digoxin and Ventricular-Fibrillation

Congestive heart failure is characterized by contractile dysfunction and frequent complex ventricular ectopy. Despite advances in therapy, mortality from heart failure is substantial, estimated at 10-80 percent per year, and sudden death is common. Magnesium is the second most common intracellular cation, strongly influences cardiac cell membrane function, and is an important catalyst of many enzymatic reactions in the myocyte. Epidemiological studies have implicated magnesium deficit in the genesis of sudden death. Patients with congestive heart failure are predisposed to magnesium deficit for many reasons, including neurohormonal activation, poor gastrointestinal absorption, and drug therapy. Hypomagnesaemia is common in these patients and has been linked to an increased frequency of complex ventricular ectopy. Several early, uncontrolled studies have suggested a beneficial effect of magnesium administration on ventricular arrhythmias in patients with congestive heart failure. Two recent randomized, double blind, placebo-controlled trials have shown that both intravenous and oral administration of magnesium chloride results in a significant reduction in the frequency and complexity of ventricular arrhythmias in patients with congestive heart failure. Magnesium administration is well tolerated and serious adverse effects are rare. The potential mechanisms of the antiarrhythmic action of magnesium and limitations of the available data are discussed. The evidence reviewed suggests that serum magnesium concentrations should be monitored and corrected in patients with congestive heart failure. Ventricular arrhythmias may respond to acute intravenous magnesium administration, which should be considered as early therapy. Further study is needed to define magnesium dose and the effect of concomitant potassium administration. A prospective clinical trial is warranted to determine the chronic effects of magnesium administration in patients with heart failure.

Topics: Absorption; Aged; Anti-Arrhythmia Agents; Death, Sudden; Digoxin; Diuretics; Heart Failure; Humans; Kidney Tubules; Magnesium; Magnesium Deficiency; Middle Aged; Prognosis; Ventricular Fibrillation

Topics: Administration, Oral; Animals; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Cardiac Catheterization; Cardiac Surgical Procedures; Coronary Disease; Depression, Chemical; Digitalis; Digoxin; Heart; Heart Diseases; Humans; Injections, Intravenous; Ouabain; Phenytoin; Plants, Medicinal; Plants, Toxic; Ventricular Fibrillation

Topics: Action Potentials; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bradycardia; Digitalis Glycosides; Digoxin; Fever; Heart Atria; Heart Block; Humans; Hypotension; Lung Diseases, Obstructive; Methoxamine; Pacemaker, Artificial; Procainamide; Propranolol; Pulmonary Embolism; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Ventricular Fibrillation

Topics: Arrhythmias, Cardiac; Bradycardia; Cardiac Complexes, Premature; Child; Child, Preschool; Deafness; Digoxin; Electric Countershock; Electrocardiography; Female; Heart Failure; Heart Ventricles; Humans; Infant; Infant, Newborn; Lidocaine; Male; Propranolol; Tachycardia; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

Topics: Atrial Fibrillation; Atrial Flutter; Cardiac Surgical Procedures; Digitalis; Digitalis Glycosides; Digoxin; Electrocardiography; Heart Block; Heart Failure; Humans; Isoproterenol; Lanatosides; Mitral Valve Stenosis; Pacemaker, Artificial; Tachycardia; Thoracic Surgery; Toxicology; Ventricular Fibrillation

VF is induced during ICD implantation to determine efficacy of therapy. Establishing the best clinical method of induction of VF would potentially be beneficial in reducing the number of induction attempts and reducing the frequency of inadvertent induction of VT. Commonly used methods to induce VF include shock in the T wave vulnerable period (T shock) and high frequency stimulation. This study compared the efficacy of T shock with a new induction method using a 9-V DC pulse. The study was a randomized, prospective, case crossover trial in patients receiving ICDs. VF was induced by T shock and DC in a randomized sequence during an ICD implant. VF was induced at least four times in each patient (two T shocks and two DC inductions) and with each induction; attempts were continued with modifications until successful. A paired evaluation between the T shock/DC induction was performed in 37 patients (28 men, age 64 +/- 12 years) with a left ventricular ejection fraction of 0.40 +/- 0.20. Arrhythmia indications were VT (n = 23), VF (n = 10), and VT/VF (n = 4). Drug therapy included amiodarone (n = 10), metoprolol (n = 6), digoxin (n = 1), and lidocaine (n = 1). The average T shock voltage was 207.0 +/- 16.1 V. The S1 cycle drive length was consistently 400 ms, and the mean S2 coupling interval was 317.8 +/- 19.6 ms. The length of time DC applied averaged 3.8 +/- 1.4 seconds. A total of 148 episodes of VF were included in the analysis. T shock induced VF with a cycle length of 213.5 +/- 35.1 ms, and DC induced VF with a cycle length of 214.6 +/- 34.5 ms (P = 0.86). Although VF was eventually induced for each randomization, the number of attempts required were dependent on the method of induction. The successful DC first attempt VF induction rate was 96%, with three patients requiring two attempts during one of the DC inductions. T shock had a 68% first attempt success rate with 21 patients requiring multiple T shocks to induce VF. All nine female patients had at least one unsuccessful first attempt T shock, which contributed to an overall unsuccessful first attempt induction rate significantly higher in women then men (36.1% vs 12.5%, P = 0.001). A constant DC voltage induction of VF may be more effective than T shock for induction of VF in a clinical setting because it reduces the number of attempts required to induce VF. By either method, VF appears to be more difficult to induce in women. DC induction has the advantage of simple programming of only duration

Topics: Amiodarone; Defibrillators, Implantable; Digoxin; Electric Countershock; Female; Humans; Lidocaine; Male; Metoprolol; Middle Aged; Prospective Studies; Ventricular Fibrillation

A population of 283 patients with recent onset (< 72 hours) AF, without heart failure, who received a single 450- or 600-mg oral dose of propafenone, or digoxin 1 mg, or placebo for conversion to sinus rhythm (SR), was studied to determine whether a routine admission to the hospital for drug administration is justified. Previous bradyarrhythmias or sick sinus syndrome (SSS), and concomitant use of antiarrhythmic drugs were exclusion criteria. None of the 283 patients studied experienced VT or VF and none of them needed implantation of a temporary pacemaker. Periods of atrial tachyarrhythmias with regularization of atrial waves and 1:1 AV conduction were observed in only two cases, both receiving placebo. No predictor of proarrhythmia was found among the clinical variables considered (age, etiology, arrhythmia duration, atrial dimension, and blood potassium). No serious hemodynamic adverse effects were noted in either group. The rates of conversion to SR after 4 hours were: 80 (57%) of 141 patients who received propafenone and 35 (25%) of 142 patients who received digoxin or placebo (P < 0.001). Acute oral treatment with propafenone is simple and effective for the conversion of recent onset AF to SR in patients without clinical signs of heart failure. The routine admission of these patients to the hospital is not necessary. Home-based administration of oral propafenone to a selected group of patients could significantly increase the cost effectiveness of this treatment.

