenously, for 5 to 7 consecutive days (total n = 11). A cohort of postinfarction dogs pretreated with digoxin alone served as a control group (total n = 26). Pre vs postdigoxin electrophysiologic testing indicated reductions in myocardial refractoriness in ventricular noninfarct and infarct zones in both treatment groups, whereas the administration of nadolol tended to reverse the reductions in ventricular refractoriness. Arrhythmia-related deaths in response to posterolateral myocardial ischemia were reduced from 12 of 20 (60%) in the digoxin control group to 2 of 10 (20%) in the digoxin + nadolol group (p = 0.039). Serum digoxin concentrations (1.29 +/- 0.14 ng/ml vs 1.39 +/- 0.24 ng/ml), underlying anterior myocardial infarct size (6.9 +/- 1.5% vs 4.6 +/- 0.9% of left ventricle), and developing posterolateral myocardial infarct size (22.8 +/- 2.5% vs 17.5 +/- 3.6% of left ventricle) did not differ significantly between the digoxin and digoxin + nadolol groups. Acute beta-adrenoceptor blockade with nadolol appears to reduce digitalis-mediated ischemic postinfarction mortality, possibly because of a salutary increase in ventricular refractoriness.

Topics: Animals; Arrhythmias, Cardiac; Cardiac Pacing, Artificial; Digitalis; Digoxin; Dogs; Drug Administration Schedule; Electric Stimulation; Electrocardiography; Electrophysiology; Myocardial Infarction; Nadolol; Plants, Medicinal; Plants, Toxic

Topics: Digoxin; Heart Failure; Humans; Myocardial Infarction

In the present study, dogs were pretreated with intravenous digoxin, 0.0125 mg/kg/day, for 6 to 7 consecutive days to achieve clinically relevant serum concentrations; untreated animals were used as control subjects. After pretreatment, nine digoxin-pretreated dogs and nine control dogs were anesthetized and subjected to a 60-minute occlusion of the left circumflex coronary artery, followed by 6 hours of reperfusion. Anatomic myocardial infarct size, expressed as a percentage of the areas at risk of infarction and as a percentage of the total left ventricle were: 20.2 +/- 3.3% control vs 35.4 +/- 6.2% digoxin-pretreated (p less than 0.05) and 8.6 +/- 1.3% control vs 14.7 +/- 2.5% digoxin-pretreated (p less than 0.05), respectively (2.04 +/- 0.37 ng/ml serum digoxin). Regional myocardial blood flow in the nonischemic and ischemic zones tended to be lower in digoxin-pretreated than in control animals at baseline testing and were significantly reduced in the anterior subendocardial sites of digoxin-pretreated dogs during ischemia and reperfusion. These data suggest that an exacerbation or enhancement of myocardial ischemia-reperfusion injury may occur in the presence of clinically observable serum digoxin concentrations.

Topics: Animals; Blood Pressure; Coronary Circulation; Digoxin; Dogs; Male; Myocardial Infarction; Myocardium; Potassium; Sodium

As part of an ongoing community-wide study of time trends in the incidence and case-fatality rates of patients hospitalized with acute myocardial infarction (MI) in all 16 Worcester, Massachusetts, metropolitan hospitals during the years 1975, 1978, 1981, and 1984, changes over time in the therapeutic management of 3263 patients with validated acute myocardial infarction were examined. Beta-blocker (21%, 1975; 52%, 1984) and nitrate (56%, 1975; 93%, 1984) therapy use increased dramatically over time. Use of antiplatelet agents was inconsistent over time, while use of digoxin remained stable, being used in approximately 40% of all patients over the four periods studied. Use of antiarrhythmic medications other than lidocaine decreased consistently over time (31%, 1975; 22%, 1984). Lidocaine use increased between 1975 (31%) and 1978 (52%) and then leveled off to being used in approximately 45% of hospitalized patients with acute MI in 1981 and 1984. A variety of demographic (e.g., age, sex, teaching hospital) and clinical characteristics (e.g., MI order, MI type, MI location, peak CPK findings, occurrence of acute clinical complications) were also associated with the use of these therapies for the combined study periods. The results of this population-based study suggest considerable changes over time in the therapeutic management of patients hospitalized with acute myocardial infarction and of numerous patient demographic and clinical factors associated with their use.

Topics: Adrenergic beta-Antagonists; Aged; Anti-Arrhythmia Agents; Blood Platelets; Depression, Chemical; Digoxin; Female; Humans; Lidocaine; Male; Massachusetts; Middle Aged; Myocardial Infarction; Nitrates

Certain approaches to analysis of the drug concentration-response relationship based on the mechanism of the effect realization and the results of their clinical trials are discussed. The studies are exemplified by a model for quantitative analysis of the concentration-response relationship developed for diuretics and by the results of the clinical trial of the principle of the maximum providing prediction of the steady-state level of the drugs in blood and estimation of the drug effect.

Topics: Aged; Digoxin; Diuresis; Dose-Response Relationship, Drug; Furosemide; Humans; Mathematics; Myocardial Infarction; Time Factors

The hemodynamic effects of digitalis were examined in ten patients with acute cardiac failure. Administration of 10 micrograms/kg of digoxin iv resulted in significant increases in cardiac index, stroke volume index, and left ventricular stroke work index within one hour in five patients with acute myocardial infarction (AMI) and five patients with atherosclerotic heart disease without AMI. These increases were maintained 2 h after digoxin therapy. Indirect assessment of global myocardial oxygen supply (coronary perfusion pressure) and demand (heart rate X systolic arterial pressure X wedge pressure product) did not reveal adverse changes. Digoxin therapy results in rapid improvement in cardiac function during acute cardiac failure in patients with and without AMI.

Topics: Cardiac Output; Digoxin; Heart Failure; Hemodynamics; Humans; Myocardial Contraction; Myocardial Infarction; Myocardium; Oxygen Consumption; Prospective Studies

To determine the relative value of clinical findings, results of low-level treadmill electrocardiographic (ECG) exercise testing and left ventricular (LV) ejection fraction (EF) for predicting cardiac events in the year after an acute myocardial infarction (AMI), 72 patients who had had an uncomplicated AMI were studied with either radionuclide angiography or 2-dimensional echocardiography to assess LVEF and a low-level treadmill exercise test before hospital discharge. All patients were followed for 1 year. Nineteen patients (26%) had at least 1 cardiac event: coronary artery bypass grafting (11 patients), recurrent AMI (6 patients) or cardiac death (6 patients). Multiple logistic regression analysis revealed that total cardiac events were predicted by exercise ECG ST-segment depression or angina, prior AMI, ventricular ectopic activity during exercise and digoxin therapy (cumulative r = 0.58, p less than 0.001). Coronary artery bypass grafting was predicted by exercise ECG ST-segment depression or angina (r = 0.29, p = 0.01). Recurrent AMI was predicted by exercise ECG ST-segment depression or angina, prior AMI and ventricular ectopic activity during exercise (cumulative r = 0.49, p less than 0.001). Cardiac death was predicted by an LVEF of 40% or less (r = 0.38, p = 0.01). The presence of both an LVEF of 40% or less and ECG ST-segment depression on treadmill exercise testing defined a subgroup of patients with a high incidence of early cardiac death (33%).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Coronary Artery Bypass; Digoxin; Exercise Test; Female; Heart; Heart Arrest; Humans; Male; Myocardial Infarction; Prognosis; Radionuclide Imaging; Stroke Volume

Risk of sudden death was assessed in 533 patients who survived 10 days after acute myocardial infarction (AMI) and were followed for up to 24 months (mean 18) in the Multicenter Investigation of the Limitation of Infarct Size. Analysis of clinical and laboratory variables measured before hospital discharge revealed that the QT interval, either corrected (QTc) or uncorrected for heart rate, did not contribute significantly to prediction of subsequent sudden death or total mortality. In this population, frequent ventricular premature complexes (more than 10 per hour) on ambulatory electrocardiographic monitoring and left ventricular (LV) dysfunction (radionuclide LV ejection fraction of 0.40 or less) identify patients at high risk of sudden death. In patients with these adverse clinical findings, the QTc was 0.468 +/- 0.044 second among those who died suddenly and 0.446 +/- 0.032 second in survivors, and was not statistically significant as an additional predictor of sudden death. Consideration of the use of type I antiarrhythmic agents, digoxin, presence of U waves and correction for intraventricular conduction delay did not alter these findings. Although QT-interval prolongation occurs in some patients after acute myocardial infarction, reduced LV ejection fraction and frequent ventricular premature complexes are the most important factors for predicting subsequent sudden death in this patient population.

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Death, Sudden; Digoxin; Electrocardiography; Follow-Up Studies; Heart Ventricles; Humans; Myocardial Infarction

A submaximal treadmill exercise test performed before hospital discharge after an uncomplicated myocardial infarction is often utilized to estimate prognosis and guide management, but there is little experience with a maximal exercise test performed 6 months after infarction to identify prognosis later in the convalescent period. The performance characteristics during an exercise test 6 months after myocardial infarction were related to the development of death, recurrent nonfatal myocardial infarction and coronary artery bypass surgery in the subsequent 12 months (that is, 6 to 18 months after infarction) in 473 patients. Mortality was significantly greater in patients who exhibited any of the following: inability to perform the exercise test because of cardiac limitations, the development of ST segment elevation of 1 mm or greater during the exercise test, an inadequate blood pressure response during exercise, the development of any ventricular premature depolarizations during exercise or the recovery period and inability to exercise beyond stage I of the modified Bruce protocol. By utilizing a combination of four high risk prognostic features from the exercise test, it was possible to stratify patients in terms of risk of mortality, from 1% if none of these features were present to 17% if three or four were present. Recurrent nonfatal myocardial infarction was predicted by an inability to perform the exercise test because of cardiac limitations, but not by any characteristics of exercise test performance. Coronary artery bypass surgery was associated with the development of ST segment depression of 1 mm or greater during the exercise test. Although clinical evidence of angina and heart failure 6 months after infarction was predictive of subsequent mortality among all survivors, among the low risk group without severely limiting cardiac disease, the exercise test provided unique prognostic information not available from clinical assessment alone. Therefore, a maximal exercise test performed 6 months after myocardial infarction is a valuable, noninvasive tool to evaluate prognosis. It provides information that is independent of and additive to clinical evaluation performed at the same time.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Angina Pectoris; Blood Pressure; Coronary Artery Bypass; Digoxin; Electrocardiography; Exercise Test; Female; Follow-Up Studies; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Random Allocation; Recurrence; Risk

The results of exercise electrocardiography were studied in a random sample of 317 subjects with clinical suspicion of coronary artery disease. In 278 patients with coronary artery disease the rate of false negative tests was 18% with and 12% without previous myocardial infarction. If ST elevation was considered a negative response, the corresponding values were 25% and 13%, respectively, p less than 0.01. The greatest prevalence of negative tests was seen after anterior myocardial infarction: 27% or 42% when ST elevation was not included into positive responses. The sensitivity of exercise-induced ST depression for the presence of multivessel disease was lower after anterior infarction (67%) than in other patients with previous infarction (86%), p less than 0.01. The corresponding specificities were 71% and 22%, respectively, p less than 0.005. If ST elevation was included into positive responses these differences were abolished. In subjects without myocardial infarction the sensitivity was 89% and specificity 43%. Digitalized patients had somewhat higher sensitivity in the exercise electrocardiogram than those without digoxin, 90% vs. 81% (p less than 0.05), but the difference was not seen with exclusion of ST elevation. The specificity was not influenced by digitalis. beta-blockade had no effect on the sensitivity or specificity, but the prevalence of postexercise ST evolution was lower with (11%) than without (30%) beta-blockade. The prevalence of slowly ascending ST depression was reduced by three factors: the presence of digitalis in patients without previous myocardial infarction, infarction itself, and the extent of coronary artery disease. We conclude that exercise electrocardiography has only a limited value in prediction of multivessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenergic beta-Antagonists; Chest Pain; Coronary Disease; Digoxin; Electrocardiography; Exercise Test; Female; Humans; Male; Middle Aged; Myocardial Infarction; Predictive Value of Tests; Time Factors

Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did not (non-AMI). An initial decrease in plasma glutamate and increase in alanine was found in AMI compared to non-AMI patients. The AMI group showed early, moderate rises of plasma FFA and citrate concentrations, positively related to the initial ST-segment elevation and to the enzymatic estimated infarct size. The AMI patients were continuously hyperglycaemic, but their relative insulin response i.e. plasma glucose/insulin ratio was identical to that of non-AMI patients. Lactate values did not differ between the two groups. Via participation in the malate-aspartate shuttle and by shunting pyruvate to alanine instead of lactate, glutamate is of importance for maintaining myocardial glucose utilization. Our finding of initial low plasma glutamate concentrations after onset of myocardial infarction suggests insufficient glutamate supply to the ischaemic myocardium. On basis of this and animal experiments, an external supply of glutamate might be a 'metabolic' treatment of AMI, alternative or additional to glucose-insulin-potassium infusion in order to promote myocardial glucose oxidation.

