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PubMed2003

Management of atrial fibrillation: review of the evidence for the role of pharmacologic therapy, electrical cardioversion, and echocardiography.

PURPOSE: This review summarizes the available evidence regarding the efficacy of medications used for ventricular rate control, stroke prevention, acute conversion, and maintenance of sinus rhythm, as well as the efficacy of electrical cardioversion and the use of echocardiography in patients with atrial fibrillation. DATA SOURCES: The Cochrane Collaboration's database of controlled clinical trials and MEDLINE. STUDY SELECTION: Primarily randomized, controlled trials of medications. DATA EXTRACTION: Paired reviewers obtained data on efficacy and safety. Strength of evidence was assessed. DATA SYNTHESIS: Recent clinical trial results showed that most patients with atrial fibrillation have similar outcomes with strategies for controlling ventricular rate compared with strategies for restoring sinus rhythm. For efficacy of primary stroke prevention, compared with placebo, evidence was strong for warfarin and suggestive for aspirin. The evidence for an increased risk for major bleeding was suggestive for warfarin and inconclusive for aspirin. For ventricular rate control, verapamil, diltiazem, atenolol, and metoprolol were qualitatively superior to digoxin and placebo, particularly during exercise. For efficacy of acute conversion, compared with placebo, evidence was strong for ibutilide, flecainide, dofetilide, propafenone, amiodarone, and quinidine. For efficacy of maintenance of sinus rhythm after conversion from atrial fibrillation, evidence was strong for amiodarone, propafenone, disopyramide, and sotalol. Echocardiography was found to be useful in estimating risk for thromboembolism and potentially useful in estimating likelihood of successful cardioversion and maintenance. CONCLUSIONS: For several key questions in the pharmacologic management of atrial fibrillation, strong evidence exists to support 1 or more treatment options.

Anti-Arrhythmia Agents↗
PubMed1999

[The new indications for permanent cardiac pacing].

In spite of conflicting data from several studies, pacing is being used in several indications beyond the classic ones, namely to treat patients with hypertrophic cardiomyopathy, severe heart failure and to prevent atrial fibrillation. In this article the authors briefly review the new indications for this therapeutic intervention and discuss the utilization criteria, the technical details and the results of trials with dual-chamber pacing in patients with hypertrophic cardiomyopathy and severe heart failure. In obstructive hypertrophic cardiomyopathy, dual-chamber pacing significantly reduces the gradient and improves symptoms. Criteria suggested for the application of pacemaker therapy are: 1) persistent symptoms in spite of an adequate medical therapy trial (i.e., B-blockers, calcium antagonists, disopyramide): 2) left ventricular tract gradients of > 30 mmHg at rest or > 50 mmHg with provocation. In heart failure (NYHA class III ou IV with ejection fraction < 35) only a small percentage seems to benefit from this new therapeutic approach. They are those with a long PR interval on the surface electrocardiogram, with presystolic mitral regurgitation and with abbreviated diastolic filling period on the mitral inflow velocity on Doppler echocardiography. On the basis of some preliminary results, it appears that pacing may decrease the frequency of paroxysms of atrial fibrillation in some patients with vagal mediated fibrillation, chronotropic incompetence and those with long interatrial conduction times. Noninvasive detection of acute cardiac allograft rejection in heart transplant recipients by the analysis of some pacing parameters with telemetry is, at present, in an experimental stage.

Arrhythmias, Cardiac↗
PubMed1999

Class I antiarrhythmic drug effects on ouabain binding to guinea pig cardiac Na+ -K+ ATPase.