Topics: Administration, Oral; Age Factors; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Function; Atrioventricular Node; Bradycardia; Cost-Benefit Analysis; Digoxin; Female; Forecasting; Heart Rate; Hemodynamics; Home Care Services; Humans; Male; Middle Aged; Pacemaker, Artificial; Patient Admission; Placebos; Potassium; Propafenone; Retrospective Studies; Sick Sinus Syndrome; Tachycardia; Tachycardia, Ventricular; Ventricular Fibrillation

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

Topics: Adult; Apocynaceae; Atrial Fibrillation; Colectomy; Digoxin; Electrocardiography; Extracorporeal Membrane Oxygenation; Fruit; Humans; Immunoglobulin Fab Fragments; Intestines; Ischemia; Life Support Care; Male; Ventricular Fibrillation

Digoxin is a cardiac glycoside that is frequently prescribed in atrial fibrillation and heart failure. Symptoms such as nausea, hyperkalaemia, cardiac arrhythmias and cardiac arrest are seen in digoxin toxicity. The treatment focuses on reduction of digoxin absorption, prevention of hypokalaemia and hyperkalaemia, treatment of symptoms and, in severe toxicity, administration of digoxin antibodies.. A 73-year-old man with a history of extensive cardiac disease was seen 45 minutes after ingesting 20 mg of digoxin. The patient developed ventricular fibrillation within 3 hours of ingestion, before arrival of the digoxin antibodies. The patient passed away despite resuscitation and administration of an insufficient amount of digoxin antibodies.. The national supply of digoxin antibodies in the Netherlands proved to be too limited for the treatment of a patient with severe digoxin toxicity. An increase in the supply, and central storage, of digoxin antibodies could promote faster administration of an adequate amount of the antibodies. Timely transportation to an extra corporeal membrane oxygenation centre should also be considered.

Topics: Aged; Arrhythmias, Cardiac; Atrial Fibrillation; Digoxin; Fatal Outcome; Heart Arrest; Humans; Male; Netherlands; Ventricular Fibrillation

Topics: Aged, 80 and over; Anti-Arrhythmia Agents; Atrial Fibrillation; Bradycardia; Cardiac Pacing, Artificial; Digoxin; Female; Humans; Ventricular Fibrillation

Topics: Aged; Digitalis; Digoxin; Electrocardiography; Female; Humans; Tachycardia; Ventricular Fibrillation

Recent investigations have demonstrated that the occurrence of implantable cardioverter-defibrillator (ICD) shocks is associated with adverse long-term outcomes. These studies have emphasized that the risk is most reasonably due to arrhythmias rather than to the shock itself. We sought to compare the impact of shock delivery for induced ventricular arrhythmias during implantation defibrillation threshold testing and noninvasive electrophysiology study (NIPS) to clinical shocks on long-term outcomes among patients with ICDs.. This was a cohort evaluation of 1,372 patients undergoing ICD implantation at a tertiary hospital from December 1997 to January 2007. The probability of all-cause mortality and hospitalization for acute decompensated heart failure (ADHF) was evaluated based upon the type of ICD shock received using multivariable Cox proportional analyses. The four shock types analyzed were implantation shocks only (n = 694), additional NIPS shocks only (n = 319), additional appropriate shocks only (n = 128), or additional inappropriate shocks only (n = 104).. The risk of death (adjusted hazard ratio [AHR] 0.91 [95% confidence interval (CI) 0.69-1.20]; P = .491) or ADHF (AHR 0.71 [95% CI 0.46-1.16]; P = .277) were similar between recipients of NIPS shocks and recipients of implantation shocks. Receiving an appropriate ICD shock increased the risk of death (AHR 2.09 [95% CI 1.38-2.69]; P <.001) and ADHF (AHR 2.40 [95% CI 1.51-3.81]; P <.002) as compared with implantation shocks and also increased the risk of death (AHR 2.61 [95% CI 1.86-3.67]; P <.001) and ADHF (AHR 2.29 [95% CI 1.33-3.97]; P = .003) as compared with NIPS shocks.. ICD shocks delivered during induced ventricular arrhythmias at the time of NIPS testing does not increase the risk of death or ADHF as compared with recipients of appropriate ICD shocks. The occurrence of spontaneous arrhythmias in vulnerable substrates may explain the increased risk.

Topics: Aged; Anti-Arrhythmia Agents; Cohort Studies; Confidence Intervals; Connecticut; Defibrillators, Implantable; Digoxin; Electrophysiology; Female; Heart Failure; Humans; Kaplan-Meier Estimate; Male; Multivariate Analysis; Phenethylamines; Prognosis; Proportional Hazards Models; Retrospective Studies; Risk Factors; Sulfonamides; Tachycardia, Ventricular; Treatment Outcome; Ventricular Fibrillation

All cardiac steroids have a similar structure, bind to and inhibit the ubiquitous transmembrane protein Na(+), K(+)-ATPase and increase the force of contraction of heart muscle. However, there are diverse biological responses to different cardiac steroids both at the cellular and at the molecular level. Moreover, we have recently shown that ouabain inhibits digoxin- and bufalin-induced changes in membrane traffic. The present study was designed to test the hypothesis that ouabain also has an inhibitory effect on cardiotoxicity induced by other cardiac steroids.. The hypothesis was tested in isolated heart muscle preparations and in an in vivo model of cardiotoxicity in guinea pigs.. Ouabain at a low dose attenuated the toxicity induced by bufalin and digoxin in heart muscle preparations. In addition, ouabain at the low dose (91 ng.kg(-1).h(-1)), but not at a higher dose (182 ng.kg(-1).h(-1)), delayed the development of digoxin-induced (500 microg.kg(-1).h(-1)) cardiotoxicity in anaesthetized guinea pigs, as manifested by delayed arrhythmia and terminal ventricular fibrillation, as well as a reduced heart rate. In addition, as observed with ouabain, the phosphoinositide 3-kinase inhibitor wortmannin (100 microg.kg(-1).h(-1)) delayed the digoxin-induced arrhythmia in anaesthetized guinea pigs.. The present study demonstrates the inhibitory effect, probably through signal transduction pathways, of ouabain on digoxin- and bufalin-induced cardiotoxicity in guinea pigs. Further understanding of this phenomenon could be beneficial for increasing the therapeutic window for cardiac steroids in the treatment of chronic heart failure.