Topics: Aged; Alanine; Blood Glucose; Citrates; Citric Acid; Digoxin; Fatty Acids, Nonesterified; Glutamates; Glutamic Acid; Humans; Insulin; Lactates; Lactic Acid; Myocardial Infarction

Topics: Animals; Antibodies; Antibodies, Monoclonal; Antibody Specificity; Cardiovascular Diseases; Coronary Disease; Digoxin; Humans; Immunization, Passive; Immunoglobulin Fragments; Myocardial Infarction; Myosins; Radionuclide Imaging; Receptors, Cell Surface; Receptors, Drug; Renin

Fourteen patients with postinfarctual ventricular aneurysm underwent equilibrium radionuclide angiocardiography at rest (ERNA) before and after oral digoxin administration in order to evaluate the effects of increasing myocardial contractility upon both ventricular aneurysm mechanical behaviour and global ventricular function. The ejection fraction (EF) was not significantly affected by digoxin therapy. However, digoxin induced changes in EF (delta EF) correlated inversely with changes in aneurysm size and directly with changes in the extent of the hypokinetic area. Two types of aneurysm were observed: high-compliance aneurysm the size of which increased after digoxin administration while both EF and the extent of the hypokinetic area fell, and low compliance aneurysm for which opposite changes occurred. This different behaviour of ventricular aneurysm may have important practical implications as surgery would be probably more effective than medical treatment in improving resting ventricular function in patients with high-compliance aneurysm.

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Female; Heart Aneurysm; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Radionuclide Imaging; Sodium Pertechnetate Tc 99m

The proarrhythmic potential of digoxin, administered in a therapeutic dosage regimen, was evaluated in conscious dogs in the subacute phase of myocardial infarction. In this evaluation, digoxin (0.0125 mg/kg/day intravenously) or vehicle were administered to conscious dogs for periods of 5 to 7 days, commencing 4 to 5 days after anterior myocardial infarction. Before treatment, programmed ventricular stimulation failed to initiate ventricular tachycardia in 26 post infarction dogs. After treatment, programmed stimulation initiated ventricular tachyarrhythmias in only 1 of 13 digoxin-treated dogs (1.36 +/- 0.17 ng/ml serum digoxin) and in 0 of 13 vehicle-treated dogs. However, the incidences of early ventricular fibrilation (4 of 10 digoxin vs 0 of 12 vehicle; p less than 0.05) and of 24-hour mortality (6 of 10 digoxin vs 2 of 12 vehicle; p less than 0.05) occurring in response to the development of posterolateral ischemia in the presence of previous anterior myocardial infarction was significantly greater in digoxin-treated (1.47 +/- 0.19 ng/ml serum digoxin) than in vehicle-treated animals. These findings suggest an enhanced susceptibility toward the development of ischemia-related lethal arrhythmias in the presence of therapeutic digoxin serum concentrations early after myocardial infarction, which is not predicted by programmed ventricular stimulation testing.

Topics: Animals; Cardiac Pacing, Artificial; Consciousness; Digoxin; Dogs; Electrocardiography; Electrophysiology; Male; Myocardial Infarction; Potassium; Risk; Tachycardia; Time Factors; Ventricular Fibrillation

Elderly and old patients with subacute myocardial infarction showed elevated gastrointestinal digoxin absorption rates and a tendency to increased bioavailability of the drug, as compared to similar parameters in infarction-free patients of the same age, so that blood digoxin peaks were higher in the former. The demonstrated absorption changes may be related to limited physical activity of the myocardial infarction patients examined. Digoxin pharmacokinetic patterns are analysed with reference to baseline myocardial contractility.

Topics: Administration, Oral; Age Factors; Aged; Biological Availability; Digoxin; Half-Life; Humans; Injections, Intravenous; Intestinal Absorption; Kinetics; Middle Aged; Myocardial Infarction; Time Factors

The efficiency of digoxin in elderly and old patients with subacute myocardial infarction is dependent on the original disorders of left-ventricular systolic phase structure. Changes in systolic phase structural parameters in the presence of supporting digoxin therapy show correspondence to changes of these parameters in response to a single digoxin dose. Digoxin's positive inotropic effect was similar in patients with the sinus rhythm and those with atrial fibrillation. The positive inotropic action of digoxin is not associated with a negative chronotropic effect in patients with sinus rhythm and normal heart rate.

Topics: Aged; Cardiac Output; Cardiac Output, Low; Digoxin; Heart Failure; Heart Ventricles; Humans; Middle Aged; Myocardial Infarction; Systole

Topics: Adult; Aged; Digoxin; Ferricyanides; Hemodynamics; Humans; Hydralazine; Male; Middle Aged; Myocardial Infarction; Nitroprusside

Beta 2-receptor stimulation is required for catecholamine-induced hypokalemia to occur. This hypokalemia is not mediated by insulin, renin or aldosterone. Catecholamine-induced hypokalemia can be prevented by selective beta 2 blockade, which does not abolish the inotropic effect of epinephrine.

Topics: Adrenergic beta-Antagonists; Digoxin; Dose-Response Relationship, Drug; Epinephrine; Heart Rate; Humans; Hypokalemia; Insulin; Isoproterenol; Myocardial Infarction; Physical Exertion; Potassium; Propanolamines; Time Factors

The importance of cardiovascular system involvement in hyperthyroidism has been recognized for many years. In the middle-aged and elderly patient, often with mild but prolonged elevation of plasma thyroid hormones, symptoms and signs of heart failure and complicating atrial fibrillation may dominate the clinical picture and mask the more classical endocrine manifestations of the disease. Pitfalls in diagnosis and the importance of early recognition and treatment are discussed. Despite experimental evidence for a short-term inotropic action of thyroid hormone excess, clinical data support the existence of a reversible cardiomyopathy in hyperthyroidism with impaired contractile reserve. Enhanced myocardial performance at rest primarily reflects the peripheral actions of thyroid hormone excess. Most, if not all, of the cardiac abnormalities return to normal once a euthyroid state has been achieved, although atrial fibrillation may persist in a minority. Optimum treatment requires rapid and definitive antithyroid therapy, usually using a large dose of radio-iodine, and rapid control of heart failure. Systemic anticoagulation is indicated in the presence of atrial fibrillation and should be continued until sinus rhythm has been present for at least three months, either spontaneously or after cardioversion.

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Arrhythmias, Cardiac; Atrial Fibrillation; Cardiomyopathies; Digoxin; Drug Therapy, Combination; Heart Diseases; Heart Rate; Hemodynamics; Humans; Hyperthyroidism; Myocardial Contraction; Myocardial Infarction; Sympathetic Nervous System; Thyroid Function Tests; Thyroid Hormones

Topics: Digoxin; Dopamine; Drug Therapy, Combination; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Nitroglycerin

To determine whether treatment with digitalis is associated with decreased survival after acute myocardial infarction (AMI), data from 504 patients who were enrolled in a postinfarction natural history study were analyzed. At the time of discharge, 229 patients (45%) were taking digitalis. After 3 years of follow-up, the cumulative survival rate for patients discharged on a regimen of digitalis was 66%, compared with 87% for those not treated (p less than 0.001). Univariate analysis showed that statistically significant differences existed between the 2 groups with respect to age, previous AMI, left ventricular failure in the coronary care unit, atrial fibrillation in the coronary care unit, peak creatine kinase levels, enlarged heart and pulmonary vascular congestion on the discharge chest x-ray, ventricular arrhythmias and treatment with diuretic, antiarrhythmic and beta-blocking drugs. Survival analysis using Cox's regression model showed that the association between digitalis and decreased survival was of borderline significance after adjustment for atrial fibrillation and left ventricular failure. Serum digoxin concentration was measured in 83% of the patients who took digitalis. Survival was inversely and significantly related to serum digoxin, i.e., the higher the serum digoxin concentration, the lower the long-term survival rate. After adjusting for atrial fibrillation and left ventricular failure, serum digoxin was not significantly related to survival. Taken together with the results of 3 other large, nonrandomized studies of digitalis treatment after AMI, this study suggests that digitalis treatment may have adverse effects on survival during follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Fibrillation; Digitalis; Digoxin; Female; Follow-Up Studies; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Plants, Medicinal; Plants, Toxic; Risk

This study investigated the effects of therapeutic and subtoxic doses of digoxin on the risk of ventricular tachycardia (VT) after graded, transthoracic shocks in anesthetized dogs. A series of direct current shocks (5, 10, 25, 50, 75, 100, 150 and 200 J) was delivered to 33 normal dogs and 6 dogs with a healed (32 +/- 7 days) myocardial infarct (MI). In 10 untreated dogs, the duration of post-shock VT was highly reproducible when 3 separate series of shocks were delivered at 2-hour intervals. In 6 normal dogs treated with oral digoxin (0.5 mg/day for 5 to 7 days), a series of shocks delivered before and during treatment (serum levels 1.5 +/- 0.5 ng/ml) resulted in the same duration of post-shock VT. In 18 normal and 6 dogs with MI, a series of shocks was given before and 90 minutes after a therapeutic dose of digoxin (0.05 mg/kg intravenously). At this dose of digitalis (serum level 2.5 +/- 1.0 ng/ml), there was no difference in the duration of post-shock VT in either normal dogs or dogs with MI. A third series of shocks was given after achieving subtoxic digitalization with additional intravenous digoxin (0.01 mg/kg) every 30 minutes until a premature ventricular stimulus evoked a repetitive ventricular response. The subtoxic doses of digitalis (serum levels 13.9 +/- 4.7 ng/ml) increased the duration of post-shock VT in both normal dogs (100%) and dogs with MI (700%) (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Arrhythmias, Cardiac; Digoxin; Dogs; Dose-Response Relationship, Drug; Electric Countershock; Electrocardiography; Heart Ventricles; Myocardial Infarction; Risk; Tachycardia

The hemodynamic effects of digoxin (0.01 mg/Kg) on congestive heart failure were compared in 32 patients with old myocardial infarction (OMI) (n = 9), dilated cardiomyopathy (DCM) (n = 10), acute myocardial infarction (AMI) (n = 5) and mitral stenosis (MS) (n = 8). The responses of heart rate (HR) and pulmonary capillary pressure (PCP) to digoxin in OMI, DCM and MS were marked but different in each of these groups and no significant changes were found in patients with AMI. The responses of cardiac index (CI) to digoxin in patients with OMI and DCM in whom left ventricular myocardial contractile force was impaired were divided into 2 groups (Group 1: CI increased more than 15% and Group 2: less than 15%). In Group 1, both CI and percent fractional shortening (%FS) before digoxin administration were lower than in Group 2, i.e., 1.97 +/- 0.27 vs 2.80 +/- 0.48 L/min/m2 (p less than 0.001) and 10.9 +/- 8.0 vs 19.5 +/- 11.9% (p less than 0.05), respectively. In MS, CI increased after digoxin administration only in the 2 patients with low CI and rapid HR in the control state. These results indicate that the mode of hemodynamic response to digoxin is considerably different in various diseases. They further suggest that digoxin should not be used in the early phase of AMI, although digoxin was of great clinical benefit in patients with OMI and DCM through such mechanisms as its positive inotropic and negative chronotropic effects and lowering of PCP.

Topics: Adult; Aged; Cardiomyopathy, Dilated; Digoxin; Female; Heart Failure; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Mitral Valve Stenosis; Myocardial Contraction; Myocardial Infarction; Pulmonary Wedge Pressure

Prenalterol was given to twenty five patients with acute myocardial infarction. Thirteen patients (group B) had signs of cardiac decompensation while twelve (group A) had not. Ejection fraction was determined with 99mTc-labelled red blood cells before and after prenalterol (50 micrograms kg-1 body weight), intravenously. In group B this procedure was repeated after digitalization 2 days later. The ejection fraction increased significantly in group A after prenalterol injection. In group B, prenalterol produced an increase, but this was not significant. After digitalis the ejection fraction increased significantly and prenalterol produced an additional significant rise. No significant changes in blood pressure occurred. Heart rate increased significantly in both groups after prenalterol injection and decreased significantly after digitalis.

Topics: Adrenergic beta-Agonists; Aged; Blood Pressure; Cardiac Output; Digoxin; Drug Therapy, Combination; Erythrocytes; Female; Heart; Heart Rate; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Practolol; Prenalterol; Radionuclide Imaging; Stimulation, Chemical; Stroke Volume; Technetium

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Arrhythmias, Cardiac; Calcium Channel Blockers; Digoxin; Drug Interactions; Humans; Hypertension; Hypoglycemic Agents; Kinetics; Liver; Myocardial Infarction

Calcium antagonists, of which the best known are verapamil, nifedipine and diltiazem, are a powerful group of cardioactive agents with a clinical spectrum of indications rather similar to those of beta-adrenoceptor blockade, including angina of effort, angina at rest, hypertension and supraventricular tachycardias (nifedipine is ineffective for the latter). In angina caused by coronary spasm, calcium antagonists are preferred to beta-blockade. Calcium antagonists have a basically different mode of action from beta-adrenoceptor blockade, although both ultimately act on the free cytoplasmic calcium ion concentration. Critical differences between the calcium antagonists are dependent on the individual properties of the calcium antagonists concerned. Different binding sites on the sarcolemma have been identified for nifedipine-like agents and verapamil, but with a different interaction with the nifedipine site. None of these sites might be relevant to the binding of calcium antagonists to the tissue of their therapeutic site of action (arterial smooth muscle for all; atrioventricular node for verapamil and diltiazem). As a group, calcium antagonists cause vascular dilation and do not cause bronchial constriction, in contrast to the beta-adrenoceptor blocking agents. In many patients, these diverse properties allow safe combination of calcium antagonists and beta-adrenoceptor blockers if due care is observed, especially in the case of nifedipine. The clinical differences between the effects of various calcium antagonists reflect: (i) the greater vasodilator capacity of nifedipine, so that at a given concentration the afterload effect dominates over possible effects on the nodal or myocardial tissue; (ii) the greater inhibition of vagal tone by nifedipine than by verapamil or diltiazem; and (iii) the greater inhibition of the atrioventricular node by verapamil and diltiazem. In angina of effort, calcium antagonists are now becoming the agents of first choice in some centers. Experimental use of calcium antagonists include the possible prevention of ventricular fibrillation, the inhibition of ischemic injury, the prevention of catecholamine mediated injury to the myocardium and decreased arterial calcinosis.

