cardiovascular-agents and Tachycardia

Since 1953, sinus tachycardia has been defined as a heart rate (HR) in sinus rhythm of >100 beats per minute (bpm). However, this number has never been formally evaluated, and no established threshold values for special groups, such as those with heart failure (HF) accompanied by a reduced ejection fraction (HFrEF). Herein, we provided evidence that lowering the HR of patients with HFrEF to <70 bpm with medications such as ivabradine improves outcomes. Numerous large-scale trials and smaller clinical studies have shown that reducing the HR in patients with HFrEF improves cardiovascular and overall outcomes. Evidence suggests that a HR of <70 bpm is appropriate for patients with HFrEF. Examination of HF registries indicates that in a large proportion of these patients the HR exceeds 80 bpm, and no consideration is given to lowering the HR, due in large part to lack of physician awareness of the benefits of a lower HR. Evidence indicates that the first-line medication for lowering HR in patients with HFrEF is ivabradine. In conclusion, the improved prognosis following appropriate HR management in patients with HFrEF suggest that the cut-off value for sinus tachycardia in these patients should be redefined as 75 bpm. Maintaining a HR of <70 bpm in patients with HFrEF is associated with improved cardiovascular and overall outcomes.

Topics: Cardiovascular Agents; Digoxin; Heart Failure; Heart Rate; Humans; Ivabradine; Stroke Volume; Tachycardia

Resting heart rate (HR) is considered a powerful predictor of mortality both in healthy subjects and in cardiovascular (CV) patients, including those affected by heart failure (HF). Its reduction below 70 bpm is the treatment target in chronic HF with reduced ejection fraction (HFrEF) when sinus rhythm is present. In acute HF (AHF) HR is usually elevated but its role as risk marker is still unknown. Notably, in unstable patients, beta-blockers can be reduced or stopped, thus enhancing this phenomenon. Moreover, some data in literature suggest that HR reduction during hospitalization or HR at discharge or in the vulnerable phase after it are more predictive of early-term events and may be therapeutic targets. On the other hand, ivabradine is a pure HR-lowering drug with no effects on inotropism. Its role in the AHF setting has been recently investigated and is the object of this review.

Topics: Acute Disease; Adrenergic beta-Antagonists; Cardiovascular Agents; Heart Failure; Heart Rate; Hospitalization; Humans; Ivabradine; Myocardial Contraction; Patient Discharge; Prognosis; Tachycardia

Despite improvements in the therapy of underlying heart disease, sudden cardiac death is a major cause of death worldwide. Disturbed Na and Ca handling is known to be a major predisposing factor for life-threatening tachyarrhythmias. In cardiomyocytes, many ion channels and transporters, including voltage-gated Na and Ca channels, cardiac ryanodine receptors, Na/Ca-exchanger, and SR Ca-ATPase are involved in this regulation. We have learned a lot about the pathophysiological relevance of disturbed ion channel function from monogenetic disorders. Changes in the gating of a single ion channel and the activity of an ion pump suffice to dramatically increase the propensity for arrhythmias even in structurally normal hearts. Nevertheless, patients with heart failure with acquired dysfunction in many ion channels and transporters exhibit profound dysregulation of Na and Ca handling and Ca/calmodulin-dependent protein kinase and are especially prone to arrhythmias. A deeper understanding of the underlying arrhythmic principles is mandatory if we are to improve their outcome. This review addresses basic tachyarrhythmic mechanisms, the underlying ionic mechanisms and the consequences for ion homeostasis, and the situation in complex diseases like heart failure.

Topics: Action Potentials; Calcium; Calcium Channels; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cardiovascular Agents; Death, Sudden, Cardiac; Electrocardiography; Epigenesis, Genetic; Excitation Contraction Coupling; Heart Conduction System; Homeostasis; Humans; Ion Channel Gating; Myocytes, Cardiac; Sodium; Sodium Channels; Tachycardia; Tachycardia, Ventricular

Cardiac arrhythmias comprise of a heterogeneous group of disorders which manifest in a wide range of clinical presentations. They can be associated with underlying cardiac disease and portend a grave prognosis, with some arrhythmias being rapidly fatal. Other arrhythmias, however are relatively benign and can be asymptomatic or may be a mere inconvenience for the patient. All primary care physicians can expect to encounter some forms of arrhythmias during the course of their practice. This review article provides a brief overview of the commonly seen tachyarrhythmias for the general practitioner and provides relevant updates on the recent developments in our understanding of their mechanisms and management.

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Cardiovascular Agents; Catheter Ablation; Electric Countershock; Electrocardiography; Heart Ventricles; Humans; Risk Factors; Tachycardia

Topics: Adult; Androstenes; Anxiety; Blood Volume; Cardiovascular Agents; Catheter Ablation; Combined Modality Therapy; Confusion; Contraindications; Diagnosis, Differential; Fatigue; Female; Hemodynamics; Humans; Leg; Mast Cells; Norepinephrine; Norepinephrine Plasma Membrane Transport Proteins; Posture; Renin-Angiotensin System; Sodium Chloride; Sympathetic Nervous System; Syncope; Syndrome; Tachycardia

Quality improvement in cardiology over the past decade focused on management of acute coronary syndrome with invasive and innovative medical therapies, optimizing treatment of congestive heart failure and the development of repair procedures in valvular heart disease. On the other hand cardiologist and the attendant physicians are confronted with changes in the characteristics of patients in the light of demographic facts. Comorbidity and polypharmacy raise the need for clear concepts. Therapeutic and diagnostic tools of geriatric medicine may help in that context.

Topics: Aged; Aged, 80 and over; Bradycardia; Cardiovascular Agents; Drug Interactions; Drug Therapy, Combination; Frail Elderly; Heart Diseases; Humans; Long QT Syndrome; Prescription Drugs; Syncope; Tachycardia

Topics: Acute Coronary Syndrome; Aged; Cardiovascular Agents; Humans; Hypertension; Intraoperative Period; Male; Myocardial Infarction; Tachycardia

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Bradycardia; Calcium Channel Blockers; Cardiovascular Agents; Humans; Tachycardia

Thirty-eight articles have been published on the association between elevated heart rate and mortality. After adjustment for other risk factors, most studies found an independent association between heart rate and all-cause and/or cardiovascular mortality. This relationship has been found to be generally weaker among females. The four studies performed in hypertensive patients found a positive association between heart rate and all-cause mortality or cardiovascular mortality. In spite of this evidence, elevated heart rate remains a neglected cardiovascular risk factor in both genders. The pathogenetic mechanisms connecting high heart rate, hypertension, atherosclerosis and cardiovascular events have also been elucidated in many studies. Several trials retrospectively showed the beneficial effect of cardiac-slowing drugs, such as beta-blockers and non-dihydropyridine calcium antagonists on mortality, notably in patients with coronary heart disease, or heart failure, but no published data are available in patients with hypertension free of coronary heart disease. Although it has not been proven in existing trials, it would seem reasonable to recommend in hypertensive subjects with heart rate > 80-85 b/min, antihypertensive agents that decrease the heart rate. The f-channel blockers, selective heart rate-lowering agents with no effect on blood pressure, could also be profitably used in hypertensive subjects with fast heart rate.