Topics: Androstadienes; Animals; Arrhythmias, Cardiac; Bufanolides; Cardiotonic Agents; Digoxin; Dose-Response Relationship, Drug; Guinea Pigs; Heart Rate; Male; Myocardium; Ouabain; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Signal Transduction; Sodium-Potassium-Exchanging ATPase; Ventricular Fibrillation; Wortmannin

Of 209 patients with heart failure treated with combined cardiac resynchronization therapy and implantable cardioverter-defibrillator therapy, appropriate cardioverter-defibrillator shocks occurred at 34-month follow-up in 22 of 121 patients (18%) on statins and in 30 of 88 patients (34%) not on statins (P = .009). Deaths occurred in 3 of 121 patients (2%) on statins and in 9 of 88 patients (10%) not on statins (P = .017). Stepwise Cox regression analysis showed that significant independent prognostic factors for appropriate shocks were use of statins (risk ratio = 0.46), smoking (risk ratio = 3.5), and diabetes (risk ratio = 0.34). Significant independent prognostic factors for the time to mortality were use of statins (risk ratio = 0.05), use of digoxin (risk ratio = 4.2), systemic hypertension (risk ratio = 14.2), diabetes (risk ratio = 4.3), and left ventricular ejection fraction (risk ratio = 1.1).

Topics: Aged; Aged, 80 and over; Cardiac Pacing, Artificial; Cardiotonic Agents; Combined Modality Therapy; Defibrillators, Implantable; Diabetes Complications; Digoxin; Female; Heart Failure; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Male; Middle Aged; Odds Ratio; Proportional Hazards Models; Risk Assessment; Risk Factors; Smoking; Stroke Volume; Tachycardia, Ventricular; Time Factors; Treatment Outcome; Ventricular Fibrillation; Ventricular Function, Left

Survival following out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation (VF) is poor and dependent on a rapid emergency response system. Improvements in emergent early response have resulted in a higher percentage of patients surviving to admission. However, the admission variables that predict both short- and long-term survival in a region with high discharge survival following OHCA require further study in order to identify survivors at subsequent highest risk.. All patients with OHCA arrest in Olmsted County Minnesota between 1990 and 2000 who received defibrillation of VF by emergency services were included in the population-based study. Baseline patient admission characteristics in survivor and nonsurvivor groups were compared. Survivors to hospital discharge were prospectively followed to determine long-term survival.. Two hundred patients suffered a VF arrest. Of these patients, 145 (73%) survived to hospital admission (7 died within the emergency department) and 79 (40%) were subsequently discharged. Sixty-six (83%) were male, with an average age of 61.9 +/- 15.9 years. Univariate predictors of in-hospital mortality included call-to-shock time (6.6 vs. 5.5 min, p = 0.002), a nonwitnessed arrest (75.4 vs. 92.4%, p = 0.008), in-field use of epinephrine (27.8 vs. 93.4%, p < 0.001), age (68.1 vs. 61.9 years, p = 0.017), hypertension (36.1 vs. 14.1%, p = 0.005), ejection fraction (32.4 vs. 42.4, p = 0.012), and use of digoxin (34.9 vs. 12.7%, p = 0.002). Of all these variables, hypertension [hazard ratio (HR) 4.0, 95% CI 1.1-14.1, p = 0.03], digoxin use (HR 4.5, 95% CI 1.3-15.6, p = 0.02), and epinephrine requirement (HR 62.0, 95% CI 15.1-254.8, p < 0.001) were multivariate predictors of in-hospital mortality. Nineteen patients (24%) had died prior to the survey follow-up. Five patients experienced a cardiac death, resulting in a 5-year expected cardiac survival of 92%. Multivariate variables predictive of long-term mortality include digoxin use (HR 3.02, 95% CI 1.80-5.06, p < 0.001), hypertension (HR 2.06, 95% CI 2.12-3.45, p = 0.006), and call-to-shock time (HR 1.18, 95% CI 1.01-1.38, p = 0.038).. A combined police/fire/EMS defibrillation program has resulted in an increase of patients surviving to hospital admission after OHCA. This study confirms the need to decrease call-to-shock times, which influence both in-hospital and long-term mortality. This study also identifies the novel demographic variables of digoxin and hypertension, which were also independent risk factors of increased in-hospital and long-term mortality. Identification of these variables may provide utility in identifying those at high-risk of subsequent mortality after resuscitation.

Topics: Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Digoxin; Electric Countershock; Emergency Medical Services; Female; Heart Arrest; Hospital Mortality; Humans; Hypertension; Male; Middle Aged; Patient Admission; Predictive Value of Tests; Research Design; Risk Factors; Survival Analysis; Time Factors; Treatment Outcome; Ventricular Fibrillation

Topics: Anti-Arrhythmia Agents; Chronic Disease; Digoxin; Electric Countershock; Humans; Thrombophlebitis; Ventricular Fibrillation

Topics: Anti-Arrhythmia Agents; Digoxin; Humans; Thrombophlebitis; Ventricular Fibrillation

We have investigated the effects of nitric oxide synthase inhibitor (L-NAME), nitric oxide precursor (L-arginine) and nitric oxide donor (sodium nitroprusside) on digoxin-induced arrhythmias both in guinea-pig isolated hearts and in anaesthetised animals. Sodium nitroprusside (0.1 mumol kg-1 min.-1 for 70 min.) caused a marked inhibition in mortality and arrhythmia score but L-NAME (10 mg kg-1) and L-arginine (30 mg kg-1 intravenous bolus followed by 10 mg kg-1 min.-1 for 60 min.) treatments were ineffective in anaesthetised guinea-pigs. None of the drugs markedly affected the time of onset of first arrhythmias or ventricular fibrillation incidence. In isolated heart experiments, nitric oxide generated by either L-arginine (1 mM) or sodium nitroprusside (1 mM) significantly reduced the arrhythmia score whereas L-NAME (1 mM) had no effect. Ventricular fibrillation incidence was totally abolished by sodium nitroprusside and none of the hearts treated with L-arginine had an irreversible ventricular fibrillation. L-NAME decreased ventricular tachycardia duration but increased ventricular fibrillation duration. There were no marked changes in the time of onset of first arrhythmias with these drugs in in vitro experiments. These results suggest that nitric oxide may play a modulatory role in the digoxin-induced arrhythmias in guinea-pigs.

Topics: Animals; Arginine; Arrhythmias, Cardiac; Blood Pressure; Digoxin; Guinea Pigs; In Vitro Techniques; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitroprusside; Time Factors; Ventricular Fibrillation

In the present study, the possible role of oxygen-derived free radicals (OFR) on digoxin- (0.6 mg/kg(-1) IV bolus) induced arrhythmias of anesthetized guinea-pigs has been investigated. Guinea-pigs (300400 g) of either sex were anesthetized with urethane (1.5 g/kg(-1),IP), and their trachea for respiration, left common carotid artery for blood pressure monitoring, and right jugular vein for drug administration were cannulated. ECG and haemodynamics were recorded throughout the experiments. None of the agents used [N-acetyl-L-cysteine (20 mg/kg(-1)IV bolus), or SOD (30,000 IU/kg(-1) IV bolus) + catalase (15,000 IU/kg(-1) IV bolus)] significantly inhibited the arrhythmias except desferrioxamine which reduced the incidence of ventricular fibrillation and arrhythmia score. Desferrioxamine, by acting intracellularly unlike other agents used, might prevent the reduction of Fe(+3) by ascorbate and superoxide anion thus inhibiting the formation of cytotoxic hydroxyl radical in this experimental setting.