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Animals; Arrhythmias, Cardiac; Calcium; Calcium Channel Blockers; Catecholamines; Coronary Disease; Coronary Vasospasm; Coronary Vessels; Digoxin; Drug Interactions; Heart; Heart Failure; Humans; Hypertension; Myocardial Contraction; Myocardial Infarction; Myocardium; Prazosin; Sinoatrial Node; Structure-Activity Relationship; Ventricular Fibrillation

Topics: Adult; Cardiac Complexes, Premature; Cardiomyopathy, Dilated; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction

A thirty-six year old woman who had an acute myocardial infarction during the early postpartum period is described. Review of literature on the incidence of postpartum myocardial infarction, the possible mechanisms and its clinical implications are summarized.

Topics: Adult; Aspirin; Digoxin; Electrocardiography; Ergonovine; Female; Heart Aneurysm; Humans; Isosorbide Dinitrate; Myocardial Infarction; Nifedipine; Pregnancy; Puerperal Disorders

Digoxin was determined in postmortem serum samples from 100 patients who died suddenly of cardiac disease. Twenty patients had digoxin levels below the therapeutic range. Twenty-one patients had normal values within the therapeutic range (1.2-2.5 nmol/l). In ten cases there was probably an overdosage. Another 15 patients had markedly elevated levels. No digoxin concentration was found (below 0.5 nmol/l) in 34 patients. The importance of determination of digoxin levels both by the clinician and the pathologist is stressed as well as the necessity of using a correct sampling technique at autopsy.

Topics: Aged; Death, Sudden; Digoxin; Female; Forensic Medicine; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Animals; Cesium Radioisotopes; Coronary Circulation; Digoxin; Disease Models, Animal; Dogs; Electrocardiography; Heart Ventricles; Hemodynamics; Microspheres; Myocardial Contraction; Myocardial Infarction; Strontium Radioisotopes

Topics: Arrhythmias, Cardiac; Digoxin; Humans; Male; Middle Aged; Myocardial Infarction; Nursing Assessment

This brief review summarizes recent literature about plasma catecholamines as indices of sympathetic nervous and sympathoadrenomedullary activity in clinical cardiologic disease states. Many reports have described high plasma levels of norepinephrine, the neurotransmitter of the sympathetic nervous system, in acute myocardial infarction, congestive heart failure, the mitral valve prolapse syndrome, and early essential hypertension. Fewer studies have reported values for plasma epinephrine, which is the product of sympathoadrenomedullary secretion. The relationship between circulating catecholamine levels and activity of the sympathetic nervous system is obscured by ignorance about catecholamine removal mechanisms and regionalization of sympathetic outflow. Further, whether increased sympathetic outflow increases cardiovascular risk or reflects compensatory recruitment or a non-specific stress response is poorly understood.

Topics: Cardiovascular Diseases; Catecholamines; Coronary Disease; Digoxin; Epinephrine; Humans; Hypertension; Mitral Valve Prolapse; Myocardial Infarction; Norepinephrine

Forty-three patients in the acute phase of myocardial infarction who were resistant to conventional doses of lidocaine received Ajmaline intravenously (50 mg bolus followed by constant infusion rate of 1-1.5 mg/min). Dangerous ventricular arrhythmias were abolished in 72% of this group of patients (group A). In the remaining patients (28%), Ajmaline was found to be ineffective (group B). There was no reduction of systolic or diastolic blood pressure and there was an insignificant increase in heart rate. Atrio-ventricular or intraventricular conduction defects appeared in 46% of the patients described. There was a statistically significant increase in occurrence of heart blocks in group B patients and among these complete left bundle branch block (CLBBB) was the most prevalent. Atrio-ventricular or intraventricular conduction defects were transient, appearing between 8-36 h (mean 23 h), and were not accompanied by reduction of ventricular rate. Conduction defects disappeared within several hours (up to 24 hours) after Ajmaline was discontinued. It is concluded that Ajmaline administered by this regimen is an effective alternative agent for patients with ventricular arrhythmia not controlled by lidocaine in the acute phase of myocardial infarction.

Topics: Ajmaline; Cardiac Complexes, Premature; Digoxin; Heart Conduction System; Heart Failure; Humans; Lidocaine; Myocardial Infarction; Time Factors; Ventricular Fibrillation

Specific binding sites have been demonstrated to exist in the heart for several drugs and hormones such as beta-blocking agents, cardiac glycosides, catecholamines, insulin, glucagon and acetylcholine. The specific binding sites for cardiac glycosides in the human heart have certain properties which make it likely that they are the pharmacological receptors for the therapeutic and toxic actions of digitalis glycosides: they are located in the cell membrane and bind cardioactive steroids reversibly with high affinity: half-maximal receptor binding occurs at approximately 2 nM (approximately 1.5 ng/ml) for digoxin; potassium decreases receptor affinity, calcium increases it; specific binding of ouabain, digoxin or digitoxin is related to inhibition of (Na+ + K+)-ATPase activity--which is supposed to be the receptor enzyme for cardiac glycosides. Human left ventricle contains approximately 1.5 x 10(14) binding sites/g wet weight, right ventricle approximately 0.9 x 10(14). In disease the number of receptors may decrease (hypothyroid states, myocardial infarction) or increase (hyperthyroidism, chronic hypokalaemia). Certain drugs (such as phenytoin) or different temperatures or pH changes cause a change in digitalis-receptor affinity. Thus, the number of receptors and possibly their properties are subject to regulation in clinically relevant situations. Further investigations will probably reveal those pathophysiological states, which allow the explanation of toxicity or digitalis refractoriness.

Topics: Animals; Binding Sites; Cats; Cell Membrane; Cells, Cultured; Digitoxin; Digoxin; Guinea Pigs; Humans; Hypokalemia; Myocardial Infarction; Myocardium; Ouabain; Receptors, Drug; Sodium-Potassium-Exchanging ATPase; Thyroid Diseases

Topics: Cardiac Output; Digoxin; Echocardiography; Female; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction

Topics: Aged; Amiodarone; Atrial Fibrillation; Benzofurans; Digoxin; Female; Humans; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction

Topics: Aged; Digoxin; Electrocardiography; Female; Heart Valve Diseases; Humans; Male; Medigoxin; Middle Aged; Mitral Valve; Myocardial Infarction; Tachycardia; Time Factors

Topics: Aged; Digoxin; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Myocardial Infarction; Substance Withdrawal Syndrome

Topics: Aged; Coronary Disease; Digoxin; Echocardiography; Female; Humans; Male; Medigoxin; Middle Aged; Myocardial Contraction; Myocardial Infarction; Stimulation, Chemical; Time Factors

The prognostic importance of ventricular arrhythmias detected during 24 hour ambulatory monitoring was evaluated in 395 patients with and 260 patients without significant coronary artery disease. Ventricular arrhythmias were found to be strongly related to abnormal left ventricular function. A modification of the Lown grading system (ventricular arrhythmia score) was the most useful scheme for classifying ventricular arrhythmias according to prognostic importance. When only noninvasive characteristics were considered, the score contributed independent prognostic information, and the complexity of ventricular arrhythmias as measured by this score was inversely related to survival. However, when invasive measurements were included, the ventricular arrhythmia score did not contribute independent prognostic information. Furthermore, ejection fraction was more useful than the ventricular arrhythmia score in identifying patients at high risk of sudden death.

Topics: Adrenergic beta-Antagonists; Ambulatory Care; Angina Pectoris; Arrhythmias, Cardiac; Cardiac Catheterization; Cardiac Output; Coronary Disease; Death, Sudden; Digoxin; Electrocardiography; Female; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Prognosis

Atrial synchronous pacemakers have been known to cause a variety of cardiac arrhythmias. Of particular concern are those arrhythmias involving a pacemaker stimulus occurring on a T wave, because these may lead to ventricular tachycardia. The Medtronic 2409 ASVIP pacemaker is an atrial synchronous pacemaker with several features designed to decrease the likelihood of such arrhythmias. We report a patient in whom a normally functioning Medtronic 2409 ASVIP pacemaker, despite these features, induced recurrent ventricular tachycardia. Conditions which predisposed this patient to pacemaker-induced re-entrant arrhythmias are discussed.

Topics: Digoxin; Electric Countershock; Electrophysiology; Female; Heart Block; Heart Failure; Heart Ventricles; Humans; Middle Aged; Myocardial Infarction; Pacemaker, Artificial; Procainamide; Tachycardia

Although most cases of sustained atrial fibrillation are associated with mitral valve disease, hypertension, cardiac failure and atherosclerotic heart disease, some cases occur in the absence of any identifiable organic pathology. The consequences of atrial fibrillation include reduction in cardiac output, systemic emboli and an exaggerated ventricular response to exercise. In most clinical situations, digoxin is the drug of choice for controlling the ventricular response. Cardioversion should be undertaken in appropriately selected patients.

Topics: Age Factors; Aged; Atrial Fibrillation; Cardiomegaly; Digoxin; Electric Countershock; Electrocardiography; Heart Failure; Humans; Hypertension; Male; Middle Aged; Mitral Valve Stenosis; Myocardial Infarction; Verapamil

Results of haemosorption in treating digitalis intoxication are analyzed. In 2 patients haemosorption was used for 90 min at the volume speed of 100 ml/min. Digoxin clearance at the start of haemosorption was 98.4 and 83.8 ml/min, at the end 85.7 and 70.3 ml/min. Digoxin concentration decreased by 44.8 and 13.0%. Hemosorption enabled performing electric defibrillation with restoration of the sinus rhythm.

Topics: Aged; Digitalis Glycosides; Digoxin; Electrocardiography; Heart Failure; Hemoperfusion; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Diazepam; Digoxin; Diuretics; Dyspnea; Emergencies; Epinephrine; Glucocorticoids; Humans; Lidocaine; Myocardial Infarction; Nitrates; Pulmonary Edema; Theophylline

A prospective study of 182 patients undergoing cardiac surgery was performed. The patients were divided into three groups. Group I consisted of 83 patients who had never been treated with digitalis. Group II comprised 59 patients who were taking digoxin before operation and had medication discontinued 24 to 48 hours prior to surgery; they did not receive maintenance digoxin in the postoperative periods. Group III was made up of 40 patients who were given prophylactic digoxin in the perioperative period; none had taken digoxin before. Sixty of 83 group I patients (72%) and two of the group III patients (5%) developed postoperative supraventricular tachyarrhythmia. Digoxin was reinstituted in 56 of group II patients (95%) for supraventricular arrhythmia and/or heart failure. Of the various factors evaluated, only valvular surgery and ECG evidence of myocardial infarction were associated with postoperative supraventricular tachyarrhythmias.

Topics: Adult; Aged; Arrhythmias, Cardiac; Cardiac Surgical Procedures; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction; Postoperative Complications; Premedication; Preoperative Care; Prospective Studies

Topics: Angina Pectoris; Coronary Circulation; Coronary Disease; Digoxin; Hemodynamics; Humans; Middle Aged; Myocardial Infarction

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atropine; Bradycardia; Cardiac Complexes, Premature; Digoxin; Heart Block; Heart Failure; Humans; Lidocaine; Myocardial Infarction; Propranolol; Tachycardia

The comparative effects of normothermic intermittent ischemic arrest (IIA) and cardioplegia (C) on left ventricular (LV) performance were assessed by gated cardiac blood pool imaging in 57 patients undergoing aortocoronary bypass surgery. In 34 patients, IIA was employed; 23 patients received C. Patients were studied preoperatively, sequentially in the immediate postoperative period at 30-minute intervals, and at 1 week after the operation, C and IIA groups did not differ in mean (+/- SEM) age, anginal class, number of diseased vessels, previous myocardial infarction, or preoperative ejection fraction (EF)(50 +/- 3% vs 50 +/- 2% [p = ns]). Aortic cross clamp time was greater with C than IIA (50 +/- 5 minutes vs 28 +/- 3 minutes [p = 0.001]). During the six sequential postoperative studies, transient LV dysfunction (greater than or equal to 7% decrease in absolute EF) was observed in 10 patients receiving C and in 16 patients receiving IIA. By time of discharge, 24 of 26 patients had returned to preoperative EF. Mean EF at discharge in the cardioplegia group did not differ compared to preoperative EF; in the IIA group, EF increased compared to preoperative EF (50 +/- 2% vs 55 +/- 2% [p < 0.01]). These data suggest that in patients with normal preoperative LV performance both C and IIA afford satisfactory myocardial preservation during aortocoronary bypass surgery.