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Antihypertensive Agents; Calcium Channel Blockers; Cardiovascular Agents; Clinical Trials as Topic; Coronary Artery Disease; Drug Therapy, Combination; Heart Diseases; Heart Rate; Humans; Hypertension; Risk Factors; Survival Rate; Tachycardia

The management of bradycardia-tachycardia syndrome (BTS) includes bradycardia and tachyarrhythmia therapy. At present, the treatment for symptomatic bradycardia in BTS patients is permanent cardiac pacing. The pharmacological treatment of atrial tachyarrhythmias comprises of rhythm and rate control, and prevention of thromboembolism. Patients with BTS often require both pacemaker and drug therapy. This article reviews the interactions of pacing and drug therapies in BTS. Drugs that alter cardiac electrophysiological properties may influence pacemaker indications, pacing mode selection, efficacy of pacing algorithms and pacing performance. Pacing by preventing drug-induced bradycardia increases the safety of pharmacotherapy and, thus, allows the intensification of those treatments. Pacing therapy and antiarrhythmic drugs used together as a hybrid therapy have a synergistic effect in the prevention of atrial tachyarrhythmias. Atrial-based pacing may reduce atrial tachyarrhythmia burden, allowing reduction of rhythm and rate control. Contemporary pacemakers' memory functions may help guide rhythm and rate control, as well as anticoagulation pharmacotherapy.

Topics: Bradycardia; Cardiac Pacing, Artificial; Cardiovascular Agents; Humans; Pacemaker, Artificial; Syndrome; Tachycardia

Alcoholic heart disease is caused by a lifestyle in which alcoholics are continue to consume an excessive amount of alcohol over a long period of time. Total abstinence is a very effective way to treat them to prevent the development of the final stage of this disease. In contrast, repetitive drinking of massive amount of alcohol is very harmful and causes exacerbation of this disease. From our clinical studies, six candidates were nominated as symptoms of alcoholic heart disease, namely(1) tachyarrhythmias (incidence: 33%), (2) left ventricular hypokinesis(17%), (3) QT interval prolongation(17%), (4) hyperthickened LV wall(13%), (5) LV dilatation with pump failure: alcoholic cardiomyopathy(0.1%), and (6) sudden cardiac death (unknown %). In the beginning of alcoholic heart disease, the patient usually complains of no symptoms, and physical signs are quite poor. Ordinarily, either transient atrial fibrillation and/or left ventricular hypertrophy which is initially documented by electrocardiography or echocardiography is one of the first signals in the diagnosis. Without such early signals, an early diagnosis is impossible. To make a definite diagnosis of alcoholic heart disease, a clinical follow-up is by all means necessary. Improvement of cardiac function after total abstinence, it's worsening after drinking again, and again improvement after abstinence a second time is a diagnostic clue. In this follow-up study, electrocardiography and echocardiography were employed as important ways to gather date. In treatment, total abstinence is essential. To achieve this therapeutic goal, education of the patient is necessary, because approximately 70 per cent of patients with alcoholic heart disease fail to continue abstinence within two years even if they have good training.

Topics: Cardiomyopathy, Alcoholic; Cardiovascular Agents; Diagnosis, Differential; Heart Ventricles; Humans; Myocardium; Prognosis; Tachycardia; Temperance; Ventricular Function, Left

Sudden cardiac death continues a major health problem. It is the leading cause of mortality in patients with coronary artery disease. In patients with the most malignant forms of ventricular tachyarrhythmias (ventricular tachycardia with syncope or aborted sudden death), anti-arrhythmics have been shown to be effective in preventing recurrences of these arrhythmias when tested according to a systematic protocol. Empiric therapy, on the other hand, is ineffective and dangerous because of the limited efficacy and the pro-arrhythmic potency of all anti-arrhythmic drugs. Asymptomatic ventricular arrhythmias, especially complex forms, after myocardial infarction characterize patients at increased risk for sudden cardiac death. In this situation most anti-arrhythmics do not improve prognosis. Amiodarone is so far the only anti-arrhythmic drug which has been shown to be beneficial in postinfarct patients, whereas Flecainide and Encainide were deleterious in a population at relatively low risk. Beta blocking agents, however, are effective in reducing mortality and incidence of sudden cardiac death in patients after myocardial infarction.

Topics: Adrenergic beta-Antagonists; Anti-Arrhythmia Agents; Calcium Channel Blockers; Cardiac Complexes, Premature; Cardiovascular Agents; Death, Sudden; Humans; Tachycardia; Ventricular Fibrillation

Topics: Adolescent; Adult; Aged; Cardiovascular Agents; Child; Child, Preschool; Electrocardiography; Female; Humans; Infant; Infant, Newborn; Male; Middle Aged; Pacemaker, Artificial; Tachycardia

Electroconvulsive therapy (ECT) is often associated with acute hyperdynamic responses, and we hypothesize that diltiazem can blunt this response. We measured the effect of a 10-mg dose of diltiazem on heart rate and mean arterial pressure during ECT. Furthermore, we assessed seizure duration by using both the cuff method and two-lead electroencephalogram. We studied 18 patients with a randomized, double-blinded, placebo-controlled cross-over study design. Diltiazem significantly reduced heart rate and mean arterial pressure just after medication, and it also significantly reduced the increases in these variables after ECT, as compared with the placebo. The use of diltiazem was, however, associated with a shortened seizure duration, possibly making ECT less effective. Because of the reduction in seizure duration, the routine administration of diltiazem may not be advisable because it can possibly interfere with the psychotherapeutic efficacy of ECT. However, diltiazem medication for ECT is potentially useful for reducing tachycardia and hypertension in high-risk patients.. Diltiazem can blunt acute hyperdynamic responses after electroconvulsive therapy, but seizure duration is also significantly reduced, possibly making this therapy less effective.