The notion that the inhibition of the Mg2+ -dependent ATP-hydrolytic function of the myocardial Na+ -K+ ATPase by class I antiarrhythmic agents occurs as a result of their binding to the same receptor sites as the digitalis glycosides was tested by performing competitive binding assays of [3H]ouabain (OUA) with eight drugs: disopyramide, encainide, lidocaine, lorcainide, phenytoin, procainamide, quinidine, and tocainide in guinea pig heart microsomal preparations. In the first set of experiments, 10-200 microM concentrations of the drugs were preincubated with the enzyme and displacement assays performed with 250 nM OUA. The drugs showed receptor occupancy of 19-32% at 50 microM, 25-44% at 100 microM, and 37-56% at 200 microM. Then, 10-500 nM concentrations of OUA were preincubated with the enzyme, and competitive assays were performed using 200 microM concentrations of the drugs. OUA occupied 39-51% of the receptor sites at 100 nM, 44-67% at 250 nM, and 62-82% at 500 nM, displacing the drugs in a concentration-dependent fashion. The results show that antiarrhythmic drugs interact with the same or similar receptor sites as ouabain on the Na+ -K+ ATPase, pointing to a possible contribution of these interactions to the mechanism for their inhibitory actions on the enzyme, and perhaps their arrhythmogenic effects.

Animals↗
PubMed1979

[Electrophysiological effects of anti-arrhythmia agents in man. Attempt at classification].

The electrophysiological effects of anti-arrhythmic drugs in man may be classified in three groups: -- Group I: comprising drugs whose characteristic action is on the AV node (beta blockers, verapamil, digitalis) The nodal conduction time (A-H interval) and refractory periods are increased. -- Group II: comprising drugs acting on the His-Purkinje system, the AV nodal conduction staying unchanged. This group has two sub-groups. Sub-group A: these drugs delay the His-Prukinje conduction (increased H-V interval). Examples are quinidine, procainamide, disopyramide, ajmaline, chloro-acetyl-ajmaline. In addition these drugs usually increase the atrial refractory periods and those of accessory pathways. Sub-group B: the His-Purkinje conduction is unchanged but the refractory periods are modified: lengthened (bretylium tosylate) or shortened (diphenylhydantoin, lignocaine, mexiletine). -- Group III: which includes amiodarone and aprindine whose effects are mixed: on the one hand AV nodal depression, and on the other, alteration of the His-Purkinje conduction manifested by an increased H-V internal (aprindine) or refractory periods (amiodarone). These preparations also increase the refractory periods of accessory AV pathways and amiodarone increase the refractory periods of the atria. This type of classification could help towards a more rational clinical approach to the use of anti-arrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed2000

Mitral valve repair and septal myectomy for hypertrophic obstructive cardiomyopathy.

Combined mitral valve repair using the sliding leaflet technique and septal myectomy were employed to successfully treat left ventricular outflow tract (LVOT) obstruction and mitral regurgitation due to hypertrophic obstructive cardiomyopathy (HOCM). A 46-year-old man was diagnosed with HOCM along with congestive heart failure and was treated medically. These symptoms, however, were resistant to medical treatments with a beta-blocker, a Ca-antagonist, and disopyramide, and he was referred to our hospital for surgery. Doppler echocardiography demonstrated an LVOT obstruction at rest with a peak pressure gradient of 138 mmHg. The interventricular septum thickness was 14 mm. Mitral regurgitation of 3+ with severe SAM was also observed. Temporary dual chamber pacing was tried without significant improvement. Following these examinations, the patient underwent surgery. A transaortic septal myotomy-myectomy was performed first, and the mitral valve was then approached through the left atrium. Mitral valve repair was performed with the sliding leaflet technique to reduce the height of the posterior leaflet from 2 cm to 1 cm. Postpump transesophageal echocardiography revealed no MR and a peak LVOT gradient of 15 mmHg. The patient recovered well except for a residual mild SAM, and MR2+. We therefore concluded that this surgical approach might provide results which are superior to those of myectomy alone.

Cardiomyopathy, Hypertrophic↗
PubMed2000

[Angelman syndrome and severe vagal hypertonia. Three pediatric case reports].