Topics: Aorta; Blood Pressure; Cardiac Output; Coronary Artery Bypass; Digoxin; Electrocardiography; Female; Heart Arrest, Induced; Heart Rate; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Postoperative Care; Pulmonary Wedge Pressure; Radionuclide Imaging; Time Factors

Topics: Analgesics; Atropine; Digoxin; Dobutamine; Dopamine; Drug Therapy, Combination; Heart Failure; Heart Rupture; Hemodynamics; Humans; Hypertension; Hypotension; Myocardial Infarction; Propranolol; Shock, Cardiogenic; Vasodilator Agents

Topics: Acute Disease; Body Surface Area; Digoxin; Electrocardiography; Humans; Myocardial Infarction; Necrosis; Propranolol

In the acute stage of transmural myocardial infarction, 22 patients ranging in age from 34 to 76 (mean 61.6) were given propranolol- because of its alleged myocardium-protecting properties - intravenously at a dosage of 0.03 to 0.1 mg/kg body weight under conditions of continuous hemodynamic control. Subsequently, the influence of digoxin, administered i. v. at a dosage of 0.01 my/kg body weight, on the negative-inotropic propranolol effects was examined. A hemodynamic comparison was made of the effects of propranolol before and after digitalis administration. In patients with compensated cardiac function (group 1, 16 patients), the propranolol-induced drop in the left ventricular stroke-work-index and rise in the left-ventricular filling pressure was completely compensated again by digitalis. The frequency-decreasing propranolol effect was nor influenced by digitalis. In patients with cardiac decompensation (group 2, 6 patients) digitalis only led to a renewed compensation of the left-ventricular stroke-work-index, the rise of the left-ventricular filling pressure remained unaffected. It follows from that, in cases of myocardial infarction without cardial decompensation, propranolol requires concomitant digitalisation. In cases of already existent myocardial insufficiency, propranolol can produce an unfavorable increase of the decompensation signs.

Topics: Acute Disease; Adult; Aged; Digoxin; Drug Therapy, Combination; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Propranolol

The left ventricular filling pressure (LVFP) was measured within 12 hours of onset of acute myocardial infarction (AMI) in 99 patients, including 21 nonsurvivors. Initial LVFP for survivors was 18 +/- 6 mm Hg (mean +/- SD) and for nonsurvivors was 24 +/- 8 mm Hg (p less than 0.005). Of the total population, 87% had initial LVFP of 12 mm Hg or greater and all nonsurvivors were in this group. Life table analysis was employed to determine LVFP related mortality rates. If initial LVFP was less than or equal to 18 mm Hg, 72-hour mortality rate was 4% and 30-day mortality rate was 10%. For initial LVFP greater than 18 mm Hg, 72-hour mortality rate was 21% and 30-day mortality rate was 33% (p less than 0.005 for both 72 hours and 30 days). When final LVFP was analyzed 30-day mortality rate for final LVFP less than or equal to 18 mm Hg was 5%. Mortality rate of 60% was observed for final LVFP greater than 18 mm Hg. We compared sequential measurements of LVFP in a subset of survivors and nonsurvivors and observed that long-term average trend was for survivors to decrease their LVFP. We conclude that AMI mortality rate is related to LVFP and that LVFP greater than 18 mm Hg is associated with very high mortality rate when compared to LVFP less than or equal to 18 mm Hg. Thus reduction of LVFP either spontaneously or as result of therapy may lower AMI mortality rate.

Topics: Actuarial Analysis; Acute Disease; Aged; Blood Pressure; Digoxin; Female; Furosemide; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Nitrates; Prognosis; Sympathomimetics; Time Factors

We studied the interference of the sample matrix on digoxin radioimmunoassays using four commercial kits. Plasma samples from non-digitalized patients of the following categories were assayed: uncomplicated essential hypertension treated with spironolactone, uremia, and acute myocardial infarction (AMI). Digoxin 2.50 nmol/L was added to all samples. Digoxin in plasma from patients on spironolactone was overestimated by two of the kits (means 2.77 and 2.68 nmol/L, respectively; p less than 0.01) and underestimated in samples from uremic patients by one kit (2.32 nmol/L; p less than 0.01). The digoxin content of AMI plasma was overestimated by one kit (2.62 nmol/L; p less than 0.05). Significant differences were found between radioimmunoassays when estimating digoxin concentration in the same category of patient and within individual methods used for different categories. Precision expressed as 95% confidence intervals ranged from 0.43 to 0.80 nmol/L for the kits. Thus, deviations in recorded digoxin concentrations from the true values found, but were of secondary importance because of the relatively low precision of the assays.

Topics: Digoxin; False Positive Reactions; Humans; Hypertension; Myocardial Infarction; Radioimmunoassay; Reagent Kits, Diagnostic; Spironolactone; Uremia

Fifty-five patients were hospitalized in a Coronary Care Unit within the first 24 hours after onset of symptoms of an acute myocardial infarction. The sum of positive and negative ST-segment deflections of their twelve leads electrocardiograms (epsilon ST12) showed a maximum within the 3rd hour from the onset of symptoms. Thereafter, in the first 24 hours, there was a marked reduction in epsilon ST12, with a steep and significant fall within the 7th hour from symptoms. In the following nine days of this study, the patients showed 4 different epsilon ST trends, but there was no significant correlation with CPK curves, or with the kind of therapy the patients underwent. An irregular trend of epsilon ST12 or a secondary late rise (after 36 hours from symptoms) suggest an unfavorable prognosis (1 death in the epsilon ST-3 group, and 2 deaths + 1 ventricular fibrillation in the epsilon ST-4 group). No significant difference results between the patients treated with high doses Heparin plus Acetyl-Salicylic-Acid (A.S.A.), and the patients treated with A.S.A alone, though the first treatment seems to reduce the values of epsilon ST12 more rapidly; perhaps this behaviour is due to the use of antiplatelet drug A.S.A in both groups, and to the relatively small number of patients.

Topics: Aged; Aspirin; Digoxin; Diuretics; Electrocardiography; Female; Heparin; Humans; Male; Middle Aged; Myocardial Infarction; Nitro Compounds; Oxygen Inhalation Therapy

Topics: Adult; Catecholamines; Digoxin; Dobutamine; Female; Heart Failure; Humans; Myocardial Infarction

Left ventricular responses to dynamic and static exercises were compared in 20 patients three weeks after myocardial infarction. Radiocardiography was used to determine the ventricular volumes at rest and during hand grip and bicycle exercise tests. The dynamic exercise increased cardiac output (p less than 0.001), and the end-diastolic volume of the left ventricle increased (p less than 0.005) from the resting value while the ejection fraction decreased (p less than 0.005). Static hand grip exertion did not increase cardiac output or the end-diastolic volume. Decrease of the stroke volume and the ejection fraction (p less than 0.001 both) again reflected pump dysfunction during the afterload stress. Our data revealed that patients with recent myocardial infarction had a range of ventricular responses to dynamic exercise. Poor response in the ejection fraction was noted in anterior infarction and in those patients using digoxin and/or diuretics after infarction. During static exercise, on the other hand, impairment of cardiac performance was constant, irrespective of the site of infarction. Reduction of the ejection fraction was greater during static exercise in the patients receiving digoxin and/or diuretics than in those not taking these drugs.

Topics: Adult; Digoxin; Diuretics; Exercise Test; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction

The cardiovascular responses to dynamic and static exercises were studied in 20 patients by exercise tests performed at 3 weeks and 12 weeks after acute myocardial infarction. The left ventricular size and volume output were determined by radiocardiography. The mean cardiac output during dynamic exercise at the second study was 24% (p less than 0.05) higher than at the first study, mainly because the peak heart rate was 19% (p less than 0.05) higher. The left ventricular end-diastolic volume or its response to ergometric exercise did not change during the 3-month follow-up and the ejection fraction and stroke volume showed minor changes only. During static exercise a 3% better increase in cardiac output was seen from 3 to 12 weeks, without any improvement in ejection fraction. At the 12-week study the changes in cardiac performance during ergometric exercise were not related to the site of infarction or drug therapy. During static exercise slight improvement of cardiac output, stroke volume and ejection fraction responses were seen in the course of time, but only in the patients with inferior infarction and in those not receiving digoxin and/or diuretics. The mean cardiac output during dynamic exercise improved by one-quarter, mainly due to a higher peak heart rate, in the course of the 3-month follow-up after myocardial infarction. Otherwise, haemodynamic variables during dynamic or static exercises within 3 months showed insignificant sequential changes only.

Topics: Adult; Digoxin; Diuretics; Exercise Test; Follow-Up Studies; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Aged; Digoxin; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction

Three hundred fifty-eight of 429 (83%) consecutive patients with acute myocardial infarction (MI) and a normal PR interval received various antiarrhythmic drugs (AD), including lidocaine and/or procainamide, quinidine, digoxin, propranolol or disopyramide. There was no significant difference in the incidence of progression to any degree of atrioventricular (AV) block or to higher degrees of AV block (Mobitz II or third-degree AV block) between those treated and not treated with AD: 38 of 358 (11%) and six of 358 (1.7%) with AD vs 11 of 71 (15%) and two of 71 (2.8%) in the untreated group, respectively. Similarly, there was no significant difference in progression between treated and untreated patients with anterior MI, 14 of 144 (10%) vs five of 32 (16%); inferior MI, 21 of 111 (19%) vs five of 26 (19%), or subendocardial MI, three of 103 (3%) vs one of 12 (8%). Bundle branch block (BBB) (without AV block) was initially present in 89 of 249 (21%). The incidence of AV block (seven of 24, 30%) was higher in treated patients with newly acquired BBB (27 patients) than in the untreated patients (none of three, p less than 0.05). The commonly used ADs did not adversely affect AV conduction in patients with acute MI with narrow QRS and either normal, first-degree, or Mobitz I AV block. Moreover, no subset of patients grouped by infarct location, specific AD used, or BBB (except perhaps for those with newly acquired BBB) appeared to be at risk of development of AV block during AD therapy.

Topics: Aged; Anti-Arrhythmia Agents; Bundle-Branch Block; Digoxin; Disopyramide; Heart Block; Heart Conduction System; Humans; Lidocaine; Male; Middle Aged; Myocardial Infarction; Procainamide; Propranolol; Quinidine; Time Factors

The use of digitalis after acute myocardial infarction is controversial. The effect of digoxin on computer-quantitated thallium-201 perfusion scintigrams (Tl-201), left ventricular (LV) ejection fraction (EF), and percentage of abnormally contracting LV regions (% ACR) was determined in 23 patients. A correlation was established between creatine kinase MB isoenzyme release and initial radionuclide-gated blood pool wall motion estimates of EF (r = -0.73) and % ACR (r = 0.71). After radionuclide assessments, 14 patients received digoxin 18 +/- 23 hours (mean +/- SD) after the rise in CK-MB from baseline, while the remaining nine patients served as controls. In the control group, the mean EF was 0.33 +/- 0.12 on the first study and 0.30 +/- 0.08 on the second study (p = NS). In the digoxin group, the EF after digoxin administration (mean 0.33 +/- 0.11) was significantly different from the initial EF (mean 0.29 +/- 0.09, p less than 0.03); however, digoxin had no apparent effect on infarct size as assessed by sequential % ACR and Tl-201 perfusion data. These data indicate that digoxin resulted in a minimal but significant improvement in EF that did not occur at the expense of LV perfusion or regional wall motion.

Topics: Adult; Aged; Digitalis Glycosides; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction; Radionuclide Imaging

In 25 digitalized patients with ischaemic heart disease who had survived a myocardial infarction for 2 to 4 weeks, the systolic time intervals (STI) and changes of glycoside plasma level were measured before and up to 5 hrs after oral intake of a maintenance dose of digitoxin (n = 18) or of digoxin (n = 7). Between the changes of STI and the increase in digitoxon and digoxin plasma level no significant correlations were found. Therefore it is concluded that neither shortening of STI during the test period nor PEP/LVET are reliable criteria of individualizing and optimizing the therapy with cardioactive glycosides.

Topics: Adult; Aged; Digitalis Glycosides; Digitoxin; Digoxin; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Myocardial Contraction; Myocardial Infarction

The hemodynamic effects of dobutamine were compared with those of digoxin in six patients with cardiac failure within 24 hours of onset of acute myocardial infarction. Dobutamine (8.5 microgram per kilogram of body weight per minute) was given intravenously for 30 minutes and then discontinued until hemodynamics returned toward base line. Digoxin (12.5 microgram per kilogram) was then given intravenously, and hemodynamics were recorded for 90 minutes. Dobutamine decreased left ventricular filling pressure (from 22.3 to 9.8 mm Hg, P < 0.02) and systemic vascular resistance (1686 +/- 188 to 1259 +/- 108 dynes . sec . cm-5), and increased cardiac index (from 2.4 to 3.2 liters per minute per square meter of body-surface area, P < 0.005) and stroke work index (from 24.6 to 36.6 g . m per square meter, P < 0.02), without changing heart rate or arterial pressure. In contrast, digoxin had no effect on filling pressure (18.3 versus 17.0) and only a slight effect on cardiac index (2.2 versus 2.4, P < 0.05) and stroke work index (21.9 versus 27.6, P < 0.05). Thus, dobutamine markedly increased cardiac output, decreased filling pressure, and relieved pulmonary congestion. Digoxin, did not affect preload or afterload.

Topics: Aged; Blood Pressure; Catecholamines; Digoxin; Dobutamine; Female; Heart Failure; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Vascular Resistance

In a prospective survey of treatment on a coronary care unit 23.6% of patients who received medication had one or more side effects. In several cases these were severe enough to cause marked deterioration of the patient's clinical status. Whilst antiarrhythmic therapy is an integral part of modern coronary care its potential hazards should be recognized, particularly in the elderly patient.