Topics: Animals; Antioxidants; Arrhythmias, Cardiac; Digoxin; Electrocardiography; Female; Free Radical Scavengers; Free Radicals; Guinea Pigs; Male; Reactive Oxygen Species; Tachycardia, Ventricular; Ventricular Fibrillation

The effectiveness and safety of antiarrhythmic agents, mostly digoxin and amiodarone given to prevent recurrences, were compared in 141 infants of less than 1 year (77% < 1 month) with re-entrant supraventricular tachycardia.. Digoxin was the drug of first choice in 114 patients at a dose of 10-20 micrograms/kg/d and was effective in 74 cases (65%). Amiodarone was used as first line therapy or after failure of digoxin. It was given at a maintenance dose of 250 mg/m2/d, alone in 22 infants and together with digoxin in another 36; it was effective in 56 cases (96.5%). Early adverse events occurred in six patients receiving digoxin: ventricular fibrillation requiring cardioversion in three, two of whom had Wolff-Parkinson-White syndrome, significant sinus bradycardia in two, accidental overload in one. At further follow-up, one child treated with digoxin but having also gastroesophageal reflux, died suddenly at 3 months of age; autopsy was normal and the digoxin blood level was 3 ng/mL. Among the 58 infants who received amiodarone, there were no proarrhythmia, a slight and transient increase in TSH in six infants and only one required a short-term treatment for hypothyroidism. Prophylactic therapy was maintained for 6 to 12 months and only ten patients had recurrences in the year following withdrawal.. Amiodarone was found to be safer and more effective than digoxin. No significant side-effect was demonstrated in infants receiving a short-term treatment. Amiodarone may be proposed as first line therapy for prophylaxis of re-entrant supraventricular tachycardia in infancy, especially for those patients with reentry and Wolff-Parkinson-White syndrome.

Topics: Amiodarone; Anti-Arrhythmia Agents; Digoxin; Electric Countershock; Electrocardiography; Humans; Infant; Practice Guidelines as Topic; Recurrence; Retrospective Studies; Tachycardia, Supraventricular; Ventricular Fibrillation

Toxicity from toad venom poisoning is similar to digoxin toxicity and carries a high mortality rate. We report on six previously healthy men who developed vomiting and bradycardia after ingesting a purported topical aphrodisiac. Each patient had positive apparent digoxin levels and the first four patients died of cardiac dysrhythmias. The last two patients recovered following treatment with digoxin Fab fragments. We analyzed samples of the purported aphrodisiac and found that it was identical to Chan Su, a Chinese medication made from toad venom. To our knowledge, this is the first reported use of digoxin Fab fragments to treat toad venom poisoning.

Topics: Adolescent; Adult; Amphibian Venoms; Animals; Aphrodisiacs; Bradycardia; Bufanolides; Bufonidae; Bufotenin; Digoxin; Fatal Outcome; Humans; Immunoglobulin Fab Fragments; Male; Materia Medica; Ventricular Fibrillation; Vomiting

Topics: Adenosine; Anti-Arrhythmia Agents; Cardiovascular Agents; Contraindications; Digoxin; Drug Interactions; Humans; Infant, Newborn; Tachycardia, Supraventricular; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

We describe a patient with unexpectedly high serum digoxin after cardiac surgery. To control atrial fibrillation in the immediate postoperative period, she was given a brief trial of digoxin (four 0.25-mg doses) over 12 h. Serum digoxin 6 h later was 2.5 micrograms/L. Two days later, the patient developed ventricular fibrillation, which progressed to cardiac arrest. During or immediately after resuscitation, blood was drawn for a digoxin measurement, and the concentration reported was 9.3 micrograms/L; this result was verified by repeated analysis. Digoxin decreased rapidly and progressively to near 4.0 micrograms/L over the next several hours and thereafter decreased slowly to 1.0 microgram/L over the next 11 days, despite no digoxin being administered. The unexpectedly high digoxin raised questions about the accuracy of the digoxin measurement, particularly about the possible influence of the digoxin-like immunoreactive factor. Analytical approaches to distinguishing true digoxin from this factor and other artifacts of digoxin measurement were applied to this patient, with unanticipated results.

Topics: Aged; Cardiac Surgical Procedures; Digoxin; False Positive Reactions; Female; Fluoroimmunoassay; Heart Arrest; Humans; Radioimmunoassay; Ventricular Fibrillation

To analyze if patient selection bias could contribute to the improved prognosis reported for ventricular tachycardia (VT) and ventricular fibrillation (VF) when therapy is guided by electrophysiologic studies (EPS), we studied 90 consecutive patients admitted to a tertiary referral center with recent VT/VF who were candidates for EPS. Seventeen patients (19%) died during the initial hospital admission, and 30 (33%) died after discharge. Survival probability was 0.83 (95% confidence interval [CI], 0.74-0.90); 0.67 (95% CI, 0.56-0.75); and 0.53 (95% CI, 0.42-0.63) at 1 month, 1 year, and 3 years, respectively. Of the 56 patients (62%) who underwent EPS during their initial hospitalization, only 1 died during that admission. Patients in whom EPS could not be performed had characteristics associated with a poorer prognosis. NYHA functional class (p = 0.005), inability to perform baseline EPS (p = 0.003) and use of digoxin (p = 0.016) were independent predictors of death. Early in-hospital mortality in patients with VT/VF remains high. Thus, omission of these deaths in reports of EPS-guided therapy creates incomplete, biased cohorts. Furthermore, there may be a bias toward a healthier population among hospital survivors undergoing EPS. These findings may contribute to better outcomes in current series compared to historical controls.

Topics: Aged; Analysis of Variance; Anti-Arrhythmia Agents; Cardiac Care Facilities; Cause of Death; Cohort Studies; Defibrillators, Implantable; Digoxin; Electrophysiology; Female; Follow-Up Studies; Humans; Male; Middle Aged; Multivariate Analysis; Prognosis; Retrospective Studies; Selection Bias; Survival Analysis; Tachycardia, Ventricular; Ventricular Fibrillation

A 50-year-old, previously healthy, woman swallowed 1 g digoxin powder, dissolved in water, with suicidal intent. On admission to hospital one hour later, having vomited three times at home, the prominent signs were somnolence and hypersalivation. Serum digoxin level was 3.37 ng/ml. There followed repeated episodes of asystole alternating with ventricular fibrillation requiring cardiopulmonary resuscitation over 90 min and adrenaline administration. Repeated electrical defibrillation, administration of dopamine, phenytoin and lidocaine, as well as transitory transvenous electrical stimulation became necessary. Anti-digoxin antibody fragments were administered, initially 80 mg, to a total of 3,280 mg over 24 hours. After 3 days of intensive care and a further 21 days in hospital she was discharged and referred to psychiatric treatment. This case demonstrates that even severe digoxin poisoning can be successfully treated without sequelae by the appropriate administration of digoxin antidote. The main problems in this case were regulation of the dosage and acquiring the necessary amount of antidote which greatly exceeded the hospital's own depot.