Angelman's syndrome is an association of severe mental retardation with absence of language, ataxia, convulsions and hyperactive, joyful behaviour with frequent bouts of laughing. Genetic diagnosis is possible in about 80% of cases. No cardiovascular abnormalities have been described in this syndrome to date. The authors report the cases of three children with Angelman's syndrome who presented with severe malaise due to increased vagal tone. The age of onset of symptoms was between 20 months and 8 years. One of the children had malaises triggered by bouts of laughing. The diagnosis was confirmed in all three cases by the results of Holter 24 hour ECG recording and oculo-cardiac reflex. The treatment chosen was Diphemanil (Prantal) in the two patients under 2 years of age (after failure of a trial of betablockers in one case) and Disopyramide for the oldest child with excellent results in all cases. However, one child died suddenly at the age of 6, two years after stopping diphemanil. Based on these observations, the authors suggest that all malaises in patients with Angelman's syndrome should be investigated by Holter ECG and oculo-cardiac reflex (or tilt test). In view of the potential gravity of the syncopal attacks, long-term medical treatment seems to be justified.

Age of Onset↗
PubMed2000

[Unwanted drug interaction between anti-arrhythmic drugs and drugs used for heart failure].

The appearance of adverse drug reactions may depend on the category of used drugs as well as on the coexistence of a pathological stage. Clinically important are: interactions of digitalis glycoside drugs leading to the occurrence or intensification of toxic symptoms characteristic for those drugs; interactions of antiarrhythmic drugs which may cause proarrhythmic effects and hypotension, and also interactions of nitrates resulting in lowering of the blood pressure. Quinidine, verapamil, nitrendipine, amiodaron, propafenone, captopril, spironolactone decrease renal clearance of digoxin, and amilorid/triamteren lower the extrarenal clearance of this drug. Thus the outcome of those concommitant therapies is the increase of digoxin serum concentration and appearance of toxic symptoms. Clinically dangerous, in the course of the antiarrhythmic therapy, is the increased risk of the arrhythmia appearance when two or more antiarrhythmic drugs are applied concomitantly. Antiarrhythmic drugs class IA (quinidine, disopyramide), class III (sotalol, amiodarone), class IV (calcium channel blockers) used at the same time with potassium depleters diuretics or beta-blocking agents result in the inhibition of repolarization and the increased duration of activation potential with the risk of developing arrhythmia of the torsade de pointes types. Nitrates interactions are mainly of the pharmacodynamic character. Most common adverse drug reaction, observed during the concomitant nitrates and another circulatory drug therapy, is excessive lowering of the blood pressure. These may lead to the decrease in the therapeutic efficacy of these combinations. Interactions of circulatory drugs are numerous, sometimes difficult to predict and they may lead to the intensification of the adverse drug reaction and lowering of their therapeutic efficacy.

Anti-Arrhythmia Agents↗
PubMed1997

[The blocking effects of six antiarrhythmic drugs on transient outward current in rat ventricular myocytes].

The effects of six antiarrhythmic drugs on transient outward current (Ito) in rat ventricular myocytes were examined by using the patch-clamp whole-cell recording technique. Quinidine, nifedipine, and imipramine resulted in a concentration-dependent inhibition of Ito with IC50s of 5.4, 10.9 and 6.0 mumol.L-1, respectively. All three agents produced a concentration-dependent increase in the rate of inactivation of Ito. Disopyramide, procainamide and E-4031 produced little inhibition of Ito even when present at 100 mumol.L-1. The results from this study show that quinidine, nifedipine and imipramine are potent inhibitors of Ito and that inhibition is mediated through preferential interaction with the open channel.

Animals↗
PubMed2002

[Antiarrhythmic drugs in atrial fibrillation].

Antiarrhythmic drugs in atrial fibrillation are relatively old and have well-specified indications. Class I antiarrhythmic drugs (IA: quinidine, disopyramide; IC: cibenzoline, flecainide, propafenone) are first indicated in patients without history of myocardial infarction and heart failure. In this last case, a b-blocker or amiodarone are indicated. Amiodarone is also indicated after failure of class I antiarrhythmic drugs. The association of class I antiarrhythmic drugs or amiodarone with a small dose of b-blocker is suitable if possible. However, the association of amiodarone with half-dose of a class I antiarrhythmic drug should remain rare, because the prognosis of chronic atrial fibrillation is unknown; the benefits to risks ratio of antiarrhythmic treatment should be discussed for each patient.