Topics: Adrenergic beta-Antagonists; Adult; Age Factors; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atropine; Coronary Care Units; Digoxin; Humans; Lidocaine; Middle Aged; Myocardial Infarction; Prospective Studies

In 1976, 130 patients aged 70 or older were admitted to the Coronary Care Unit (CCU) at Toronto Western Hospital. Arrhythmias were noted in all but 24 percent. Digoxin was given to 53 patients, lidocaine to 24, propranolol to 28, and quinidine to 11. In 2 patients, cardioversion by direct current was required for supraventricular arrhythmias. In 26 patients, temporary pacemakers were used. Of 13 patients who experienced at least one cardiac arrest in the CCU, 10 survived to be discharged to the ward. In total, only 12 of the 130 elderly patients died in the hospital, and in only 3 of these was arrhythmia the primary cause of death. The treatment of arrhythmias in the elderly is as successful and rewarding as in younger patients. Indications for the various antiarrhythmic drugs are similar. Except for digoxin, the dosages of such drugs for the elderly are the same as those for younger patients. Adverse effects apparently are not more common in the elderly.

Topics: Aged; Arrhythmias, Cardiac; Atropine; Cardiac Pacing, Artificial; Coronary Care Units; Digoxin; Electric Countershock; Electrocardiography; Female; Humans; Lidocaine; Male; Myocardial Infarction; Ontario; Procainamide; Propranolol; Quinidine

Topics: Acute Disease; Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Ferricyanides; Heart Failure; Hemodynamics; Humans; Infusions, Parenteral; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Nitroprusside; Pulmonary Circulation; Vascular Resistance

Topics: Animals; Coronary Vessels; Digoxin; Dogs; Iodine Radioisotopes; Myocardial Infarction; Myocardium

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).

Topics: Adult; Aged; Anti-Arrhythmia Agents; Cardiac Pacing, Artificial; Coronary Angiography; Digoxin; Diuretics; Electric Countershock; Female; Heart Aneurysm; Heart Ventricles; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Tachycardia

A patient with alternating atrial and ventricular tachycardia is described. He had an acute myocardial infarction and was taking digitalis. The atrial tachycardia, which was occasionally associated with aberrant ventricular conduction, was able to interrupt the ventricular tachycardia though the reverse was not true, suggesting a retrograde conduction block. This patient shows that atrial and ventricular arrhythmias can alternate and, since tachycardia with aberrant ventricular conduction can closely resemble ventricular tachycardia, intra-atrial electrocardiography may be necessary to establish an accurate diagnosis.

Topics: Digoxin; Electrocardiography; Heart Atria; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Tachycardia

The effect of digoxin on the cardiac index and diastolic pressure in the pulmonary artery was studied in 17 patients with acute myocardial infarction on the 1st-3rd day of the disease by the method of thermodilution. Twelve of these patients had clinical manifestations of congestive circulatory insufficiency. Digoxin was infused intravenously in a dose of 0.5 mg. Its infusion led to reduction of diastolic pressure in the pulmonary artery from 19.0 to 16.7 mm Hg and rise of cardiac index from 2.26 to 2.4 1/min/m2 (statistically untrustworhty difference). In all cases digoxin concentration in blood serum examined by the radioimmune method was therapeutical (1.64 ng/ml, on the average). The positive hemodynamic effect of digoxin infused in a dose producing its therapeutic concentration in blood is negligible.

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction; Pulmonary Circulation; Stroke Volume; Systole

The effects of acute myocardial infarction on the pharmacokinetics of digoxin were studied. Digoxin, 0.75 mg, was given orally to 12 patients with left-sided cardiac failure due to acute myocardial infarction and to 9 healthy control subjects. Serum concentration of digoxin in the first 4 hours and the area under the serum concentration-time curve in the first 12 hours after administration of the drug were lower in patients with infarction than in control subjects (P less than 0.01). The 24 hour area under the concentration curve, the amount excreted in urine and the renal clearance did not differ between the groups. The 24 hour area under the concentration curve correlated with the predigoxin pulmonary capillary wedge pressure and with heart rate (P less than 0.01). The decrease of renal clearance of digoxin was related to the serum activity of MB isoenzyme of creatine kinase (P less than 0.001). Morphine reduced and delayed the peak serum concentrations of digoxin (P less than 0.001). Thus, the absorption of oral digoxin was slower and the peak concentrations remained lower in patients with acute myocardial infarction than in healthy control subjects. However, the total amount of digoxin absorbed was unchanged.

Topics: Administration, Oral; Adult; Aged; Blood Pressure; Cardiac Output; Creatine Kinase; Digoxin; Female; Heart Failure; Heart Rate; Humans; Isoenzymes; Male; Middle Aged; Myocardial Infarction; Pulmonary Circulation; Time Factors

Topics: Adult; Aged; Digoxin; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction

The hemodynamic effects of nitroglycerin and nifedipin and the application of both substances during a long term training program in patients with angina pectoris, myocardial infarction, and myocardial dysfunction (=48) were studied. Cardiac output, heart rate, and arterial blood pressure showed no significant changes after application of nitroglycerin and nifedipin. After nitroglycerin, however, there were significant drops of pulmonary arterial pressure and right atrial pressure during rest and exercise, whereas no changes were seen after nifedipin. With the application of nitroglycerin (but not with nifedipin) prior to the daily physical training program on a bicycle ergometer, all patients with angina pectoris and myocardial dysfunction showed an increasing training effect during the long term program and their angina pectoris improved.

Topics: Angina Pectoris; Blood Pressure; Cardiac Complexes, Premature; Cardiac Output; Digoxin; Exercise Therapy; Heart Rate; Humans; Myocardial Infarction; Nifedipine; Nitroglycerin; Pulse; Pyridines

Atrioventricular nodal alternating Wenckebach periods were defined as episodes of 2:1 atrioventricular block in which there was a gradual increase in transmission intervals of conducted beats ending in two or three consecutively blocked atrial impulses. This is one of the mechanisms whereby 2:1 atrioventricular block progresses into 3:1 or 4:1 atrioventricular block. Alternating Wenckebach periods appear during rapid atrial pac,ng (even in the absence of depressed atrioventricular nodal function), provided that the atria can be captured at a rate fast enough to allow for the occurrence of this phenomenon. Treatment of atrial flutter with digoxin and quinidine produces alternating Wenckebach's periods, with associated electrocardiographic changes specific for the type of drug given. In patients with "atrial tachycardia with atrioventricular block" due to digitalis intoxication or with primary disease of the conducting system or with acute myocardial infarction, there are coexisting severe arrhythmias and clinical symptoms requiring almost immediate pharmacologic or electrical therapy. We conclude that atrioventricular nodal alternating Wenckebach's periods are common and frequentyly transient and that they occur in a variety of clinical conditions, most of which are benign; however, contrary to what is commonly accepted, some episodes appear in clinical settings requiring prompt pharmacologic or electrical treatment.

Topics: Acute Disease; Atrial Flutter; Atrioventricular Node; Bundle of His; Digitalis Glycosides; Digoxin; Electrocardiography; Heart Atria; Heart Block; Heart Conduction System; Heart Diseases; Humans; Myocardial Infarction; Pacemaker, Artificial; Purkinje Fibers; Quinidine; Tachycardia

Topics: Catecholamines; Digoxin; Female; Humans; Male; Myocardial Infarction; Oxygen Consumption

Topics: Acute Disease; Digoxin; Drug Therapy, Combination; Electric Countershock; Humans; Lidocaine; Myocardial Infarction; Procainamide; Ventricular Fibrillation

Topics: Aged; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction

Topics: Acute Disease; Cardiac Output; Digitalis Glycosides; Digoxin; Furosemide; Heart Failure; Heart Rate; Heart Ventricles; Humans; Myocardial Contraction; Myocardial Infarction; Oxygen Consumption; Shock, Cardiogenic; Stimulation, Chemical

Haemodynamic tests were performed at rest and during exercise in 41 patients with arterial hypertension and early impairment of left-ventricular function, before and after administration of a single dose of 0.6 mg beta-methyl-digoxin. After clinical, ECG and coronary-angiographic studies, the patients were assigned to two groups. Group I: 17 patients with transmural infarcts in the chronic stage or with angina. Cardiac output was within normal limits at rest and on exercise and was not significantly altered by administration of beta-methyl-digoxin. There was no significant fall during exercise of the abnormally elevated pulmonary "wedge" pressure or of other pressures in the lesser circulation after digitalis. Group II: 24 patients without signs of coronary heart disease. They, too, had a normal cardiac output at rest and on exercise, not significantly changed by digitalisation with beta-methyl-digoxin. But pulmonary "wedge" pressure and right-atrial mean pressure were significantly reduced during exercise. Before beta-methyl-digoxin the mean "wedge" pressure rose on exercise to an average of 27.3 +/- 5.4 mm Hg, but after beta-methyl-digoxin to only 21.7 +/- 5.1 mm Hg (P less than 0.001). The mean right atrial pressure changed similar. These results indicate that acute digitalisation at the stated dosage in general has an effect on abnormal myocardial function only if there is no additional coronary heart disease.

Topics: Adult; Angina Pectoris; Blood Pressure; Capillaries; Cardiac Output; Digoxin; Electrocardiography; Humans; Hypertension; Lung; Middle Aged; Myocardial Infarction; Physical Exertion; Time Factors

Topics: Digoxin; Diuretics; Humans; Myocardial Infarction

The pharmacokinetics of digoxin, the most frequently used digitalis preparation, are reviewed. The dominate serum turnover time is about 34 hours, and is not affected by the route of administration. Excretion is largely as unchanged digoxin in the urine and this excretion is compromised in renal failure. Serum levels of digoxin (determined by radioimmunoassay) are generally available and are useful clinically in assessment of both toxicity and the state of underdigitalization, even though significant overlap exists. Special problems are presented in patients with myocardial infarction, pulmonary heart disease, and thyroid disease.

Topics: Acute Kidney Injury; Aging; Digitalis Glycosides; Digoxin; Heart Rate; Kidney; Kinetics; Myocardial Contraction; Myocardial Infarction; Obesity; Pulmonary Heart Disease; Structure-Activity Relationship; Thyroid Diseases; Water-Electrolyte Balance

Topics: Adult; Aged; Amiodarone; Atrial Fibrillation; Atrial Flutter; Benzofurans; Digoxin; Female; Humans; Male; Middle Aged; Myocardial Infarction; Pulmonary Heart Disease; Rheumatic Heart Disease

In 59 digitalized and 3 non digitalized patients the effect of digitalis during the 1st to 4th days after transmural myocardial infarction was controlled. Rhythm disturbances in acute myocardial infarction may arise secondary to a complicating cardiac failure and may be influenced by digitalis. In 9 of 17 cases (53 p.c.) with ventricular or supraventricular extrasystoles daily doses of 0,4 mg beta-Methyldigoxin or 0,4 mg Digoxin i.v. resulted in undisturbed sinus rhythm. In two cases supraventricular tachycardia and extrasystoles with rapid ventricular rate were abolished by 1,2 mg beta-Methyldigoxin within 12 hours, in three other cases an improvement was recorded. Dysrhythmias or other complications did not occur in previously non digitalized patients. When the antiarrhythmic effect of digitalis cannot be obtained cardiodepressive complications by treatment with typical antiarrhythmic agents are diminished. In patients on digitalis and in cardiogenic shock, digitalization should be performed carefully. Intoxication leads to a diminution of cardiac output and to cardiac dysrhythmias.

Topics: Acute Disease; Adult; Aged; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Digitalis Glycosides; Digoxin; Drug Interactions; Female; Heart Block; Humans; Male; Middle Aged; Myocardial Infarction; Premedication; Shock, Cardiogenic; Tachycardia

In 20 patients with acute myocardial infarction hemodynamic controls were performed after digitalisation and following i.v. injection of 0,4 mg of Prindolol. Circulatory changes were most pronounced 5-15 min after Prindolol injection and consisted of decrease in heart rate of 7%, mean arterial blood pressure of 6%, cardiac output of 10,5%, stroke volume index of 5,1% and left ventricular work of 18%. An increase of pulmonary wedge pressure of 17%, pulmonary pressure of 9%, mean right atrial pressure of 16% and peripheral arterial resistance of 6% were calculated. In 5 cases a favourable effect on extrasystoles and in 2 cases on sinus tachycardia were observed. Not infrequently, during the initial phase of acute myocardial infarction, a hyperadrenergic state may be noted. Prindolol may be indicated, when circulatory changes or arrhythmias are suspect to be the result of this hyperadrenergic stimulation. A simultaneous digitalisation may inhibit a more intensive cardiodepression.

Topics: Acute Disease; Adult; Aged; Blood Pressure; Cardiac Complexes, Premature; Cardiac Output; Digitalis Glycosides; Digoxin; Female; Heart Rate; Heart Ventricles; Hemodynamics; Humans; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Pindolol; Pulmonary Artery; Shock, Cardiogenic; Tachycardia; Time Factors; Vascular Resistance

In recent years it has become possible by means of a radioimmunoassay to measure Digoxin concentration in the serum of digitalized patients. With this method it could be shown that the resorption of Digoxin is decreased by partial resection of the samll intestines, by malabsorption syndromes, after ingestion of Neomycin, Colestyramine and antacids. In renal insufficiency, however, the elimination half-life period of Digoxin is increased conspiciously (from about 35 hours up to about 120 hours). This results in a raised serum concentration of cardiac glycosides unless the dosage is decreased considerably. The incidence of Digitalis intoxication in Digitalis treated patients has been reported to rank as high as 20%. There is, however, no strict correlation between the serum glycoside level and the clinical symptoms, because the glykoside concentration in the serum does not represent the pharmacologically active concentration at the receptor. Experimental investigations of cardiac glycoside binding to the receptor for cardiac glycosides in human heart cell membranes revealed, that receptor bound Digoxin for instance is diminished in serious renal insufficiency and it depends on the serum concentration of potassium, calcium and magnesium. In hypoxia, after myocardial infarction and in myxedema the sensitivity for cardiac glycosides is increased. The opposite is true in hyperthyreoidism, fever and in children. All of these factors have to be kept in mind and paid attention to in the clinical evaluation of the measured Digoxin concentration in the serum.