Topics: Acute Disease; Antidotes; Combined Modality Therapy; Digitalis; Digoxin; Drug Overdose; Drug Therapy, Combination; Female; Gastric Lavage; Humans; Middle Aged; Plants, Medicinal; Plants, Toxic; Poisoning; Powders; Suicide, Attempted; Ventricular Fibrillation

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

A complication of transesophageal atrial pacing in an infant with Wolff-Parkinson-White syndrome (WPW) is reported. A newborn infant born with fetal hydrops had recurrent supraventricular tachycardia (SVT) that required repeated successful conversion by transesophageal atrial pacing. Because of secondary left ventricular dysfunction, digoxin was administered. During repeat transesophageal atrial pacing for recurrent SVT, ventricular fibrillation occurred. Although it is unclear which of several possible contributing factors was responsible for the ventricular fibrillation, recommendations are appropriate to minimize the risk in infants with WPW.

Topics: Cardiac Pacing, Artificial; Digoxin; Esophagus; Female; Humans; Infant, Newborn; Recurrence; Tachycardia, Supraventricular; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

To investigate the mechanism of pressure related ventricular arrhythmias by examining them during atrioventricular (AV) block.. Complete AV block, where all ventricular beats are ectopic, was induced by AV node ablation and/or by toxic digitalisation, and rhythm changes were studied while arterial blood pressure was repeatedly raised and lowered.. 15 anaesthetised mongrel dogs, weight 15-28 kg, were used. AV block was induced in eight by chemical or mechanical ablation of the AV node. In five of these and in seven other dogs, 5.0-7.5 mg digoxin was also given.. Following AV block due to ablation, a heart rate increase (or no change) was found in 87.5% of 56 arterial pressure increases produced by elevation of an open arterial blood reservoir or by metaraminol infusion, but in only 21.8% of 55 pressure decreases caused by arterial bleeding (p much less than 0.001). Following AV block due to digitalisation, the equivalent figures were 96% of 50 pressure increases and 27.3% of 55 pressure decreases (p much less than 0.001). While arterial pressure was increased there was moderate acceleration of the escape rhythm, then appearance of premature ventricular beats, then non-sustained and finally sustained ventricular tachycardia. The reverse occurred, with some hysteresis, on decreasing the arterial pressure. In five of the digitalised animals, arterial pressure reduction to nearly zero caused reproducible sudden arrest, with resumption of the ordinary escape rhythm on increasing the pressure again.. The findings suggest the possibility of two kinds of ectopic rhythm in AV block: the "normal" escape rhythm which is only moderately affected by arterial pressure changes; and an "abnormal" faster pressure dependent rhythm which is generated by high arterial pressure and abolished by pressure near zero, as if there were a mechano-electrical association. This abnormal rhythm may prevail completely in digitalis toxicity so that if cardiac arrest occurs, no automaticity can be expected to appear unless arterial pressure is raised.

Topics: Animals; Arrhythmias, Cardiac; Atrioventricular Node; Blood Pressure; Digoxin; Dogs; Electrocardiography; Formaldehyde; Heart Block; Heart Rate; Heart Ventricles; Mechanoreceptors; Tachycardia; Ventricular Fibrillation

Flecainide acetate has a recognized proarrhythmic effect in patients treated for ventricular tachycardia. Three patients developed severe ventricular arrhythmias while taking flecainide for atrial fibrillation. Patient 1 had normal ventricular function and idiopathic atrial fibrillation. Treadmill exercise tests during digoxin therapy showed no ventricular arrhythmia; however, during flecainide therapy the patient developed ventricular flutter at his peak exercise level that required cardioversion. Patient 2 had normal ventricular function and a prosthetic mitral valve. During therapy with flecainide, 150 mg twice daily, he had an episode of sustained ventricular tachycardia, also at his peak exercise level. Patient 3 had paroxysmal atrial fibrillation and hypertrophic cardiomyopathy but no previous ventricular arrhythmia. She died suddenly within 10 days of starting flecainide therapy. Judged from previous findings none of these patients was considered at high risk for proarrhythmia. These cases suggest a possible relation between vigorous exercise, atrial fibrillation, and the proarrhythmic properties of flecainide and indicate the limitations of classifying patients as "high-risk" or "low-risk" for proarrhythmic complications of anti-arrhythmic therapy.

Topics: Adult; Atrial Fibrillation; Digoxin; Drug Therapy, Combination; Electrocardiography; Exercise Test; Female; Flecainide; Heart Ventricles; Humans; Male; Tachycardia; Ventricular Fibrillation

Topics: Aged; Digoxin; Humans; Magnesium; Male; Ventricular Fibrillation

Severe digitalis intoxication today is preferentially treated by intravenous infusion of Fab fragments of digoxin antibodies (Digitalis Antidot BM). The kinetics of Fab fragments in the circulation are well known when kidney function is normal or slightly impaired. There are no data available, however, in complete renal failure. We observed a patient with life-threatening digitalis intoxication (serum digoxin, 3.7 ng/ml) and anuria, who was treated successfully by 160 mg Fab fragments i.v. Serum digoxin and Fab fragment concentrations could be followed for 229 h. The extrarenal clearance of Fab fragments was lower (5.6 ml/min) than in patients with normal kidney function (10.9 ml/min). This finding suggests that lower doses than usual might be sufficient for treating patients with severe digitalis intoxication and renal failure.

Topics: Acute Kidney Injury; Digoxin; Humans; Immunoglobulin Fab Fragments; Infusions, Intravenous; Male; Metabolic Clearance Rate; Middle Aged; Ventricular Fibrillation

1. Increased local thromboxane (Tx) formation has been considered to be a contributing factor in digitalis-induced arrhythmias. 2. A potent Tx synthetase inhibitor (TxSI), UK 38,485 (0.1, 1.0 or 10.0 mg/kg per h, administered intravenously) and a Tx receptor antagonist (TxRA), ICI 185,282 (1, 2 or 10 mg/kg bolus and 1, 2 or 10 mg/kg per h, administered intravenously) were tested for their ability to reduce digoxin-induced arrhythmias in anaesthetized guinea-pigs. 3. Electrocardiograms, mean blood pressure, heart rate and arrhythmias were recorded, starting 30 min before digoxin administration and continued for 60 min afterwards. 4. ICI 185,282, at the doses used, significantly delayed the time of onset of arrhythmias, and reduced the incidence of ventricular fibrillation, mortality and arrhythmia score. In contrast, UK 38,485 was found to be effective on all measured variables only at the dose rate of 1.0 mg/kg per h, except for time required for the development of arrhythmias. These protective effects of both TxSI and TxRA were not found to be dose-dependent. 5. Arterial blood pressure and heart rate changes caused by either UK 38,485 or ICI 185,282 infusions did not have any marked effects on digoxin-induced arrhythmias. 6. These data suggest that endogenously released TxA2 and prostaglandin endoperoxides may play an important role in digoxin-induced arrhythmias in guinea-pigs.