Topics: Adult; Aged; Blood Pressure; Cardiovascular Agents; Cross-Over Studies; Diltiazem; Double-Blind Method; Electroconvulsive Therapy; Electroencephalography; Female; Heart Rate; Hemodynamics; Humans; Hypertension; Male; Middle Aged; Seizures; Tachycardia

The arrhythmogenic hazard of adenosine treatment in an emergency room (ER) has not been established. Thus, in this study, we set out to prospectively determine the prevalence and clinical consequences of the arrhythmogenic effects associated with urgent adenosine treatment in the ER. One hundred and sixty consecutive patients treated with adenosine for regular wide or narrow complex tachyarrhythmias at our ER were included in the study. An initial bolus of 3 mg of adenosine was used, up to a maximum dose of 18 mg (mode 6 mg). Proarrhythmia was defined as the new appearance of any brady- or tachyarrhythmia within 1 minute from the bolus administration of adenosine. Of the 160 study patients, 84% had narrow complex tachycardia and 16% had wide complex tachycardia. Adenosine was effective in the diagnosis and/or treatment of the underlying arrhythmia in 92%. The overall prevalence of adenosine-induced proarrhythmia was 13%, including prolonged AV block inducing asystole > 4 seconds (7%), paroxysmal atrial fibrillation (1%) and non-sustained ventricular tachycardia (5%). All adenosine-induced arrhythmias were transient and subsided spontaneously. It is concluded, firstly, that adenosine-induced proarrhythmia proved to be frequent in a consecutive ER series, and included potentially dangerous arrhythmias. Secondly, nevertheless, all adenosine-induced arrhythmias subsided spontaneously and did not require treatment. Therefore, urgent adenosine treatment is safe and can be recommended in an emergency setting, provided a strict protocol of administration under close monitoring by highly trained personnel.

Topics: Adenosine; Adult; Age Distribution; Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cardiovascular Agents; Comorbidity; Diabetes Mellitus; Drug Therapy, Combination; Drug Tolerance; Electrocardiography; Emergency Service, Hospital; Female; Humans; Hypertension; Hyperthyroidism; Italy; Logistic Models; Male; Middle Aged; Prevalence; Prospective Studies; Pulmonary Disease, Chronic Obstructive; Sex Distribution; Tachycardia; Treatment Outcome

The lateral hypothalamus (LH) is a diencephalic structure that has been considered part of the central circuitry regulating the baroreflex function. However, the local neurochemical mechanisms involved in baroreflex control by this hypothalamic area are poorly understood. Therefore, in the present study we investigated the role of corticotropin-releasing factor (CRF) neurotransmission within the LH acting via local CRF

Topics: Aminopyridines; Animals; Baroreflex; Blood Pressure; Bradycardia; Cardiovascular Agents; Corticotropin-Releasing Hormone; Heart; Heart Rate; Hypothalamic Area, Lateral; Male; Peptide Fragments; Rats; Rats, Wistar; Receptors, Corticotropin-Releasing Hormone; Synaptic Transmission; Tachycardia

Topics: Cardiovascular Agents; Catecholamines; Humans; Ivabradine; Male; Middle Aged; Norepinephrine; Octreotide; Organometallic Compounds; Paraganglioma; Tachycardia

Tachycardia is associated with cardiovascular mortality. Tachycardia is also a known clozapine adverse effect. However, whether clozapine-associated tachycardia is persistent is not known. Thirty clozapine-treated patients with clinical tachycardia were investigated with 24-hour ambulatory electrocardiography (ECG). Baseline peripheral heart rate (HR) was 106.7±7.8. The ambulatory ECG 24-hour-HR was 98.7±9.7. Baseline HR and 24-hour-HR correlated strongly (r=0.74, p=0.000003). Daytime HR was 106.4±9.9 and nighttime HR 89.2±12.0. Low dose bisoprolol reduced HR significantly. The high 24-hour-HR indicates a persistent tachycardia. Tachycardia should not discourage from clozapine use but the findings indicate a need of guidelines for detection and treatment of clozapine-associated tachycardia.

Topics: Adult; Antipsychotic Agents; Bisoprolol; Cardiovascular Agents; Clozapine; Electrocardiography, Ambulatory; Female; Heart Rate; Humans; Male; Photoperiod; Tachycardia; Time Factors

A 26-year-old man presented to our syncope service with debilitating daily palpitations, shortness of breath, presyncope and syncope following a severe viral respiratory illness 4 years previously. Mobitz type II block had previously been identified, leading to a permanent pacemaker and no further episodes of frank syncope. Transthoracic echocardiography, electophysiological study and repeated urine metanepherines were normal. His palpitations and presyncope were reproducible on deep inspiration, coughing, isometric hand exercise and passive leg raises. We demonstrated rapid increases in heart rate with no change in morphology on his 12 lead ECG. His symptoms were resistant to fludrocortisone, flecainide, β blockers and ivabradine. Initiation of clonidine in combination with ivabradine led to rapid resolution of his symptoms. We suggest that an excessive respiratory sinus arrhythmia was responsible for his symptoms and achieved an excellent response with the centrally acting sympatholytic clonidine, where previous peripherally acting treatments had failed.

Topics: Adrenergic alpha-2 Receptor Agonists; Adult; Benzazepines; Cardiovascular Agents; Clonidine; Cough; Drug Therapy, Combination; Dyspnea; Echocardiography; Electrocardiography; Humans; Inhalation; Ivabradine; Male; Syncope; Tachycardia; Tachycardia, Sinus; Treatment Outcome

Topics: Animals; Atrial Flutter; Cardiovascular Agents; Dog Diseases; Dogs; Echocardiography; Electrocardiography; Heart Murmurs; Lameness, Animal; Tachycardia; Tricuspid Valve Insufficiency

Liposomes are nanosystems that allow a sustained release of entrapped substances. Gamma-aminobutyric acid (GABA) is the most prevalent inhibitory neurotransmitter of the central nervous system (CNS). We developed a liposomal formulation of GABA for application in long-term CNS functional studies. Two days after liposome-entrapped GABA was injected intracerebroventricularly (ICV), Wistar rats were submitted to the following evaluations: (1) changes in mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) to ICV injection of bicuculline methiodide (BMI) in anesthetized rats; (2) changes in cardiovascular reactivity to air jet stress in conscious rats; and (3) anxiety-like behavior in conscious rats. GABA and saline-containing pegylated liposomes were prepared with a mean diameter of 200 nm. Rats with implanted cannulas targeted to lateral cerebral ventricle (n = 5-8/group) received either GABA solution (GS), empty liposomes (EL) or GABA-containing liposomes (GL). Following (48 h) central microinjection (2 μL, 0.09 M and 99 g/L) of liposomes, animals were submitted to the different protocols. Animals that received GL demonstrated attenuated response of RSNA to BMI microinjection (GS 48 ± 9, EL 43 ± 9, GL 11 ± 8%; P < 0.05), blunted tachycardia in the stress trial (ΔHR: GS 115 ± 14, EL 117 ± 10, GL 74 ± 9 bpm; P<0.05) and spent more time in the open arms of elevated plus maze (EL 6 ± 2 vs. GL 18 ± 5%; P = 0.028) compared with GS and EL groups. These results indicate that liposome-entrapped GABA can be a potential tool for exploring the chronic effects of GABA in specific regions and pathways of the central nervous system.