Topics: Cardiac Complexes, Premature; Cells; Digoxin; Humans; Intestinal Absorption; Kidney; Male; Myocardial Infarction; Myocardium

Nine children with endocardial fibroelastosis were followed from the time of admission with congestive heart failure until either death or discharge. Review of multiple clinical features showed that only the electrocardiographic pattern could be correlated with death or survival. The presence of a delayed transition zone with anterior force loss on the initial electrocardiogram ('infarct pattern') was noted in all the children who died. Progression of these changes with a pattern of anterolateral 'infarct' in two and inferior wall 'infarct' in two occurred before death. Necropsy on three of the four children confirmed the diagnosis of endocardial fibroelastosis. There was extensive fibrosis and thinning of the left ventricular myocardium as well as involvement of the mitral valve structures. Review of published cases supports the view that an 'infarct' pattern in a child with endocardial fibroelastosis is usually associated with death and that this pattern is a negative prognostic sign for survival.

Topics: Cardiomegaly; Child; Child, Preschool; Digoxin; Electrocardiography; Endocardial Fibroelastosis; Female; Follow-Up Studies; Heart Failure; Humans; Infant; Male; Myocardial Infarction; Prognosis

Topics: Arrhythmias, Cardiac; Digitalis Glycosides; Digoxin; Diuretics; Drug Therapy, Combination; Heart Diseases; Heart Failure; Humans; Myocardial Infarction; Potassium

Topics: Aged; Aging; Anesthesia; Arrhythmias, Cardiac; Blood Circulation; Cardiovascular Physiological Phenomena; Digoxin; Heart Failure; Humans; Hypertension; Myocardial Infarction; Pacemaker, Artificial; Propranolol; Risk

Topics: Aged; Coronary Disease; Digoxin; Exercise Therapy; Female; Humans; Male; Middle Aged; Myocardial Infarction; Oxyfedrine

Of 32 patients with acute myocardial infarction complicated by sinoatrial disease, 23 survived. All 23 had inferior infarction. During follow-up lasting 4 to 6 years only one patient developed severe chronic sinoatrial disease (sick sinus syndrome) necessitating permanent pacemaker treatment; twelve others died during this time. In 2 of them death was sudden 5 and 6 months after infarction. Atrial pacing studies in 7 of the 11 patients still alive showed no gross abnormalities. A review of 71 patients with chronic sinoatrial disease treated with a permanent pacemaker revealed only 5 with previous documented infarction. The present data suggest that sinus node dysfunction in patients surviving acute infarction is most often only temporary as is atrioventricular block. Occasionally, however, severe chronic sinoatrial disease requiring a permanent pacemaker may develop later, and this course of events is most likely to occur in those patients who had additional complications during the acute infarct.

Topics: Adult; Aged; Arrhythmia, Sinus; Digoxin; Electrocardiography; Female; Heart Rate; Humans; Male; Middle Aged; Myocardial Infarction; Pacemaker, Artificial; Prognosis

Topics: Angina Pectoris; Digoxin; Humans; Myocardial Infarction; Physical Exertion; Vectorcardiography

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Female; Furosemide; Heart Rate; Humans; Hydrogen-Ion Concentration; Male; Microcirculation; Middle Aged; Myocardial Infarction; Osmotic Pressure; Oxygen; Pulmonary Circulation; Pulmonary Edema; Respiration; Shock, Cardiogenic; Water-Electrolyte Balance

The effects of bypass graft surgery versus continued medical management in 40 patients with stable angina were evaluated at 2 years: 17 of 20 surgical patients (85%) and 18 of 20 medical patients (90%) were alive, and 5 of 20 surgical patients (25%) and 2 of 20 medical patients (10%) had developed myocardial infarction; 8 of 17 surgical patients (47%) and 4 of 18 medical patients (22%) had no angina, and 13 of 17 surgical patients (76%) and 9 of 18 medical patients (50%) had no angina or greater than 25% increase in exercise time until angina. No statistically significant differences were demonstrated between the medical and surgical groups for all variables submitted to statistical analysis.

Topics: Angina Pectoris; California; Coronary Artery Bypass; Digoxin; Follow-Up Studies; Humans; Male; Middle Aged; Myocardial Infarction; Physical Exertion; Saphenous Vein; Statistics as Topic; Time Factors; Transplantation, Autologous

Of the 27 patients described, 23 were in cardiogenic shock, 2 had severe left ventricular failure, and 2 had medically refractory ventricular tachycardia. Utilizing intraaortic counterpulsation, adequate systemic blood pressure was initially restored in 19 patients. Nine of these were subsequently weaned from circulatory assistance, but only three were discharged from the hospital and are currently alive. The remaining 10 patients who derived initial benefit from circulatory assistance were balloon-dependent in that they could not be weaned from circulatory assistance. Eight of these patients subsequently underwent cardiac catheterization; four had inoperable disease. The remaining four patients underwent surgery for either resection of the area of infarction and/or for myocardial revascularization; only one survived to subsequently leave the hospital. Ventricular volumes were abnormal and ejection fractions were below 30 per cent in all the patients in cardiogenic shock except one who underwent cardiac catheterization and ultimately died. Ejection fractions were greater than 30 per cent in the two patients with cardiogenic shock who were weaned from balloon support and survived to leave the hospital without surgery. Both of these patients had inferior myocardial infarction. The data obtained from this experience suggest that intraaortic counterpulsation is a very useful adjunct to currently existing medical measures to treat both cardiogenic shock and medically refractory left ventricular failure but that most patients have such extensive disease that they can neither be weaned from balloon support nor undergo successful infarctectomy or myocardial revascularization.

Topics: Adult; Aged; Assisted Circulation; Blood Pressure; Cardiac Catheterization; Cardiac Volume; Digoxin; Diuretics; Female; Heart Failure; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Plasma Substitutes; Shock, Cardiogenic; Tachycardia

A dose-response relation between cardiac glycosides and systolic time intervals has previously been established in short-term studies in which the glycoside was administered intravenously in these studies there was uncertainty regarding the steady state kinetics, and maintenance of the early serum levels would have resulted in toxicity. Accordingly, we studied the effect on systolic time intervals of small increments of serum digoxin within the therapeutic range. Serum digoxin concentration and systolic time intervals were measured in 21 patients receiving 0.25 mg of the glycoside daily. The daily dose was increased to 0.5 mg and measurements were repeated 5 to 7 days later. Serum digoxin concentration with the smaller dose was 0.56 plus or minus (standard error) 0.06 ng/ml and increased to 1.18 plus or minus 0.11 ng/ml with the larger dose. Associated with the increased serum digoxin was a mean decrease in duration of total electromechanical events of 6.3 plus or minus 2.9 msec (P smaller than 0.025), which resulted from a mean shortening of left ventricular ejection time of 5.6 plus or minus 3.0 msec (P smaller than 0.05). The mean decrease in preejection phase of 1.1 plus or minus 2.1 msec was insignificant (P larger than 0.2). Repeated measurements in control patients showed no change in serum digoxin concentration or systolic time intervals. In nine patients the digoxin dose was randomly varied between 0 and 0.75 mg and measurements were made 4 to 5 days after drug administration at each dose level. The correlation coefficient between changes in serum digoxin and changes in left ventricular ejection time was minus 0.55 (P smaller than 0.01) the data indicated that increasing the maintenance dose of digoxin while keeping the serum level within therapeutic range will result in improved ventricular function as assessed by determination of systolic time intervals.

Topics: Adult; Aged; Carotid Arteries; Coronary Disease; Digoxin; Dose-Response Relationship, Drug; Electrocardiography; Heart; Heart Failure; Heart Ventricles; Humans; Hypertension; Injections, Intravenous; Middle Aged; Myocardial Infarction; Phonocardiography; Pulse; Radioimmunoassay

The effects of digoxin priming dose of 0.04 mg/kg body weight followed by infusion of 0.02 mg/kg per min) on local tension and length characteristics of the nonischemic, border and ischemic left ventricular zones were studied in 30 dogs using Walton-Brodie strain gauge arches and mercury-in-Silastic segment length gauges. Total tension in the nonischemic zone increased to 130.9 plus or minus 5.3 percent (P smaller than 0.001) of the control level in association with parallel changes in preejection and ejection tension and rate of rise of tension when infusion of digoxin was instituted 15 to 30 minutes after ligation. Consistent increases in tension variables were noticed when infusion of digitalis was initiated 45 to 60 minutes or 2 to 3 hours after ligation. Segment length remained unchanged. In the border zone, total tension decreased to 68.9 plus or minus 5.9 percent (P smaller than 0.01) after infusion of digitalis. When infusion of digitalis was instituted 45 to 60 minutes or 2 to 3 hours after occlusion, similar increases in total tension and other tension variables were seen. Segment length again showed no significant changes. There was an increase in total tension in 5 of the 12 ischemic zones studied when digitalis was infused 15 to 30 minutes after coronary arterial ligation, whereas a consistent (3 to 5 percent) decrease in tension was observed when infusion of digitalis was instituted 45 to 60 minutes and 2 to 3 hours after coronary occlusion. There was no increase in segment length. In summary, digitalis uniformly increased contraction of the nonischemic and border zones after coronary arterial ligation, but the effects on contraction and aneurysmal bulging in the ischemic zone were minimal.

Topics: Animals; Coronary Vessels; Digoxin; Dogs; Electrocardiography; Ligation; Myocardial Contraction; Myocardial Infarction; Time Factors

Forty-nine patients admitted to a Coronary Care Unit with myocardial infarction complicated by left ventricular failure, were treated with 1.75 mg Lanoxin over 36 hours. Serum digoxin levels were measured by radioimmunoassay at 8, 24, and 48 hours. No difference in serum levels was observed between those patients who received 'old' (reduced bioavailability) and those who received 'new' Lanoxin. Serum levels were significantly higher at 8 and 24 hours in those patients who received their first dose intramuscularly compared with those who received their first dose orally, irrespective of the bioavailability of the oral preparation used. No correlation was observed between serum digoxin levels and serum urea or creatinine during the 48-hour period of study. The incidence of arrhythmias is reported, but no conclusion can be drawn as to whether or not the glycoside contributed to this in any way. The use of digoxin in patients with acute myocardial infarction complicated by left ventricular failure is justifiable in the light of available evidence. However, in view of the possible predisposition of such patients to toxicity, lower serum levels than were achieved in many of our patients seem desirable and a modified dosage schedule is suggested.

Topics: Administration, Oral; Arrhythmias, Cardiac; Creatinine; Digoxin; Heart Arrest; Humans; Injections, Intramuscular; Middle Aged; Myocardial Infarction; Radioimmunoassay; Urea

To determine the prognostic significance of ventricular arrhythmias persisting during the hospital ambulatory phase of acute myocardial infarction, 64 patients with acute myocardial infarction underwent continuous 10-hour Holter monitoring an average of 11 days after discharge from the coronary care unit (CCU). Patients were categorized according to the results of ambulatory monitoring: 27 patients had ventricular extrasystoles, which were complicated (multifocal, R on T, paired, more than 5/min), or ventricular tachycardia; 22 had uncomplicated premature ventricular contractions; and 15 exhibited no ventricular arrhythmias. The 64 patients were followed prospectively for an average course of 25.8 months; 12 died suddenly; 8 died of other causes, and 44 survived. In all patients who died suddenly, ventricular ectopy was recorded on Holter monitoring before their discharge from the hospital (complicated premature ventricular contractions, eight patients; uncomplicated premature ventricular contractions, four patients); there were no sudden deaths in the patients without ventricular arrhythmias. Patients who died suddenly and those survived were similar in respect to age (60, 62 years), sex, location of infarction, presence of coronary risk factors, severity of acute myocardial infarction (Q waves, cardiac enzymes), serum cholesterol levels, evidence of cardiomegaly on roentgenograms, presence of ventricular gallop and drug therapy received. The occurrence of acute arrhythmias in the CCU did not separate patients who died suddenly from those who survived; there were no differences in ventricular tachycardia or ventricular fibrillation (3 or 12 patients who died suddenly, 6 of 44 patients who survived) or complicated premature ventricular contractions (4 or 12 patients who died suddenly, 18 of 44 patients who survived). Electrocardiograms obtained late in the hospital course revealed no differences in the extent of Q or T wave changes between these two groups. However, the extent of S-T segment abnormality was greater in patients who died suddenly than in patients who survived (5.6 compared to 1.8 leads/standard tracing, p smaller than 0.02) suggesting that the arrhythmias in the former were related to persistent ischemia or segmental ventricular dyssynergy. Thus, in this relatively small number of patients, ventricular arrhythmias persisting late in the hospital course of patients admitted for acute myocardial infarction are shown to predispose to subsequen

Topics: Acute Disease; Adult; Aged; Arrhythmias, Cardiac; Aspartate Aminotransferases; Creatine Kinase; Death, Sudden; Digoxin; Diuretics; Female; Follow-Up Studies; Heart Failure; Hospitalization; Humans; L-Lactate Dehydrogenase; Male; Middle Aged; Myocardial Infarction; Potassium; Procainamide; Quinidine; Sodium; Time Factors

26 mongrel dogs were given a single dose of 0.03mg/kg tritium-labelled digoxin, beta-methyldigoxin, digitoxin or ouabain 2 hrs or 95 hrs following experimental coronary occlusion. Examination of the epicardial ECG was performed by moving from intact to ischemic or necrotic zones. 60 min after glycoside administration the animals were sacrificed and tissue samples from the marked heart muscles areas and from the skeletal muscle were analysed for glycoside content. The early glycoside uptake in acute ischemic or necrotic myocardium was diminished independently of the physicochemical properties of the glycoside. Significantly higher glycoside concentrations (ng/g wet weight) were measured in the injured myocardium 3 hrs after coronary occlusion than 96 hrs afterward (p less than 0.005). The values in acute ischemic myocardium varied considerably. This nonhomogeneity of glycoside uptake in the acute ischemic heart muscle may partly explain the increased sensitivity to glycosides in myocardial infarction. The decline of glycoside concentration correlates with the alterations in the epicardial ECG. The cardiac effects of cardenolides 60 min after intravenous administration was caused by the unchanged glycoside. In contrast to the myocardium, glycoside accumulation could not be found in the skeletal muscle. The concentrations of digoxin, beta-methyldigoxin and digitoxin in the skeletal muscle were significantly higher than the concentration of ouabain, which was rapidly eliminated via the urine.