Adrenergic beta-Antagonists↗
PubMed2002

[Role amiodarone in sinus rhythm maintenance after successful cardioversion in patients with chronic non-valvular atrial fibrillation].

UNLABELLED: Antiarrhythmic drugs prophylaxis may improve late outcome of electrical cardioversion (CV) in persistent atrial fibrillation (AF). We conducted a prospective study of the efficacy of sequential antiarrhythmic drug therapy in sinus rhythm (SR) maintenance after a successful elective CV in patients (pts) with persistent nonvalvular AF. Investigated group and methods. 104 pts (60.4 +/- 7.9 years old) with persistent AF underwent CV. Following SR restoration pts received one of these antiarrhythmic drugs (Drug I): propafenone, sotalol, disopyramide. In case of arrhythmia recurrence we performed a second CV and pts received another drug from the mentioned before (Drug II). If treatment proved to be unsuccessful pts received amiodarone (Drug III) and a third CV was attempted. Following an unsuccessful first CV pts received loading dose amiodarone and another CV was attempted. In case of SR restoration amiodarone was administered continuously. RESULTS: First CV was successful in 53.8% pts. Following 1 year 27 pts (48.2%) presented with SR treated with Drug I (median not exist); Drug II proved to be effective in 2 pts (7.0%) (median 14 days). Amiodarone as the third antiarrhythmic agent (Drug III), administered in pts who had previously AF recurrence during the first two antiarrhythmic agents, occurred effective in additional 13 pts (median 307 days) who remained free from AF for one year from the initiation of sequential antiarrhythmic therapy. 48 pts in whom the first CV was ineffective, received amiodarone. During the loading period SR was restored in 10 pts (20.8%). The remaining 38 pts underwent repeated CV and SR was restored in 24 (62.3%) of them. Long-term amiodarone treatment maintained SR during the follow-up period in 24 (70.6%) pts. In total, amiodarone helped to maintain SR in 56.0% of pts. CONCLUSIONS: Sequential antiarrhythmic drug therapy improve arrhythmia prognosis in AF within a 12 months observation period. Amiodarone seems to be the most effective antiarrhythmic drug also in pts who required a second CV proceeded by amiodarone treatment to restore SR.

Aged↗
PubMed2003

[Drug therapy of atrial fibrillation].

The authors summarize the up-to-date knowledge relating to the pharmacological treatment of atrial fibrillation. They emphasize that drug treatment continues to be in the forefront of the therapy of the arrhythmia, which can now be considered to constitute a cardiovascular epidemic. In the era following the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AF-FIRM) trial, the strategy of pharmacological treatment will certainly change: in place of "rhythm control", which in recent decades has been overforced in patients identical with the elderly, cardiac patients with an impaired left ventricular function who were enrolled into AFFIRM, there will be a more frequent use of ventricular "rate control". Naturally, this does not mean that, in certain patient groups, an effort should not be made to restore and maintain the sinus rhythm. In cases involving congestive heart failure and structural heart disease complicated by a depressed left ventricular systolic function, atrial fibrillation is currently treated with antiarrhythmic drugs possessing low proarrhythmic activity that prolong refractory period (Class 3), and with the even safer mortality-reducing beta-receptor blockers. The classical antiarrhythmic drugs (quinidine, procainamide, disopyramide) are being increasingly forced into the background, and the areas of indication of the novel Na(+)-channel blocker antiarrhythmics (propafenone, flecainide) have also narrowed: they are administered only in the event of atrial fibrillation in patients with a structurally intact heart or left ventricular hypertrophy. After a brief survey of the more important aspects of ventricular rate control, and of the drugs available, the research trends aimed at the progression of the pharmacological treatment of atrial fibrillation are outlined. The clinical introduction of procedures based on myocardial gene therapy is now a realistic therapeutic approach as concerns atrial fibrillation too.