Topics: Animals; Anxiety; Arterial Pressure; Bicuculline; Cardiovascular Agents; Catheters, Indwelling; Central Nervous System Agents; Exploratory Behavior; GABA Agents; gamma-Aminobutyric Acid; Heart Rate; Infusions, Intraventricular; Kidney; Liposomes; Male; Microinjections; Rats, Wistar; Stress, Physiological; Sympathetic Nervous System; Tachycardia

Topics: Benzazepines; Bisoprolol; Cardiovascular Agents; Comparative Effectiveness Research; Drug Monitoring; Drug Therapy, Combination; Exercise Tolerance; Female; Heart Rate; Humans; Ivabradine; Male; Middle Aged; Myocardial Ischemia; Myocardial Revascularization; Postoperative Complications; Tachycardia; Treatment Outcome

Drug-induced torsades de pointes (TdP) and related clinical entities represent a current regulatory and clinical burden.. As part of the FP7 ARITMO (Arrhythmogenic Potential of Drugs) project, we explored the publicly available US FDA Adverse Event Reporting System (FAERS) database to detect signals of torsadogenicity for antipsychotics (APs).. Four groups of events in decreasing order of drug-attributable risk were identified: (1) TdP, (2) QT-interval abnormalities, (3) ventricular fibrillation/tachycardia, and (4) sudden cardiac death. The reporting odds ratio (ROR) with 95 % confidence interval (CI) was calculated through a cumulative analysis from group 1 to 4. For groups 1+2, ROR was adjusted for age, gender, and concomitant drugs (e.g., antiarrhythmics) and stratified for AZCERT drugs, lists I and II (http://www.azcert.org , as of June 2011). A potential signal of torsadogenicity was defined if a drug met all the following criteria: (a) four or more cases in group 1+2; (b) significant ROR in group 1+2 that persists through the cumulative approach; (c) significant adjusted ROR for group 1+2 in the stratum without AZCERT drugs; (d) not included in AZCERT lists (as of June 2011).. Over the 7-year period, 37 APs were reported in 4,794 cases of arrhythmia: 140 (group 1), 883 (group 2), 1,651 (group 3), and 2,120 (group 4). Based on our criteria, the following potential signals of torsadogenicity were found: amisulpride (25 cases; adjusted ROR in the stratum without AZCERT drugs = 43.94, 95 % CI 22.82-84.60), cyamemazine (11; 15.48, 6.87-34.91), and olanzapine (189; 7.74, 6.45-9.30).. This pharmacovigilance analysis on the FAERS found 3 potential signals of torsadogenicity for drugs previously unknown for this risk.

Topics: Adverse Drug Reaction Reporting Systems; Amisulpride; Antipsychotic Agents; Arrhythmias, Cardiac; Benzodiazepines; Cardiotoxins; Cardiovascular Agents; Databases, Pharmaceutical; Death, Sudden, Cardiac; Female; Humans; Male; Olanzapine; Phenothiazines; Risk; Sulpiride; Tachycardia; Torsades de Pointes; United States; United States Food and Drug Administration; Ventricular Fibrillation

Vasopeptidase inhibition (VPI), a therapeutic strategy by dual inhibition of both ACE and neutral endopeptidase 24.11, has not shown a prognostic benefit over ACE inhibition in chronic severe heart failure (CHF). Nevertheless, the effects of early treatment by VPI on cardiac remodelling have not been well assessed. We analysed the effects of early chronic VPI (50 mg/kg/day Omapatrilat) on cardiac remodelling and neurohumoral function during the progression of rapid ventricular pacing-induced heart failure in rabbits (early left ventricular dysfunction [ELVD]: 10 days at 330 bpm, CHF: further 10 days at 360 bpm). VPI-treated animals (ELVD-VPI n = 6; CHF-VPI n = 8) and placebo treated animals (ELVD n = 6; CHF n = 7) were compared with control rabbits (CTRL n = 5). LV fractional shortening (FS) and enddiastolic diameter (LVEDD) were assessed by echocardiography (12 MHz probe). LV BNP- and LV IL-6 gene expression was analysed quantitatively by real time PCR. Neurohumoral function was assessed by ANP, cGMP, plasma renin activity (PRA) and Aldosterone. In ELVD, LVEDD and atrial mass were significantly increased (both p < 0.05). This increase was markedly attenuated by VPI (both p < 0.05 vs. placebo). CHF was associated with a further increase in atrial mass and an increase in LV mass (both p < 0.05), which was again attenuated by VPI (atrial mass, p < 0.05 vs. untreated). LV BNP mRNA was significantly increased in CHF (p < 0.05 vs. control), and chronic VPI completely abolished this increase in ELVD and significantly attenuated it in CHF (p < 0.05 vs. CHF-placebo). Beyond that, the increase of cGMP was augmented by chronic VPI (p < 0.05 vs. placebo in CHF) in heart failure and that of Aldosterone was attenuated (p < 0.05 vs. placebo in ELVD), whereas PRA was temporarily increased (p < 0.05 vs. placebo in ELVD). Combined inhibition of ACE and NEP by VPI significantly inhibits early cardiac remodelling and LV BNP gene expression. If initiated early enough, it may slow down cardiac remodelling and represents a promising therapeutic strategy in progressive heart failure.

Topics: Aldosterone; Angiotensin-Converting Enzyme Inhibitors; Animals; Cardiomegaly; Cardiovascular Agents; Disease Models, Animal; Gene Expression Regulation; Heart Failure; Male; Natriuretic Peptide, Brain; Neprilysin; Pyridines; Rabbits; Renin; Renin-Angiotensin System; RNA, Messenger; Tachycardia; Thiazepines; Ventricular Dysfunction, Left; Ventricular Remodeling

Topics: Anti-Bacterial Agents; Bacteremia; Borrelia; Cardiopulmonary Resuscitation; Cardiovascular Agents; Ceftriaxone; Child; Combined Modality Therapy; Cytokines; Doxycycline; Endotoxins; Female; Humans; Hypotension; Positive-Pressure Respiration; Pulmonary Edema; Relapsing Fever; Shock, Cardiogenic; Tachycardia; Unconsciousness

Elevated catecholamine levels are a well-recognized cause of various types of cardiomyopathy. Causes of catecholamine elevation include tumors, toxins, drugs, emotional stress, and sepsis. Milnacipran is a dual and equipotent inhibitor of norepinephrine and serotonin uptake. It is frequently prescribed as therapy for fibromyalgia, and the drug has a good safety profile. Herein, we report the case of a 42-year-old woman with undefined connective-tissue disease and fibromyalgia who developed a severe and reversible cardiomyopathy while taking recommended doses of milnacipran. The cardiomyopathy was associated with a hyperadrenergic state manifested by tachycardia, hypertension, and elevated plasma catecholamine levels. The discontinuation of milnacipran and the initiation of anti-failure therapy resulted in complete resolution of the cardiomyopathy in 6 months. To our knowledge, this is the first report of milnacipran as a possible cause of catecholamine-induced cardiomyopathy.