Topics: Animals; Cardiac Glycosides; Chromatography, Thin Layer; Coronary Vessels; Digitoxin; Digoxin; Dogs; Electrocardiography; Ligation; Muscles; Myocardial Infarction; Myocardium; Ouabain; Time Factors; Tritium

Alpha,alpha-Dimethyl-4-(alpha,alpha,beta,beta-tetrafluorophenethyl)benzylamine (MK-251) has been found to prevent certain types of experimentally induced ventricular arrhythmias and at maximally effective doses possesses substantial hemodynamic safety in contrast to standard antiarrhythmic agents. MK-251 prevented or modified ventricular arrhythmias produced by injection of tetrafluorohexachlorobutane into the coronary artery of dogs and baboons. In dogs, the dose estimated to prevent 80% of the arrhythmic impulses (ED80) was 0.5 mg/kg i.v. and 5.0 mg/kg p.o. The duration of action after oral administration of 5.0 mg/kg to the dog or baboon exceeded 5 to 6 hours. MK-251 delayed the onset of arrhythmias resulting from coronary artery ligation, reduced their severity and permitted a conversion back to normal sinus rhythm earlier than in control dogs. In cats, the doses of digoxin required to induce ventricular ectopic activity, ventricular tachycardia and ventricular fibrillation were elevated by MK-251. In anesthetized dogs, 4 times the i.v. ED80 produced no change in blood pressure, cardiac contractility or output, or in ventricular conduction. The only effect after 8 times the ED80 was a slight decrease in contractility. In contrast. lidocaine at its ED80 (0.21 mg/kg/min), decreased blood pressure and contractility; there was no change in ventricular conduction. Quinidine at the ED80 (8.8 mg/kg i.v.) and above produced hypotension, decreased contractility and prolonged conduction in a dose-related manner.

Topics: Amines; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzyl Compounds; Benzylamines; Blood Pressure; Cardiac Output; Coronary Vessels; Digoxin; Dogs; Female; Heart Conduction System; Heart Rate; Hemodynamics; Hydrocarbons, Fluorinated; Male; Myocardial Contraction; Myocardial Infarction; Papio

Physiologic concepts relating to reperfusion of ischemic areas of myocardium may be applied both to acute coronary insuficiency, manifested by angina pectoris, and to restoration of coronary blood flow by coronary bypass procedures, currently employed both in acute myocardial infarction and in chronic myocardial ischemia for relief of angina pectoris. Of the information currently available from experimental studies, much may be applicable to the clinical situation. After acutr transient coronary occlusion mechanical and electrical properties of the ischemic area rapidly return to normal, but there is prolongation of tension development and occurrence of ventricular arrhythmias; implications of these phenomena for clinical coronary ischemia deserve exploration. Following more prolonged coronary ischemia, results of experimental reperfusion appear to be variable and, although restoration of function following several hours of ischemia is possible, certain deleterious effects are often observed in the form of myocardial edema and hemorrhage. Clinical use of bypass procedures in acute myocardial infarction suggests that results may be good, but that deleterious effects are occasionally observed; occurrence of the later requires definition and explanation. Restoration of myocardial blood flow in the presence of normal left ventricular function in chronic coronary artery disease, and failure to reverse functional abnormalities when left ventricular damage has already ensued in the clinical situation, appears to be well established; however, better methods to assess the potential for recovery of function following revascularization are needed in both acute and chronic coronary artery diseases. It is anticipated that more careful exploration of pathophysiology both in the catheterization laboratory and in the operating room may aid this process.

Topics: Acute Disease; Animals; Cardiac Catheterization; Coronary Circulation; Coronary Disease; Digoxin; Electrocardiography; Heart; Heart Conduction System; Humans; Myocardial Infarction; Myocardial Revascularization; Myocardium; Oxygen Consumption

Topics: Adult; Aged; Aspartate Aminotransferases; Creatine Kinase; Diazepam; Digoxin; Female; Humans; Injections, Intramuscular; L-Lactate Dehydrogenase; Lidocaine; Male; Middle Aged; Myocardial Infarction; Pentazocine

Topics: Acute Disease; Adult; Aged; Blood Glucose; Blood Specimen Collection; Catecholamines; Cholesterol; Cyclic AMP; Cyclizine; Diazepam; Digoxin; Fatty Acids, Nonesterified; Female; Furosemide; Humans; Hydrocortisone; Insulin; Lidocaine; Lipids; Male; Middle Aged; Morphine; Myocardial Infarction; Myocardium; Time Factors; Triglycerides

Topics: Digoxin; Dose-Response Relationship, Drug; Heart Failure; Humans; Injections, Intravenous; Myocardial Infarction; Radioimmunoassay; Time Factors

Topics: Animals; Cardanolides; Chromatography, Thin Layer; Coronary Disease; Digoxin; Dogs; Electrocardiography; Myocardial Infarction; Myocardium; Tritium

Topics: Administration, Oral; Digitalis Glycosides; Digoxin; Diuretics; Heart Failure; Heart Valve Diseases; Hemodynamics; Humans; Injections, Intramuscular; Injections, Intravenous; Myocardial Infarction; Pulmonary Edema; Vagus Nerve

Topics: Autopsy; Digoxin; Female; Humans; Kidney Cortex; Liver; Male; Methods; Muscles; Myocardial Infarction; Myocardium; Radioimmunoassay; Tritium

Topics: Adult; Aged; Blood Pressure; Cardiac Catheterization; Digoxin; Diuretics; Electrocardiography; Female; Glucose; Heart Ventricles; Hemodynamics; Heparin; Humans; Intensive Care Units; Lidocaine; Male; Middle Aged; Myocardial Infarction; Oscillometry; Partial Pressure; Phonocardiography; Pulmonary Artery; Pulmonary Edema; Radiography

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Digitalis; Digoxin; Electric Countershock; Heart Block; Heart Ventricles; Humans; Lidocaine; Myocardial Infarction; Pacemaker, Artificial; Phenytoin; Phytotherapy; Plants, Medicinal; Plants, Toxic; Procainamide; Propranolol; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Ventricular Fibrillation

Topics: Animals; Blood Pressure; Cardiac Output; Digoxin; Dogs; Electrocardiography; Myocardial Infarction; Spironolactone

Topics: Aged; Arrhythmias, Cardiac; Digitalis Glycosides; Digitoxin; Digoxin; Heart Block; Heart Failure; Heart Valve Diseases; Humans; Middle Aged; Myocardial Infarction; Potassium Deficiency; Strophanthins

Topics: Arrhythmias, Cardiac; Atropine; Cardiac Glycosides; Digoxin; Home Nursing; Humans; Lidocaine; Myocardial Infarction; Ouabain; Practolol; Procainamide; Quinidine; Valsalva Maneuver

Topics: Acute Disease; Adult; Aged; Cardiac Volume; Digoxin; Heart; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Time Factors

Topics: Arrhythmia, Sinus; Arrhythmias, Cardiac; Coronary Disease; Digoxin; Diuretics; Electroconvulsive Therapy; Endocarditis, Bacterial; Heart Aneurysm; Heart Failure; Heart Valve Diseases; Heart Ventricles; Humans; Lidocaine; Myocardial Infarction; Pacemaker, Artificial; Pericarditis, Constrictive; Potassium Deficiency; Rupture; Spironolactone; Tachycardia; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

Topics: Adult; Aged; Digoxin; Electrocardiography; Female; Fluoroscopy; Hand; Heart Rate; Heart Ventricles; Humans; Kymography; Male; Middle Aged; Movement; Muscle Contraction; Myocardial Infarction; Phonocardiography; Physical Exertion; Propranolol; Television; Time Factors; Ventricular Function

Topics: Aged; Animals; Atropine; Bradycardia; Coronary Disease; Digoxin; Female; Heart Block; Heart Failure; Humans; Injections, Intravenous; Lidocaine; Male; Myocardial Infarction; Rabbits

Topics: Acute Disease; Adult; Aged; Blood Pressure; Cardiac Catheterization; Digoxin; Female; Furosemide; Germany, West; Heart Diseases; Heart Failure; Heart Septum; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Myocardial Infarction; Prognosis; Pulmonary Artery; Pulmonary Edema; Rupture, Spontaneous; Shock, Cardiogenic; Strophanthins

Topics: Aged; Digoxin; Female; Heart Block; Heart Failure; Heart Rate; Humans; Lidocaine; Male; Myocardial Infarction; Ouabain; Pacemaker, Artificial; Quinidine

Topics: Adult; Angina Pectoris; Coronary Disease; Digoxin; Drug Combinations; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Prenylamine

Topics: Administration, Oral; Coronary Disease; Digoxin; Electrocardiography; Female; Heart Failure; Humans; Injections, Intravenous; Kidney Failure, Chronic; Male; Myocardial Infarction; Phenytoin; Tachycardia

Topics: Administration, Oral; Adult; Chromatography, Thin Layer; Computers; Dialysis; Digoxin; Feces; Female; Humans; Hypertension; Injections, Intravenous; Intestinal Absorption; Intestinal Mucosa; Isotope Labeling; Kidney; Kinetics; Liver; Male; Models, Biological; Myocardial Infarction; Protein Binding; Serum Albumin; Time Factors; Tritium

Topics: Adipose Tissue; Animals; Coronary Vessels; Digoxin; Dogs; Heart Atria; Heart Ventricles; Injections, Intravenous; Ligation; Myocardial Infarction; Myocardium; Time Factors; Tritium

Topics: Angiocardiography; Atrial Flutter; Cardiac Complexes, Premature; Digoxin; Electrocardiography; Heart Aneurysm; Heart Failure; Heart Injuries; Heart Ventricles; Myocardial Infarction; Propranolol; Quinidine; Tachycardia, Paroxysmal

Topics: Aortic Valve Stenosis; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Cardiomyopathies; Coronary Disease; Digoxin; Electrocardiography; Heart; Heart Ventricles; Humans; Hypertension; Middle Aged; Mitral Valve Stenosis; Myocardial Infarction; Pulmonary Heart Disease; Time Factors

Topics: Adrenergic beta-Antagonists; Blood Circulation; Cardiac Glycosides; Digoxin; Heart Block; Humans; Male; Middle Aged; Myocardial Infarction; Propranolol; Sinoatrial Node

Topics: Aged; Digoxin; Diuretics; Female; Furosemide; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Strophanthins

Topics: Anticoagulants; Blood Pressure; Cardiac Catheterization; Cardiomegaly; Dietary Fats; Digoxin; Diuretics; Heart Septal Defects, Ventricular; Heart Septum; Heart Ventricles; Humans; Male; Middle Aged; Mitral Valve Insufficiency; Myocardial Infarction; Oxygen; Rupture; Venous Pressure

Topics: Animals; Atropine; Blood Pressure; Carbon Dioxide; Cardiac Output; Coronary Circulation; Digoxin; Disease Models, Animal; Dogs; Escherichia coli; Heart Failure; Heart Rate; Myocardial Infarction; Myocardium; Oxygen Consumption; Shock, Septic; Vascular Resistance

Topics: Aged; Arrhythmias, Cardiac; Atrial Fibrillation; Digoxin; Female; Heart Failure; Humans; Male; Myocardial Infarction; Pulse; Venous Pressure

Topics: Aged; Ambulatory Care; Arteriosclerosis; Aspartate Aminotransferases; Blood Pressure; Coronary Disease; Digoxin; Female; Humans; Male; Methods; Middle Aged; Myocardial Infarction; Radioisotopes; Rubidium; Sex Factors

Topics: Aged; Blood Urea Nitrogen; Calcium; Coronary Disease; Creatinine; Digitalis Glycosides; Digitoxin; Digoxin; Electrocardiography; Evaluation Studies as Topic; Heart Failure; Heart Valve Diseases; Humans; Kidney Failure, Chronic; Middle Aged; Myocardial Infarction; Photometry; Potassium; Radioimmunoassay; Saliva; Specimen Handling; Spectrophotometry, Atomic