Anti-Arrhythmia Agents↗
PubMed1992

[Pregnancy and cardiovascular agents].

Any treatment used in pregnant women must take into account the effects of the substance in question of the fetus and the particular sensitivity of the latter during the first three months of development. The majority of drugs used in cardiology can be prescribed during pregnancy: digitalis preparations, furosemide, certain beta-blockers, verapamil, nifedipine (except during the first three months), quinidine, disopyramide, lignocaine, flecainide, amiodarone, heparins (non-fragmented and low molecular weight), central antihypertensive agents, dipyridamole and aspirin. In contrast, some drugs should be avoided because of insufficient information regarding their maternal and fetal consequences (bumetamide, modamide, the most recent beta-blockers, cibenzoline, ticlopidine) or because of harmful adverse effects on the fetus (spironolactones, bipyridines, diltiazem) or the newborn infant (angiotensin converting enzyme inhibitors). Finally, with certain medications (propafenone, oral anticoagulants), it is important to be able to compare maternal risks due to the disease and fetal risks induced by the drug. Modification of the conditions of use of these drugs and very careful monitoring of the patient most often suffice to avoid untoward events or complications with potentially serious medicolegal consequences and which may implicate the liability of the prescriber.

Anticoagulants↗
PubMed1992

Advances in syncope: a combined approach utilizing head-up tilt testing and electrophysiologic evaluation.

The electrophysiological evaluation of syncope of unknown origin yields a diagnosis in approximately 40% of patients. In the presence of structural heart disease ventricular tachycardia is the most common etiology accounting for 20% of cases. Over the past several years head-up tilt table testing with isoproterenol provocation has highlighted the syndrome of neurocardiogenic syncope. This syndrome accounts for an additional 30-40% of patients with syncope. There is compelling evidence that this syndrome involves the Bezold-Jarisch reflex with excessive stimulation of ventricular mechanoreceptors (C-fibers) located predominantly in the inferoposterior portion of the heart. Tilt table testing is now an established tool both for diagnosis of this syndrome and for guiding therapy with beta blockers, disopyramide, theophylline, or alpha-agonists. Tilt table testing combined with invasive electrophysiological testing significantly increases the diagnostic yield in the evaluation of syncope.

Arrhythmias, Cardiac↗
PubMed2003

Hypertrophic obstructive cardiomyopathy: mechanism of obstruction and response to therapy.

Hypertrophic cardiomyopathy is a primary, usually familial, disorder of heart muscle whose primary feature is muscular hypertrophy without recognized cause that encroaches on the ventricular chamber, reducing chamber area and volume. In roughly 25% of cases, there is associated obstruction to left ventricular outflow (hypertrophic obstructive cardiomyopathy [HOCM]). This article details the mechanism of obstruction in HOCM, focusing on obstruction at the mitral valve level, and reviews the pharmacologic and surgical therapies currently available. Mainstays of pharmacologic therapy include b-blockers, calcium channel blockers (verapamil in particular), and/or disopyramide. Surgical therapies include septal myotomy/myectomy, which has become the gold standard to which other therapies are compared, and mitral valve replacement. During the past 10 years, atrio-ventricular sequential pacing and alcohol septal ablation have been proposed as less invasive alternatives to surgery. A single, optimal therapy for patients with HOCM and refractory symptoms has not been established, and decisions regarding surgical versus noninvasive therapies need to be individualized based on functional status, comorbidities, local expertise in the surgical and nonsurgical techniques, and patient preference.

Adrenergic beta-Antagonists↗
PubMed2004

Two cases of ventricular tachycardia with congenital left ventricular malformation in an adult.