Topics: Adrenergic Uptake Inhibitors; Adult; Cardiomyopathies; Cardiovascular Agents; Catecholamines; Coronary Angiography; Cyclopropanes; Female; Humans; Hypertension; Magnetic Resonance Imaging; Milnacipran; Selective Serotonin Reuptake Inhibitors; Tachycardia; Time Factors; Treatment Outcome; Up-Regulation

Topics: Adenosine; Cardiovascular Agents; Heart Arrest; Humans; Tachycardia

The incretin hormone, glucagon-like peptide (GLP)-1(7-36), is rapidly cleaved by dipeptidyl peptidase 4 (DPP-4) into GLP-1(9-36), and although it is agreed that most, if not all, of the metabolic effects are attributable to the intact peptide, the degree to which the cardiovascular effects are due to the cleavage product is unclear. The purpose of this study was to measure the regional haemodynamic effects of GLP-1(7-36), and determine the extent to which the cardiovascular effects of GLP-1(7-36) were influenced by DPP-4 inhibition and reproduced by GLP-1(9-36). Additional experiments investigated the involvement of autonomic mechanisms in the cardiovascular effects of GLP-1(7-36).. Regional haemodynamic effects of bolus doses and 4 h infusions of GLP-1(7-36) amide and GLP-1(9-36) amide were measured in conscious, chronically instrumented rats; the influence of DPP-4 inhibition and autonomic blockade on responses to GLP-1(7-36) were also assessed.. Glucagon-like peptide-1(7-36) had clear regional haemodynamic effects comprising tachycardia, a rise in blood pressure, renal and mesenteric vasoconstriction and hindquarters vasodilatation, whereas GLP-1(9-36) was devoid of any cardiovascular actions. The effects of GLP-1(7-36) were enhanced by DPP-4 inhibition, and the tachycardia and hindquarters vasodilatation were beta-adrenoceptor-mediated.. In conscious rats, the cardiovascular effects of GLP-1(7-36) resemble those of the GLP analogue, exendin-4, and are attributable to the intact peptide rather than the cleavage product, GLP-1(9-36).

Topics: Animals; Blood Pressure; Cardiovascular Agents; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Glucagon-Like Peptide 1; Male; Peptide Fragments; Peptides; Rats; Rats, Sprague-Dawley; Tachycardia; Time Factors; Vasoconstriction; Vasodilation

Few cases of anomalous origin of the left coronary artery from the pulmonary artery remain asymptomatic until adolescence, and it is very rare to find a patient with this disease reaching the age of 70 without having undergone any surgery. Up to now, there have been only three other cases of patients, more than 70 years of age, with this congenital heart effect described in medical literature. We report the clinical history and the cardiac morphofunctional findings of 12 years of follow-up after a very late diagnosis of anomalous origin of the left coronary artery from the pulmonary artery.

Topics: Aged; Cardiac Surgical Procedures; Cardiovascular Agents; Coronary Angiography; Coronary Vessel Anomalies; Electrocardiography; Female; Humans; Pulmonary Artery; Tachycardia; Tomography, X-Ray Computed; Treatment Outcome; Treatment Refusal

Topics: Algorithms; Bradycardia; Cardiovascular Agents; France; Heart Arrest; Hospital Units; Humans; Myocardial Infarction; Myocardial Reperfusion; Patient Transfer; Shock, Cardiogenic; Tachycardia

Retroconduction (ventriculo-atrial conduction) remains a problem for patients with implanted cardiac rhythm devices. Pacemaker algorithms can detect and terminate endless loop tachycardia (ELT), but actual prevention of ELT may require anti-arrhythmic drugs (AADs). Similarly, AADs can affect ICD rhythm discrimination algorithms that depend on atrio-ventricular ratios. There is concern whether these drugs remain effective during stress situations.. Electrophysiologic studies that included retroconduction testing using slow ramp pacing were done in 1332 patients. The presence or absence of retroconduction at baseline and with drug was recorded, as was the rate at block. As a stress surrogate, isoproterenol was used to test retroconduction and reversal of drug-induced block.. Procainamide, mexiletine, phenytoin, disopyramide, quinidine, beta-blockers, encainide, and amiodarone caused complete retrograde block or decreased the rate at which block occurred (mean 76% of patients, p < 0.008), whereas digoxin, lidocaine, diltiazem, and verapamil did not. Isoproterenol (in the absence of AADs) increased the rate at block in 82% of 404 patients with retroconduction at baseline (p < 0.005). Of 319 patients without retroconduction at baseline, 134 (42%) developed retroconduction after isoproterenol. Isoproterenol reversed retrograde block in 39% of patients with block on an AAD. Amiodarone, digoxin, and the combination of digoxin plus a beta-blocker were most effective at resisting this reversal of ventriculo-atrial block (80%, 68%, and 75% respectively).. Most of the AADs reviewed increase the cycle length at block or abolish retroconduction, while isoproterenol has the opposite effect. Anti-arrhythmic medications, particularly amiodarone, digoxin, and the combination of digoxin plus a beta-blocker may be considered for a patient with multiple ELT episodes or certain ICD detection problems.