Topics: Arrhythmias, Cardiac; Atropine; Diet Therapy; Digoxin; Electrocardiography; Female; Furosemide; Heart Block; Heart Failure; Heparin; Hospitalization; Humans; Hypotension; Male; Middle Aged; Monitoring, Physiologic; Myocardial Infarction; Oxygen Inhalation Therapy; Progressive Patient Care; Shock, Cardiogenic

Topics: Aged; Blood Pressure; Body Surface Area; Cardiac Output; Coronary Disease; Digoxin; Electrocardiography; Female; Heart Failure; Heart Rate; Heart Ventricles; Hemodynamics; Humans; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Potassium; Pulmonary Artery; Tachycardia; Vascular Resistance

Topics: Administration, Oral; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Digoxin; Electrocardiography; Heart Failure; Humans; Injections, Intravenous; Monitoring, Physiologic; Myocardial Infarction; Ouabain; Tachycardia, Paroxysmal

Topics: Aged; Aminosalicylic Acids; Arrhythmias, Cardiac; Arteriosclerosis; Cerebrovascular Disorders; Coronary Disease; Digoxin; Electrocardiography; Furosemide; Heart Conduction System; Humans; Hypertension; Isoniazid; Kidney Failure, Chronic; Lung Diseases, Obstructive; Middle Aged; Myocardial Infarction; Phenytoin

Topics: Digoxin; Echocardiography; Electrocardiography; Humans; Myocardial Infarction; Prognosis

Topics: Digoxin; Humans; Kinetics; Myocardial Infarction

Topics: Analgesics; Anxiety; Arrhythmias, Cardiac; Coronary Care Units; Digoxin; Diuretics; Heparin; Home Care Services; Humans; Lidocaine; Myocardial Infarction

Topics: Aged; Digoxin; Female; Humans; Myocardial Infarction

Topics: Digitalis Glycosides; Digoxin; Humans; Myocardial Infarction; Myocardium; Oxygen Consumption; Radioimmunoassay; Vascular Resistance

Topics: Angiocardiography; Carotid Arteries; Coronary Artery Bypass; Coronary Disease; Coronary Vessels; Digoxin; Electrocardiography; Female; Heart Rate; Heart Ventricles; Humans; Male; Myocardial Infarction; Phonocardiography; Pulse

Topics: Adult; Aged; Blood Pressure; Cardiac Catheterization; Cardiac Output; Digoxin; Dye Dilution Technique; Electrocardiography; Female; Heart Failure; Heart Rate; Heart Ventricles; Humans; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Vascular Resistance

Topics: Blood Pressure; Body Surface Area; Carbon Dioxide; Cardiac Catheterization; Cardiac Output; Collateral Circulation; Digoxin; Electrocardiography; Glucagon; Heart Failure; Humans; Isoproterenol; Lung; Myocardial Infarction; Norepinephrine; Oxygen; Positive-Pressure Respiration; Pulmonary Artery; Pulmonary Circulation; Shock, Cardiogenic

Topics: Aged; Analgesia; Anti-Arrhythmia Agents; Blood Volume; Bradycardia; Cardiovascular Diseases; Diazepam; Digoxin; Diuretics; Dopamine; Glucagon; Heart Failure; Humans; Hypertension; Hypotension; Male; Myocardial Infarction; Norepinephrine; Phentolamine; Plasma Substitutes; Potassium; Tachycardia

Topics: Adult; Aged; Arrhythmias, Cardiac; Bradycardia; Coronary Care Units; Digoxin; Diuretics; Electrocardiography; Female; Heart Atria; Heart Block; Heart Failure; Heart Ventricles; Hospitals, Teaching; Humans; Male; Middle Aged; Myocardial Infarction; Prognosis; Shock, Cardiogenic; Tachycardia; Ventricular Fibrillation

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Dextrans; Digoxin; Electrocardiography; Epinephrine; Heart Ventricles; Humans; Isoproterenol; Middle Aged; Myocardial Infarction; Norepinephrine; Phlebography; Pulmonary Artery; Shock, Cardiogenic; Vascular Resistance

Topics: Cardiac Output; Digitoxin; Digoxin; Heart; Heart Failure; Heart Rate; Humans; Myocardial Infarction; Potassium Chloride; Shock, Cardiogenic

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Catecholamines; Diagnosis, Differential; Digoxin; Electric Countershock; Electrocardiography; Heart Conduction System; Humans; Lidocaine; Myocardial Infarction; Potassium; Procainamide; Quinidine; Tachycardia; Time Factors

Topics: Aged; Arrhythmias, Cardiac; Digoxin; Electrocardiography; Female; Heart Atria; Humans; Lung Diseases; Male; Middle Aged; Myocardial Infarction; Quinidine; Time Factors

Topics: Acute Disease; Aged; Arrhythmias, Cardiac; Blood Pressure Determination; Coronary Care Units; Digitalis Glycosides; Digoxin; Drug Hypersensitivity; Electrocardiography; Female; Heart Block; Humans; Male; Middle Aged; Myocardial Infarction; Ouabain; Strophanthins

Topics: Acute Disease; Animals; Blood Pressure; Chronic Disease; Coronary Circulation; Coronary Vessels; Digoxin; Dogs; Electrocardiography; Electrodes; Heart Ventricles; Ischemia; Ligation; Myocardial Infarction; Time Factors; Tritium

Topics: Angina Pectoris; Atrial Fibrillation; Bradycardia; Cardiac Catheterization; Diagnosis, Differential; Diagnostic Errors; Digoxin; Electrocardiography; Humans; Hyperthyroidism; Lidocaine; Male; Middle Aged; Myocardial Infarction; Procainamide; Tachycardia; Tachycardia, Paroxysmal; Thyroxine

Topics: Adult; Aged; Angina Pectoris; Arrhythmias, Cardiac; Blood Pressure; Cardiac Complexes, Premature; Coronary Disease; Digoxin; Geriatrics; Heart Diseases; Heart Failure; Humans; Hypertension; Middle Aged; Morpholines; Myocardial Infarction; Phenethylamines; Pulmonary Heart Disease; Pulse; Tachycardia

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Flutter; Coronary Care Units; Digoxin; Heart Block; Humans; Monitoring, Physiologic; Myocardial Infarction; Ouabain; Pacemaker, Artificial

Topics: Acetanilides; Adrenergic beta-Antagonists; Aged; Amino Alcohols; Angina Pectoris; Arrhythmia, Sinus; Bundle-Branch Block; Diagnosis, Differential; Digoxin; Electric Countershock; Electrocardiography; Female; Humans; Lidocaine; Male; Middle Aged; Myocardial Infarction; Myxedema; Tachycardia; Thyroxine

Topics: Aged; Digoxin; Female; Glucagon; Hemodynamics; Humans; Isoproterenol; Male; Myocardial Infarction; Shock, Cardiogenic

The effect of digoxin on A-V conduction in 19 patients with known disease of their conduction tissue was studied while a demand pacing system was in position. Fifteen had transient complete heart block after myocardial infarction and four had chronic intermittent complete heart block. The patients were studied on return to sinus rhythm.In no instance was a return to either second- or third-degree heart block precipitated in these patients despite therapeutic levels and, in some cases, high serum level of digoxin for a period of seven days.The duration of complete heart block after myocardial infarction was 4.3 days in those taking digoxin while in heart block and 3.3 days in those who started digoxin only after return to sinus rhythm.

Topics: Aged; Digoxin; Female; Heart Block; Heart Conduction System; Humans; Male; Middle Aged; Myocardial Infarction; Pacemaker, Artificial

Topics: Adolescent; Adult; Aged; Arrhythmia, Sinus; Bundle-Branch Block; Digoxin; Electrocardiography; Female; Follow-Up Studies; Furosemide; Heart Atria; Heart Conduction System; Heart Ventricles; Humans; Male; Middle Aged; Myocardial Infarction; Pacemaker, Artificial; Procainamide

Topics: Digitalis Glycosides; Digitoxin; Digoxin; Heart Diseases; Humans; Myocardial Infarction; Myocardium

Topics: Acute Disease; Aged; Arrhythmias, Cardiac; Coronary Disease; Digitalis Glycosides; Digitoxin; Digoxin; Electrocardiography; Female; Humans; Lung Diseases; Male; Myocardial Infarction; Poisoning; Prognosis; Prospective Studies; Radioimmunoassay

Topics: Atrial Fibrillation; Atropine; Digoxin; Electric Countershock; Humans; Male; Middle Aged; Mitral Valve Stenosis; Myocardial Infarction; Ouabain; Warfarin

Topics: Aged; Calcium, Dietary; Cardiac Complexes, Premature; Diet Therapy; Digoxin; Female; Humans; Hypocalcemia; Myocardial Infarction

Topics: Bretylium Compounds; Cardiac Complexes, Premature; Digitalis Glycosides; Digoxin; Humans; Lidocaine; Myocardial Infarction; Phenytoin; Potassium Chloride; Procainamide; Propranolol; Quinidine

Topics: Acute Disease; Bradycardia; Digoxin; Female; Hearing Disorders; Heart Diseases; Heart Failure; Humans; Myocardial Infarction; Nitroglycerin; Vestibular Function Tests

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Digoxin; Female; Heart Failure; Heart Rate; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Shock, Cardiogenic

Topics: Acidosis; Bicarbonates; Blood Pressure; Cardiac Output; Digoxin; Fructose; Humans; Hypoxia; Myocardial Infarction; Oxygen; Plasma Substitutes; Shock; Tromethamine

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Digitalis Glycosides; Digoxin; Heart Failure; Humans; Intensive Care Units; Myocardial Infarction; Pacemaker, Artificial; Phenytoin

Topics: Anticoagulants; Arrhythmias, Cardiac; Atropine; Digoxin; Electric Countershock; Heart Arrest; Humans; Intensive Care Units; Isoproterenol; Levallorphan; Lidocaine; Medical Staff, Hospital; Meperidine; Myocardial Infarction; New Zealand; Nursing Service, Hospital; Oxygen Inhalation Therapy; Procainamide; Quinidine; Sympathomimetics; Ventricular Fibrillation

Topics: Adult; Cholecystectomy; Digoxin; Electric Countershock; Electrocardiography; Female; Heart Failure; Humans; Male; Metaraminol; Middle Aged; Myocardial Infarction; Quinidine; Tachycardia, Paroxysmal

Topics: Aged; Digoxin; Female; Heart Block; Heart Failure; Humans; Injections, Intramuscular; Injections, Intravenous; Lanatosides; Male; Myocardial Infarction

Topics: Aged; Blood Urea Nitrogen; Creatinine; Digoxin; Glycosides; Heart Failure; Humans; Intestinal Absorption; Kidney; Kidney Function Tests; Male; Middle Aged; Myocardial Infarction; Ventricular Fibrillation

Topics: Animals; Blood Pressure; Digoxin; Dogs; Electrocardiography; Male; Myocardial Infarction; Ventricular Fibrillation

Topics: Adams-Stokes Syndrome; Bradycardia; Digitalis; Digoxin; Electrocardiography; Heart Arrest; Heart Rate; Humans; Myocardial Infarction; Plants, Medicinal; Plants, Toxic; Procainamide; Propranolol; Quinidine; Sympathomimetics

Topics: Adult; Atrial Fibrillation; Digoxin; Electrocardiography; Humans; Male; Middle Aged; Monitoring, Physiologic; Myocardial Infarction; Physical Exertion; Propranolol; Radio; Telemetry

Topics: Digoxin; Heart Diseases; Humans; Myocardial Infarction

Topics: Adrenal Cortex Hormones; Aged; Diabetes Complications; Digoxin; Female; Heart Failure; Humans; Male; Middle Aged; Myocardial Infarction; Nitroglycerin; Shock; Vasodilator Agents

Topics: Aminophylline; Digoxin; Diuretics; Drug Therapy; Electric Countershock; Electrocardiography; Heart Failure; Humans; Hypotension; Metaraminol; Myocardial Infarction; Organomercury Compounds; Phenylephrine; Quinidine; Tachycardia; Ventricular Fibrillation

Topics: Digoxin; Drug Therapy; Electrocardiography; Heart Block; Heart Conduction System; Humans; Myocardial Infarction; Quinidine; Reserpine; Tachycardia; Tachycardia, Paroxysmal; Wolff-Parkinson-White Syndrome

Topics: Digoxin; Exercise Therapy; Humans; Myocardial Infarction; Rehabilitation

Topics: Adams-Stokes Syndrome; Arrhythmias, Cardiac; Barbiturates; Digoxin; Electrocardiography; Heart Block; Humans; Myocardial Infarction; Pacemaker, Artificial; Poisoning; Quinidine; Resuscitation; Toxicology

Topics: Adrenergic Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Digitalis; Digoxin; Electrocardiography; Ethanolamines; Geriatrics; Heart Block; Heart Failure; Hypotension; Myocardial Infarction; Nausea; Paresthesia; Sympatholytics; Toxicology; Vertigo; Vomiting

Topics: Digoxin; Humans; Myocardial Infarction; Rehabilitation

Topics: Autoimmune Diseases; Betamethasone; Dexamethasone; Digoxin; Humans; Myocardial Infarction; Radiography, Thoracic; Syndrome; Warfarin