Two patients without any risk factors for coronary artery disease presented with symptomatic, recurrent, nonsustained ventricular tachycardia. They were found to have a postero-lateral left ventricular aneurysm and diverticulum. Coronary angiography revealed normal coronary arteries. The 12-lead electrocardiogram showed sinus rhythm with frequent premature ventricular contractions. Their nonsustained ventricular tachycardias were reproduced by programmed electrical stimulation and was unresponsive to procainamide, mexiletine, and disopyramide. Aneurysmal resection and cryoablative surgery were performed. The pathological examination of the aneurysmal wall revealed focal defect of muscle fibers in case 1. On the other hand, the wall of case 2 was formed by all three cardiac layers. After surgery, ventricular programmed stimulation was negative, and premature ventricular contraction had disappeared.

Diverticulum↗
PubMed1992

[A case of repetitive monomorphic ventricular tachycardia].

We present a case treated with aprindine and metoprolol combined with a DDD type pacemaker for repetitive monomorphic ventricular tachycardia. A 50-year-old man was admitted because of palpitation and near syncope attack. Electrocardiogram showed repetitive monomorphic ventricular tachycardias (RBBB LAD type) and R-R interval of about 440 msec and I degree A-V block in sinus rhythm. Electrophysiologic study disclosed that overdrive pacing in HRA suppressed ventricular tachycardias. Left ventriculography revealed a dilated left ventricular and decreased contractility. Antiarrhythmic agents such as quinidine sulfate, procainamide, disopyramide, mexiletine, lidocaine and propranolol were not effective. But, the combination of propranolol and aprindine decreased the rate of the ventricular tachycardia. With aprindine 60 mg/day and metoprolol 60 mg/day combined with the atrioventricular sequential pacing at 85/min, ventricular tachycardia completely disappeared.

Aprindine↗
PubMed1992

[Permanent junctional reciprocating tachycardia in children and adolescents. Efficacy of medical treatment].

Between 1969 and 1991, 11 patients were followed up for permanent junctional reciprocating tachycardia. The average age at diagnosis was 2 years and 4 months (1 day to 14 years). The tachycardia was diagnosed at routine examination in 5 cases and following an episode of cardiac failure in the other 6. Digitalis was prescribed in all patients with 4 good results, 5 average and 2 poor results. One patient, who remained in mild cardiac failure with digitalis therapy, died suddenly at the age of 9 years. In more recent cases, amiodarone was used from the onset or secondarily with good results in all patients. In 2 patients, in whom amiodarone was withdrawn after 3 months and 3 years' treatment, there was a recurrence of the tachycardia. No side effects of amiodarone therapy were observed in this series. Three patients were prescribed flecainide with 1 good and 2 average results. Propranolol, used in 2 cases, was associated with 1 average and 1 poor result. Disopyramide and Verapamil were ineffective. These results suggest that amiodarone is the drug to choose in permanent junctional reciprocating tachycardia but it must be given long term. The persistence of cardiac failure, poor control of the tachycardia or secondary effects of drug therapy should lead to consideration of non-medical management of the tachycardia.

Adolescent↗
PubMed2005

[Atrial fibrillation: choice of the method of pharmacological cardioversion].

The paper considers circumstances under which it is expedient or not expedient to perform cardioversion in patients with paroxysmal or persistent atrial fibrillation. It contains discussion of benefits, limitations and drawbacks of electrical and pharmacological methods of cardioversion. American College of Cardiology/American Heart Association/European Society of Cardiology Guidelines for the Management of Patients With Atrial Fibrillation are presented. These guidelines suggest amiodarone, dofetilide, ibutilide, propafenone, flecainide, and quinidine as first line therapy because of their proven efficacy. Efficacy of intravenous disopyramide and procainamide in some patients with recent onset atrial fibrillation is recognized with certain reservations. The use of azimilide and dronedarone is considered promising. In Russia nibentan and ethacizine can be also used. Special emphasis is made on the possibility of wide use (including self-administration) of loading doses of oral propafenone for cardioversion in some categories of patients with atrial fibrillation of recent onset.

Anti-Arrhythmia Agents↗