Topics: Adrenergic beta-Agonists; Anti-Arrhythmia Agents; Atrioventricular Node; Cardiac Pacing, Artificial; Cardiovascular Agents; Combined Modality Therapy; Defibrillators, Implantable; Drug Resistance; Drug Therapy, Combination; Electrophysiologic Techniques, Cardiac; Female; Heart Block; Heart Rate; Humans; Isoproterenol; Male; Middle Aged; Pacemaker, Artificial; Research Design; Tachycardia; Treatment Outcome

Cecropia pachystachya is used in South America for relieving cough and asthma. In Argentina it is known as "ambay" and grows in the neotropical forests (Ntr C.p.) and in temperate hilly regions (Tp C.p.). To evaluate their cardiovascular profile, the effect of extracts obtained from plants growing in the neotropical region as well as in temperate areas were compared by i.v. administration in normotensive rats. The following parameters were measured: blood pressure (BP) and heart rate (HR). The hypotensive effect was stronger for Ntr C.p., which aqueous extract decreased BP at doses between 90 and 300 mg lyophilised/kg until 46.2 +/- 12% of basal. The extract of Tp C.p. reduced BP to 86.1 +/- 11% of basal (p < 0.05 respect to Ntr C.p.) at 180 mg/kg, but increased HR at 90 and 180 mg/kg (until 133.6 +/- 10.8% of basal, p < 0.05) and produced death by respiratory paralysis at 320 mg/kg (about 3g dry leaves/kg). The hypotensive effects, but not the chronotropic ones, were attenuated by pretreatment with reserpine (5 mg/kg). The plant extracts had not diuretic activity by oral administration in conscious rats, nor produced vasodilation of perfused hindquarters arterial bed precontracted with high-[K] or 100 microM phenylephrine. The results suggest that neotropical ambay is more hypotensive than the one from the temperate hilly region. When it reaches plasma, it could produce hypotension (by central blockade of sympathic innervation of vessels) and tachycardia (by central cholinergic inhibition of heart), although it happens at doses higher than the oral ethnotherapeutic (about 340 mg dried leaves/kg).

Topics: Administration, Oral; Animals; Antihypertensive Agents; Blood Pressure; Cardiovascular Agents; Cecropia Plant; Diuretics; Dose-Response Relationship, Drug; Female; Heart Rate; Injections, Intravenous; Plant Extracts; Plant Leaves; Rats; Rats, Wistar; South America; Tachycardia

Topics: Bradycardia; Cardiovascular Agents; Electrocardiography; Heart Block; Humans; Infant, Newborn; Infant, Premature; Long QT Syndrome; Mexiletine; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channel Blockers; Sodium Channels; Tachycardia; Torsades de Pointes

Topics: Adolescent; Autonomic Nervous System Diseases; Cardiovascular Agents; Child; Child, Preschool; Diagnosis, Differential; Diet; Humans; Hypotension, Orthostatic; Infant; Physical Examination; Reflex; Respiration Disorders; Syncope, Vasovagal; Tachycardia

Topics: Adult; Cardiovascular Agents; Electric Countershock; Electrocardiography; Emergency Treatment; Female; Humans; Maternal-Fetal Exchange; Pregnancy; Pregnancy Complications, Cardiovascular; Tachycardia; Treatment Outcome

Interferon-alpha (IFN-alpha) has been widely used for treatment of chronic hepatitis C in Japan. In general, cardiovascular adverse reactions are rare in association with IFN-alpha therapy. Here, a 64-year-old man with chronic active hepatitis C complained of fatigue, palpitation and depression, and developed atrial fibrillation with prominent negative T waves during IFN-alpha therapy. Echocardiogram showed septal and apical hypertrophy. Three days after discontinuation of IFN-alpha, subjective symptoms and atrial fibrillation subsided. It is unclear whether or not IFN-alpha induced the giant negative T waves with apical hypertrophy. We might observe the developing course of hepatitis C virus (HCV)-related myocardial hypertrophy by chance. Cardiovascular toxicity should be carefully monitored during IFN-alpha therapy even in patients with minor cardiac disease, such as premature ventricular contracture (PVC) and mild hypertension.

Topics: Antihypertensive Agents; Antiviral Agents; Atrial Fibrillation; Atrial Premature Complexes; Cardiovascular Agents; Electrocardiography; Hepatitis C, Chronic; Humans; Hypertension; Hypertrophy, Left Ventricular; Interferon alpha-2; Interferon-alpha; Male; Middle Aged; Recombinant Proteins; Tachycardia; Ultrasonography

Cannabinoids, including the endogenous ligand anandamide, elicit pronounced hypotension and bradycardia through the activation of CB1 cannabinoid receptors. A second endogenous cannabinoid, 2-arachidonoyl glycerol (2-AG), has been proposed to be the natural ligand of CB1 receptors. In the present study, we examined the effects of 2-AG on mean arterial pressure and heart rate in anesthetized mice and assessed the role of CB1 receptors through the use of selective cannabinoid receptor antagonists and CB1 receptor knockout (CB1(-/-)) mice. In control ICR mice, intravenous injections of 2-AG or its isomer 1-AG elicit dose-dependent hypotension and moderate tachycardia that are unaffected by the CB1 receptor antagonist SR141716A. The same dose of SR141716A (6 nmol/g IV) completely blocks the hypotensive effect and attenuates the bradycardic effect of anandamide. 2-AG elicits a similar hypotensive effect, resistant to blockade by either SR141716A or the CB2 antagonist SR144528, in both CB1(-/-) mice and their homozygous (CB1(+/+)) control littermates. In ICR mice, arachidonic acid (AA, 15 nmol/g IV) elicits hypotension and tachycardia, and indomethacin (14 nmol/g IV) inhibits the hypotensive effect of both AA and 2-AG. Synthetic 2-AG incubated with mouse blood is rapidly (<2 minutes) and completely degraded with the parallel appearance of AA, whereas anandamide is stable under the same conditions. A metabolically stable ether analogue of 2-AG causes prolonged hypotension and bradycardia in ICR mice, and both effects are completely blocked by SR141716A, whereas the same dose of 2-AG-ether does not influence blood pressure and heart rate in CB1(-/-) mice. These findings are interpreted to indicate that exogenous 2-AG is rapidly degraded in mouse blood, probably by a lipase, which masks its ability to interact with CB1 receptors. Although the observed cardiovascular effects of 2-AG probably are produced by an arachidonate metabolite through a noncannabinoid mechanism, the CB1 receptor-mediated cardiovascular effects of a stable analogue of 2-AG leaves open the possibility that endogenous 2-AG may elicit cardiovascular effects through CB1 receptors.