Topics: Anesthesia; Animals; Arrhythmias, Cardiac; Blood Pressure; Digoxin; Dioxanes; Dioxins; Dose-Response Relationship, Drug; Electrocardiography; Female; Guinea Pigs; Imidazoles; Male; Thromboxane A2; Ventricular Fibrillation

Topics: Aged; Digoxin; Humans; Ventricular Fibrillation

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

Topics: Adult; Amiodarone; Antibody Specificity; Benzofurans; Digoxin; Female; Humans; Immunoglobulin Fab Fragments; Poisoning; Ventricular Fibrillation

Topics: Digoxin; Electric Countershock; Female; Heart Rate; Humans; Middle Aged; Pacemaker, Artificial; Propranolol; Ventricular Fibrillation

Topics: Atrial Fibrillation; Digoxin; Drug Synergism; Drug Therapy, Combination; Female; Humans; Middle Aged; Ventricular Fibrillation; Verapamil

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: Aged; Coronary Disease; Digoxin; Drug Interactions; Drug Therapy, Combination; Female; Heart Arrest; Humans; Male; Ventricular Fibrillation; Verapamil

Documentation of the mechanism of sudden death is described in a patient with a prolonged QT interval. Ventricular tachycardia was initiated by a ventricular premature beat (VPB) with a prematurity index similar to previous isolated VPBs. This event occurred despite the fact that the patient was receiving phenytoin sodium, a drug known to shorten the QT interval.

Topics: Aged; Death, Sudden; Diabetes Complications; Digoxin; Electrocardiography; Epilepsy, Tonic-Clonic; Furosemide; Heart Arrest; Heart Failure; Humans; Male; Phenytoin; Potassium Chloride; Ventricular Fibrillation

A potentially fatal case of massive digitalis intoxication is presented. Recurrent ventricular fibrillation failed to respond to lidocaine or phenytoin, but responded dramatically to magnesium sulfate infusion. A review of the literature and previous clinical studies, as well as the case reported here, appears to indicate that magnesium sulfate given intravenously in adequate quantities (2 to 3 g in one minute followed by 2 g/h for 4 to 5 h) is effective in controlling ventricular irritability caused by toxic levels of digitalis preparations.

Topics: Digoxin; Electrocardiography; Humans; Infusions, Parenteral; Magnesium Sulfate; Male; Middle Aged; Suicide, Attempted; Tachycardia; Ventricular Fibrillation

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

Topics: Adult; Amiodarone; Benzofurans; Digoxin; Humans; Infusions, Parenteral; Male; Ventricular Fibrillation

Electrophysiologic studies with programmed cardiac stimulation were performed in a selected group of 17 patients with severe proximal coronary artery disease involving at least 2 major vessels and left ventricular ejection fractions greater than 30% who were undergoing coronary artery bypass graft surgery after prehospital cardiac arrest or ventricular tachycardia (VT) unassociated with acute myocardial infarction. Before surgery and without antiarrhythmic drug therapy, programmed cardiac stimulation induced ventricular fibrillation (VF) in 4 patients, and VT (greater than or equal to 5 beats) in 11 patients. Inducible VT or VF was suppressed by antiarrhythmic drugs in 7 of 13 patients in whom they were tried. Patients underwent coronary artery bypass graft surgery unassociated with perioperative myocardial infarction. When studied again an average of 19 days after surgery, 10 patients had no inducible VT or VF without antiarrhythmic drug therapy; 6 had induced VT. One patient had spontaneous VT. An effective antiarrhythmic regimen that suppressed inducible or spontaneous VT, or both, was defined by serial electrophysiologic studies in 4 patients, whereas 3 patients continued to manifest electrically inducible VT with all antiarrhythmic regimens tested. All but 1 patient, in whom postoperative VT could not be suppressed, are free of arrhythmias after a mean follow-up period of 23 months (range 6 to 53). It is concluded that myocardial revascularization alone may improve the abnormal electrophysiologic findings in certain patients; however, this effect of coronary artery bypass graft surgery is unpredictable, and pre- and postoperative electrophysiologic studies are recommended as part of the evaluation of these patients.

Topics: Aged; Amiodarone; Cardiac Pacing, Artificial; Coronary Artery Bypass; Digoxin; Electrophysiology; Female; Heart Ventricles; Humans; Male; Middle Aged; Postoperative Care; Preoperative Care; Radiography; Tachycardia; Ventricular Fibrillation

Topics: Aged; Digoxin; Electric Countershock; Female; Humans; Recurrence; Ventricular Fibrillation

A 49-year-old woman took about 12.5 mg digoxin with suicidal intent. Severe arrhythmias, including recurrent ventricular fibrillation, occurred. Sheep Fab fragments of digoxin-specific antibodies were administered i. v. at a dose of 480 mg. Serum free-digoxin concentration fell within half an hour to 0, with simultaneous rise of total digoxin from 13 micrograms/l to a maximum of 176 micrograms/l after 2 hours. At the same time there was marked improvement in the clinical condition with restoration of a stable sinus rhythm. There were no side effects to the Fab fragment administration.

Topics: Antibodies; Digoxin; Female; Humans; Immunoglobulin Fab Fragments; Middle Aged; Suicide, Attempted; Ventricular Fibrillation

An elderly woman allegedly ingested oleander leaves and died. Ventricular arrhythmias and asystole were unresponsive to cardiopulmonary resuscitation, pharmacologic agents, and cardioversion. The patient, who had no access to digoxin, had an initial serum digoxin concentration of 5.8 ng/mL. Cross-reactivities between oleander extract and pure oleandrin and digoxin in the digoxin radioimmunoassay were 100:1 and 29,000:1, respectively. We postulate that glycosides in oleander leaves produced the elevated serum digoxin concentration. Based on an assumed volume of distribution of the oleander glycosides of 1 L/kg, the calculated lethal dose absorbed by our patient was 200 times greater than lethal doses in several animal species and corresponded to the absorption of 4 g of oleander leaves.

Topics: Aged; Cardenolides; Cross Reactions; Digoxin; Female; Heart Arrest; Humans; Plant Extracts; Plant Poisoning; Plants, Medicinal; Radioimmunoassay; Ventricular Fibrillation

Digitalis poisoning is a rare problem in children, but it may be life threatening. A case of massive overdose of digoxin in a 2 1/2-year-old boy that produced prolonged ventricular fibrillation refractory to conventional therapy is reported. After two hours the boy was given digoxin-specific Fab fragments of antibody in sufficient quantity to bind his estimated dose of 10 mg. By completion of the treatment minutes later, normal rhythm and circulation were restored. The serum free digoxin level before antibody administration was greater than 100 ng/ml, and it rapidly fell to undetectable levels after antibody was given. Digoxin bound to the antibody had a clearance half-life of approximately 48 hours. The child had no apparent neurologic damage and his intellectual function was normal on discharge. He had a transient hematuria and a residual incomplete right bundle branch block. Administration of purified Fab fragments of digoxin-specific antibodies can be life saving in children with digitalis poisoning, and prolonged cardiopulmonary resuscitation in children is justified when the cause of cardiac arrest is potentially reversible.