Topics: Anesthesia; Animals; Arachidonic Acids; Blood Pressure; Camphanes; Cardiovascular Agents; Cardiovascular Diseases; Dose-Response Relationship, Drug; Endocannabinoids; Female; Glycerides; Heart Rate; Hypotension; Indomethacin; Ligands; Male; Mice; Mice, Inbred ICR; Mice, Knockout; Piperidines; Pyrazoles; Receptors, Cannabinoid; Receptors, Drug; Rimonabant; Tachycardia

Potential long-term cardioprotection was investigated in an extensive experimental study. Lactobacillus cultivation components (LCC) were administered intravenously in anesthetized rats 1, 7, and 21 days before global ischemia (GI). GI was produced by full stop flow in isolated Langendorff-perfused hearts for 20 min and was followed by reperfusion. Control animals were injected with saline. LCC reduced reperfusion tachyarrhythmia significantly and improved functional recovery of the ischemized rat heart. These beneficial effects were associated with reduction of release of norepinephrine (NE) and prostacyclin at the first minute of reperfusion, activation of myocardial catalase, and overexpression of 70-kDa heat stress protein (HSP-70) at ischemia and reperfusion (P < 0.05). This cardioprotection was documented up to 21 days after a single injection of LCC. Thus Lactobacillus cultivation components are new nontoxic materials that produce marked long-term cardioprotection against ischemia-reperfusion damage. This effect is attributed to an activation of the cellular defense system, manifested by activation of the antioxidant pathway and by expression of protective proteins. NE is involved in this process, and the data also suggest a role for prostacyclin in this model of cardioprotection. The potential of LCC and related compounds working through similar mechanisms in the prevention and therapy of various ischemic heart syndromes should be explored.

Topics: Adenosine Triphosphate; Animals; Body Temperature; Cardiovascular Agents; Catalase; Coronary Circulation; Epoprostenol; Hemodynamics; HSP70 Heat-Shock Proteins; Lactic Acid; Lactobacillus; Male; Myocardial Ischemia; Norepinephrine; Pharmaceutical Preparations; Rats; Rats, Sprague-Dawley; Recovery of Function; Reperfusion Injury; Tachycardia

Heart rate, an important risk factor of coronary mortality, is highly correlated with numerous anthropometric and biochemical variables: height, body weight and hyperlipidemia; it varies, furthermore, with smoking and age and can be modified during pharmacotherapy for hypertension. From meta-analyses on different cardiovascular treatments, given after coronary events, only the efficacy of drugs significantly reducing heart rate is borne out (beta-blockers with sympathomimetic activity, or calcium-antagonists with a prevalent vasodilatory action do not provide a protective effect). Among calcium-antagonists, while the mechanism of action is similar at the cell level (delay of opening of voltage-operated slow channels), the distribution of activity within the vascular system varies markedly. Dihydropyridines (e.g., nifedipine) exert a dominant peripheral effect, with consequent vasodilation, whereas phenylalkylamines (verapamil) have both peripheral vasorelaxant and cardiac negative chronotropic activity, because of a reduced sinus node action potential. A relative tachycardia may occur with dihydropyridines, secondary to the activation of baroreceptors; the compensatory heart mechanism operated by verapamil antagonizes this reflex tachycardia. The activity of verapamil on the atrioventricular conduction allows both a slowing of functional recovery of the channel in hyperexcitable conditions (supraventricular tachycardia), and, moreover, increased diastolic intervals, with consequent improvement of coronary flow. New molecules can selectively reduce the sinus node activity without exerting other effects (hypotensive, anti-arrhythmic). From a comparative evaluation of these molecules with verapamil, it clearly emerges how this latter can provide a more acceptable pharmacodynamic profile, both for the hypotensive activity, and also for the control of reflex tachycardia, with a consequently improvement of coronary flow.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Aged, 80 and over; Animals; Benzazepines; Blood Pressure; Calcium Channel Blockers; Cardiovascular Agents; Coronary Circulation; Dihydropyridines; Electrocardiography; Female; Heart Rate; Humans; In Vitro Techniques; Male; Middle Aged; Nifedipine; Population Surveillance; Rabbits; Sinoatrial Node; Tachycardia; Verapamil

Because of the emergency nature of the arrhythmias associated with WPW syndrome, nurses are often called upon for diagnosis and intervention in critical settings. In such cases the nurse's understanding of mechanisms, ECG recognition, and emergency treatment guarantees the patient the best possible outcome, not only in the critical setting, but in the long term as well. The most common arrhythmias of WPW syndrome are PSVT and atrial fibrillation. In PSVT a differential diagnosis is made on the ECG between (1) CMT using the AV node anterogradely and an accessory pathway retrogradely and (2) AV nodal reentry tachycardia. Helpful clues are location of the P' wave, presence of QRS alternans, the initiating P'R interval, and presence of aberrancy. Atrial fibrillation with an accessory pathway has the morphology of VT but is differentiated because the rhythm is irregular and the rate is more than 200 beats per minute. Emergency treatment consists of blocking the accessory pathway with procainamide. Emergency treatment for both types of PSVT consists of breaking the reentry circuit at the AV node (eg, vagal maneuver, adenosine, or verapamil). Procainamide can also be used to block the retrograde fast pathway in the AV node and to terminate CMT by blocking the accessory pathway. Symptomatic patients with accessory pathways are referred for evaluation and possible radio-frequency ablation.

Topics: Atrial Fibrillation; Cardiovascular Agents; Catheter Ablation; Education, Nursing, Continuing; Electrocardiography; Heart Conduction System; Humans; Tachycardia; Tachycardia, Atrioventricular Nodal Reentry; Tachycardia, Paroxysmal; Wolff-Parkinson-White Syndrome

Tachycardia caused by surgical stimulation can compromise the myocardial oxygen balance and may also lead to a reduction of cardiac output. Conventional drugs with negative chronotropic effects also cause reduction of inotropy. Recent so-called specific bradytropic agents are expected to act merely upon chronotropy without affecting pressure of the systemic or coronary circulation. The goal of this study was to investigate the effects of a calcium channel blocker. Falipamil, on the circulation controlling excessive intraoperative tachycardia. PATIENTS AND METHODS. In this study 15 patients, aged 32 to 73 years, mean 55 +/- 12 were investigated. The cardiac risk classes included classification I-III, according to Goldman. The patients underwent major abdominal or thoracoabdominal operations. Monitoring consisted of a radial arterial cannula, as well as a 7 French Swan-Ganz catheter, which was introduced via the internal jugular vein. Determination of cardiac output was done using the thermodilution technique with a Kimray Medical Association Oklahoma City model 3500; related indexes were calculated. Electrophysiological data were read from the ECG. The recorded QT interval was corrected for heart rate according to the formula of Hegglin and Holzmann. Anesthesia consisted of premedication with diazepam, 0.1 mg/kg, 1 h preoperatively. Anesthesia was induced with thiopentone, 5 mg/kg, and fentanyl, 1.5 micrograms/kg. After giving 1 mg alcuronium, succinylcholine, 1 mg/kg, was used for intubation. Anesthesia was continued using ventilation with O2: N2O 1:2 and intermittent doses of fentanyl and alcuronium. When tachycardia occurred at a rate higher than 100 beats per minute, a dose of 2 micrograms/kg fentanyl was administered to deepen the anesthesia. If this had no influence, control readings were taken and subsequently falipamil 2 mg/kg was injected. After that the hemodynamic parameters were monitored for 1, 2, 3, 5, 10, and 20 min. Statistical analysis was performed using the analyses of variance, followed by the Newman-Keuls test. The level of significance was p less than 0.05. RESULTS. The means and standard deviations of the hemodynamic parameters following induction of anesthesia (0) and at the peak rate are shown in Table 1. The mean increase in heart rate at that time was 38 +/- 18% and the QT and RR interval were reduced concomitantly. Both times the QT measured and the QT corrected for rate did not significantly differ from each other. (ABSTRACT TR

Topics: Adult; Aged; Anti-Arrhythmia Agents; Calcium Channel Blockers; Cardiovascular Agents; Female; Hemodynamics; Humans; Intraoperative Complications; Isoindoles; Male; Middle Aged; Phthalimides; Tachycardia

Magnesium chloride has been shown to terminate torsades de pointes in some patients with the acquired long QT syndrome. The mechanism for this effect is unknown. Recently early afterdepolarizations (EADs) and triggered activity (TA) have been proposed as causes of torsades de pointes. The purpose of the present study was to examine whether magnesium suppressed EADs that were initiated in vitro by different agents and if so its mechanism of action. TA arising from EADs was induced by quinidine (1 to 4 mumol/L, n = 5) at high temperature (38.5 to 40 degrees C), cesium chloride (5 to 12 mmol/L, n = 6), and 4-aminopyridine (1.5 to 5 mmol/L, n = 7) in canine cardiac Purkinje fibers superfused with modified Tyrode's solution (KCI = 2.7 mmol/L). MgCl2 (2 to 7 mmol/L) reversibly abolished TA and suppressed EADs. Tetrodotoxin (TTX; 1 to 5 mumol/L) also abolished TA elicited by 4-aminopyridine (n = 6). We then examined the effects of MgCl2, TTX, and verapamil on depolarization-induced automaticity by means of a single sucrose gap technique to gain insight into the mechanism of action of magnesium. MgCl2 (5 mmol/L) abolished automaticity arising from membrane potentials more negative than -70 mV and prolonged the spontaneous cycle length at less negative membrane potentials. The effects of TTX (1 to 5 mumol/L) resembled those of MgCl2. Verapamil (1 mumol/L) prolonged the cycle length of the initial automatic response at high levels of membrane potential and progressively reduced the amplitude of the subsequent automatic potentials. It abolished automaticity arising from less negative membrane potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 4-Aminopyridine; Action Potentials; Aminopyridines; Animals; Cardiovascular Agents; Cesium; Depression, Chemical; Dogs; Female; Heart Conduction System; In Vitro Techniques; Magnesium; Male; Purkinje Fibers; Quinidine; Tachycardia

Prompt defibrillation with lower energy levels (200 joules) initially is now recommended. Epinephrine is effective when instilled intratracheally and remains the treatment of choice for restoring cardiac rhythm. Enthusiasm for isoproterenol and calcium chloride has waned. Sodium bicarbonate and atropine are now used more cautiously. Bretylium and verapamil have improved the treatment of refractory ventricular fibrillation and paroxysmal supraventricular tachycardia, respectively.

Topics: Arrhythmias, Cardiac; Cardiovascular Agents; Electric Countershock; Heart Arrest; Humans; Male; Resuscitation; Tachycardia; Ventricular Fibrillation

The effects of two drugs that apparently block slow inward current--nifedipine and the new compound AQ-A 39--were studied on the isolated sinoatrial (SA) and atrioventricular (AV) nodes of the rabbit heart using intracellular microelectrodes. Nifedipine and AQ-A 39 both slowed the sinus rate associated with a decrease in the rate of diastolic depolarisation. Conduction through the AV node was consistently impaired; this effect was enhanced with increasing atrial rates or with decreasing coupling intervals of premature beats. The action potential amplitude was significantly reduced in SA nodal and upper (AN) AV nodal fibres but was not significantly affected in lower (NH) AV nodal and in atrial fibres. The maximum diastolic potential showed little or no alteration. In all fibre types studied, the action potential duration was shortened with nifedipine but was significantly prolonged with AQ-A 39. Prevention of AV nodal reentrant tachycardia by nifedipine was related to an increase in the effective refractory period of the AV node. AQ-A 39 prevented the tachycardia by both slowing of AV nodal conduction and by prolongation of action potential duration in the AV nodal and atrial compartments of the reentrant circuit associated with the appearance of different gap phenomena of the AV conduction. The maximum possible A-H interval was, however, not shortened by either drug and single atrial echo beats could still be initiated. The results suggest that nifedipine and AQ-A 39 both have a direct depressant action on the slow inward current-dependent electrical activity of the SA and AV node but have opposite effects on the repolarisation phase resulting in different antiarrhythmic mechanisms.

Topics: Action Potentials; Animals; Atrioventricular Node; Cardiovascular Agents; Heart Conduction System; Isoindoles; Nifedipine; Phthalimides; Pyridines; Rabbits; Sinoatrial Node; Tachycardia

Reported here are 162 cases of atrial ectopic tachycardia, a specific type of the supraventricular arrhythmia, which is characterized by the distinct P waves on the ECG, which follow at the rate of 400 and more per minute. Although atrial ectopic tachycardia is similar to the supraventricular paroxysmal tachycardia and atrial flutter, it differs from them by the mechanism of the development. Atrial ectopic tachycardia is caused by the failure or weakening the sinus node and the appearance of the ectopic focus in the atria. Such arrhythmia occurs in the following 4 types: with atrial to ventricular excitation ratio 1:1; with incomplete atrio-ventricular block; with complete atrioventricular block; and in combination with atrial fibrillation. Atrial ectopic tachycardia often takes lingering course and is hardly responsive to the medical treatment. The cases of arrhythmia, characterized by the broad P waves on the ECG tend to the progressive course. 17 cases of atrial ectopic tachycardia treated by electrostimulation (ES) which had 100% positive effect are presented and ES advantages over the drug therapy are underlined. The frequent transition of this arrhythmia into the atrial fibrillation is outlined.

Topics: Cardiovascular Agents; Coronary Disease; Electric Countershock; Electrocardiography; Female; First Aid; Heart Atria; Humans; Male; Rheumatic Heart Disease; Tachycardia

Topics: Cardiovascular Agents; Digitalis; Heart Ventricles; Tachycardia; Tachycardia, Paroxysmal

Topics: Arrhythmias, Cardiac; Cardiovascular Agents; Digitalis; Humans; Potassium; Tachycardia