Topics: Animals; Antibodies; Child, Preschool; Digoxin; Electrocardiography; Humans; Immunoglobulin Fab Fragments; Male; Sheep; Ventricular Fibrillation

Purified Fab fragments of ovine anti-digoxin antibodies (Wellcome Foundation) were used to treat a patient who attempted suicide by absorbing 10 mg of digitoxin (serum concentration 265 micrograms/l). The poor prognosis, as assessed clinically and from serum potassium levels (7.5 mEq/l), seemed to warrant such a treatment. The weak (6.85%) cross-reactivity elicited in vitro between the anti-digoxin antibodies and digitoxin was compensated by increasing the doses, but improvement was observed with 3.6 g, i.e. about half the effective dosage initially considered. The criteria of effectiveness were clinical, electrocardiographic (reversal of the ventricular fibrillation), biochemical (simultaneous and opposite changes in extra- and intracellular potassium levels, suggesting that ATPase inhibition by digitalis is a reversible process) and toxicological: there was an increase in digitoxin serum levels suggesting displacement of the drug from tissue sites to plasma and other extracellular compartments where the Fab fragments are distributed, and Fab-bound digitoxin appeared fairly rapidly in the urine, which suggested shunting of the normal hepatic metabolic pathway.

Topics: Aged; Animals; Antibodies; Cross Reactions; Digitoxin; Digoxin; Humans; Immunoglobulin Fab Fragments; Inactivation, Metabolic; Male; Potassium; Sheep; Suicide, Attempted; Ventricular Fibrillation

Topics: Digoxin; Female; Humans; Infant, Newborn; Ovum; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

Topics: Blood Pressure Determination; Digoxin; Electrocardiography; Humans; Male; Middle Aged; Ventricular Fibrillation

A 27-year-old man with typical mitral leaflet prolapse syndrome was under medical care for eight years with ventricular arrhythmias resistant to various antiarrhythmic drugs. He was started on digoxin, 0.25 mg daily, because of echocardiographically demonstrated left ventricular dilatation and functional impairment; he died of ventricular fibrillation 15 days later.

Topics: Adult; Digoxin; Electrocardiography; Humans; Male; Mitral Valve; Mitral Valve Prolapse; Ventricular Fibrillation

Topics: Animals; Digoxin; Dogs; Electric Countershock; Heart Rate; Myocardium; Procainamide; Propranolol; Ventricular Fibrillation

Topics: Adult; Arrhythmias, Cardiac; Cross Reactions; Digitoxin; Digoxin; Female; Heart Block; Humans; Immunoglobulin Fab Fragments; Potassium; Suicide, Attempted; Ventricular Fibrillation

Topics: Acute Disease; Coronary Disease; Digoxin; Humans; Lidocaine; Tachycardia; Ventricular Fibrillation

Topics: Adult; Aged; Diastole; Digoxin; Electrocardiography; Female; Humans; Male; Middle Aged; Quinidine; Tachycardia; Ventricular Fibrillation

Topics: Aged; Arrhythmias, Cardiac; Berlin; Cardiac Complexes, Premature; Digitalis Glycosides; Digoxin; Diuretics; Drug Therapy, Combination; Drug Tolerance; Female; Heart Block; Humans; Hypokalemia; Male; Myocardium; Pacemaker, Artificial; Potassium; Prospective Studies; Retrospective Studies; Ventricular Fibrillation

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

The rapid i.v. administration of digitalis has recently been shown to cause a substantial increase in coronary vascular resistance in the normal heart. This neurogenically mediated decrease in coronary blood flow would be potentially detrimental if it occurred during ischemia. The present study evaluates the effects of i.v. acetylstrophanthidin and digoxin on coronary vascular resistance during acute global ischemia in 29 dogs anesthetized with chloralose and urethane. Under these conditions, 0.5 mg of i.v. acetylstrophanthidin in 15 dogs resulted in erratic increases in coronary vascular resistance. The peak rise was 12+/-5% above control (P less than 0.01). In 7 of the 15 dogs, the initial erratic rise in coronary vascular resistance culminated in a steep rise associated with acute elevation in left ventricular end-diastolic pressure, which in four dogs terminated in ventricular fibrillation. During the nonischemic control periods, the peak rise in coronary vascular resistance with acetylstrophanthidin was 16+/-1% above control (P less than 0.01). In five dogs, prior alpha adrenergic receptor blockade with phenoxybenzamine prevented the rise in coronary vascular resistance with acetylstrophanthidin during ischemia. Similar erratic increases in coronary vascular resistance were observed with i.v. digoxin (1 mg) during ischemia in three dogs. In two of these dogs, there was a progressive rise in coronary vascular resistance associated with elevation of left ventricular end-diastolic pressure and ventricular fibrillation. The increase in coronary vascular resistance with digoxin during ischemia was abolished with phenoxybenzamine in two additional dogs. Thus, i.v. digitalis in the ischemic heart results in potentially detrimental increases in coronary vascular resistance mediated through alpha adrenergic receptor stimulation.

Topics: Animals; Coronary Circulation; Coronary Disease; Coronary Vessels; Digoxin; Dogs; Phenoxybenzamine; Receptors, Adrenergic; Receptors, Adrenergic, alpha; Stimulation, Chemical; Strophanthins; Vascular Resistance; Ventricular Fibrillation

Topics: Digoxin; Heart Diseases; Humans; Ventricular Fibrillation

The efficacy of potassium canrenoate in suppressing frequent ventricular premature depolarizations and ventricular bigeminal and trigeminal rhythms thought to be due to digitalis overdose was studied in seven men and five women (average age, 54.5 years). A mean dose of 525 mg. (1.31 mEq.) of potassium canrenoate administered intravenously effectively suppressed the ventricular rhythm disturbances in eight of the 12 patients for from several minutes to 4 hours. The mean serum digoxin level determined in seven patients was greater than 2.3 ng. per milliliter. The ability of potassium canrenoate to counteract digitalis intoxication suggests that the molecule of canrenoate is unique in the clinical setting since it shows both diuretic and antiarrhythmic properties.

Topics: Adult; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Canrenoic Acid; Digitalis Glycosides; Digoxin; Diuretics; Humans; Middle Aged; Pregnadienes; Ventricular Fibrillation

Clinical, electrocardiographic and laboratory data were found out in 52 patients with cardiac arrhythmias and conduction defects due to digoxin intoxication. Forty six nontoxic patients were also studied for comparison. Blood urea concentration was significantly higher in toxic patients as compared to nontoxic ones (P less than 0-01). Ventricular bigeminy and trigeminy (38.6%), multifocal ventricular premature beats (25%) and second or third degree A-V blocks (25%) were very much prevalent. Fairly good correlations have been observed between different cardiac arrhythmias and serum digoxin levels. Significantly higher mean serum digoxin levels were observed in patients with A-V block and multifocal ventricular premature beats as compared to patients with supraventricular arrhythmias.

Topics: Adult; Arrhythmias, Cardiac; Atrial Fibrillation; Digoxin; Female; Heart Block; Heart Failure; Humans; Male; Middle Aged; Pulmonary Heart Disease; Rheumatic Heart Disease; Tachycardia; Ventricular Fibrillation

Topics: Animals; Arrhythmias, Cardiac; Barbiturates; Bemegride; Biopharmaceutics; Blood Pressure; Cardiac Output; Digoxin; Dose-Response Relationship, Drug; Electrocardiography; Heart; Heart Arrest; Heart Rate; Specific Gravity; Vascular Resistance; Ventricular Fibrillation

Topics: Animals; Anti-Arrhythmia Agents; Cardiac Glycosides; Digitoxin; Digoxin; Electric Stimulation; Electrocardiography; Female; Guinea Pigs; Ouabain; Time Factors; Ventricular Fibrillation

Topics: Adrenocorticotropic Hormone; Autopsy; Child; Dermatomyositis; Diagnosis, Differential; Digoxin; Electrocardiography; Female; Heart Atria; Heart Failure; Heart Murmurs; Heart Neoplasms; Humans; Leg; Myxoma; Pain; Penicillins; Rest; Rheumatic Fever; Tachycardia; Ventricular Fibrillation

Topics: Administration, Oral; Aged; Arrhythmias, Cardiac; Digitalis Glycosides; Digitoxin; Digoxin; Heart Block; Heart Diseases; Heart Failure; Humans; Hyperthyroidism; Injections, Intravenous; Kidney Failure, Chronic; Middle Aged; Obesity; Ventricular Fibrillation

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: 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: Aged; Atrial Fibrillation; Digoxin; Electrocardiography; Hemodynamics; Humans; Lidocaine; Male; Practolol; Procainamide; Ventricular Fibrillation; Wolff-Parkinson-White Syndrome

Topics: Cardiomyopathies; Child; Child, Preschool; Digoxin; Electrocardiography; Female; Follow-Up Studies; Humans; Infant; Male; Myocarditis; Procainamide; Prognosis; Propranolol; Quinidine; Recurrence; Tachycardia, Paroxysmal; Time Factors; Ventricular Fibrillation

Topics: Digoxin; Electrocardiography; Female; Gastric Lavage; Half-Life; Heart; Heart Block; Humans; Male; Middle Aged; Poisoning; Radioimmunoassay; Suicide; Ventricular Fibrillation

Topics: Ajmaline; Apgar Score; Arrhythmias, Cardiac; Cesarean Section; Digoxin; Electrocardiography; Extraction, Obstetrical; Female; Fetus; Heart Block; Humans; Infant; Infant, Newborn; Lanatosides; Pregnancy; Prenatal Diagnosis; Tachycardia; Tachycardia, Paroxysmal; Ventricular Fibrillation; Verapamil; Wolff-Parkinson-White Syndrome

Topics: Administration, Oral; Age Factors; Digoxin; Electrocardiography; Heart Failure; Humans; Infant; Infant, Newborn; Injections, Intravenous; Intestinal Absorption; Ventricular Fibrillation

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: Aged; Cardiac Glycosides; Digitalis Glycosides; Digoxin; Humans; Male; Middle Aged; Neurologic Manifestations; Poisoning; Potassium; Ventricular Fibrillation

Topics: Adult; Aged; Aortic Valve; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Blood Urea Nitrogen; Digoxin; Female; Heart Block; Heart Valve Prosthesis; Humans; Male; Middle Aged; Mitral Valve; Prospective Studies; Tachycardia, Paroxysmal; Tricuspid Valve; Ventricular Fibrillation

Topics: Adolescent; Adult; Age Factors; Angiocardiography; Cardiac Catheterization; Child; Child, Preschool; Digoxin; Drug Synergism; Electric Countershock; Electrocardiography; Female; Heart Ventricles; Humans; Infant; Lidocaine; Male; Procainamide; Quinidine; Tachycardia; Time Factors; Ventricular Fibrillation

Topics: Accidents; Adolescent; Adult; Aged; Cardiac Complexes, Premature; Child, Preschool; Coronary Disease; Digoxin; Female; Half-Life; Humans; Male; Middle Aged; Poisoning; Radioimmunoassay; Suicide; Tachycardia, Paroxysmal; Ventricular Fibrillation

Topics: Aged; Atrial Fibrillation; Digoxin; Epinephrine; Humans; Hyperthyroidism; Isoproterenol; Male; Middle Aged; Propranolol; Quinidine; Ventricular Fibrillation

Topics: Adult; Aged; Anti-Arrhythmia Agents; Atropine; Digitalis Glycosides; Digoxin; Electrocardiography; Female; Heart Ventricles; Humans; Isoproterenol; Lidocaine; Male; Middle Aged; Pacemaker, Artificial; Phenytoin; Procainamide; Propranolol; Quinidine; Tachycardia; Ventricular Fibrillation

Topics: Animals; Aorta; Blood Pressure; Blood Volume; Cardiac Output; Digoxin; Dogs; Electrocardiography; Female; Heart Arrest; Heart Rate; Hemodynamics; Male; Phenytoin; Vascular Resistance; Ventricular Fibrillation

Topics: Animals; Arrhythmias, Cardiac; Cats; Digoxin; Drug Synergism; Electric Countershock; Electrocardiography; Humans; Tachycardia; Ventricular Fibrillation

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Computers; Digitalis Glycosides; Digoxin; Electrocardiography; Heart Conduction System; Heart Rate; Humans; Ventricular Fibrillation

Topics: Animals; Arrhythmias, Cardiac; Digoxin; Dogs; Ethanolamines; Extracorporeal Circulation; Heart; Heart Conduction System; In Vitro Techniques; Mephentermine; Ouabain; Sympathectomy; Ventricular Fibrillation

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; Digoxin; Drug Synergism; Electric Countershock; Ethacrynic Acid; Female; Humans; Quinidine; Syncope; Ventricular Fibrillation

Topics: Cardanolides; Digitalis Glycosides; Digoxin; Electric Countershock; Electrocardiography; Female; Humans; Male; Middle Aged; Strophanthins; Ventricular Fibrillation

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; Arrhythmias, Cardiac; Cats; Digitalis Glycosides; Digitoxin; Digoxin; Female; Lanatosides; Male; Ouabain; Reserpine; Vagus Nerve; Ventricular Fibrillation

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

Topics: Animals; Arrhythmias, Cardiac; Digoxin; Dogs; Electric Countershock; Electric Stimulation; Electrocardiography; Electrophysiology; Heart Block; Heart Conduction System; Quinidine; Tachycardia; Ventricular Fibrillation

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