Efficacy and safety of quinidine therapy for maintenance of sinus rhythm after cardioversion. A meta-analysis of randomized control trials.

Abstract

Because individual studies evaluating the role of quinidine in the maintenance of sinus rhythm after cardioversion from chronic atrial fibrillation have involved relatively few patients, a meta-analysis of randomized control trials was performed. Six trials published between 1970 and 1984 were selected by two blinded reviewers based on study design and statistical analysis. Data from these six trials involving 808 patients were pooled after testing for homogeneity of treatment effects across trials. Life table estimates of the percent of patients still in sinus rhythm at 3, 6, and 12 months after cardioversion were constructed for quinidine and control groups. The proportion of patients remaining in sinus rhythm in the quinidine group was 69O, 58%, and 50% at 3, 6, and 12 months postcardioversion respectively. The proportion of patients remaining in sinus rhythm in the control group was 45%, 33%, and 25% at the same time intervals. The pooled rate difference, or difference in proportion of patients in sinus rhythm between quinidine and control groups, was 24%, 23%, and 24% at 3, 6, and 12 months of follow-up (p<0.001 at all time intervals). The unadjusted total mortality rate in the quinidinetreated patients was 2.9%o and in the control group was 0.8%. The odds of dying in the quinidine-treated group were approximately three times that of the control group ("typical" odds ratio= 2.98, p<0.05). Thus, quinidine treatment is more effective than no antiarrhythmic therapy in suppressing recurrences of atrial fibrillation but appears to be associated with increased total mortality. (Circulation 1990;82:1106-1116 54%.3-5 In some studies administration of quinidine was stopped because of an unacceptably high incidence of toxicity that included ventricular fibrillation, syncope, and death.5,6 Nevertheless, a precise estimate of mortality secondary to quinidine is lacking in the literature. This is particularly relevant in light of recent observations regarding the proarrhythmic potential of antiarrhythmic agents and the recently published report of the Cardiac Arrhythmia Suppression Trial,7 which demonstrated increased mortality in patients randomized to encainide and flecainide treatment for suppression of ventricular arrhythmias after myocardial infarction.

Effects of Antiarrhythmic Drugs on Fibrillation in the Remodeled Atrium

“…Because the same agents affect ventricular electrophysiology, they risk promoting ventricular tachyarrhythmias and thereby directly increasing cardiac mortality. 22 Pharmacological therapy to prevent remodeling is attractive because it would target the processes that promote the occurrence and maintenance of AF at a more fundamental level. 23 In the present study, we found that amiodarone prevented tachycardia-induced atrial electrophysiological remodeling, in terms of both atrial electrical properties and ion-channel subunit expression.…”

Effect of Low-Dose Amiodarone on Atrial Fibrillation or Flutter in Japanese Patients With Heart Failure.

“…6 Therefore, the prevention or conversion of AF or flutter is important in the management of heart failure. Many class I antiarrhythmic agents convert AF and maintain sinus rhythm (SR) through a slowing of conduction velocity, but may also worsen heart failure through their significant negative inotropic effects [7][8][9] and thus increase the risk of death in patients with heart failure. 7 Randomized control trials for prevention of cardiac death in patients with impaired cardiac function have suggested that amiodarone therapy is suitable for management of AF in patients with heart failure, [10][11][12][13][14] and it was reported in the recent DIAMOND trial that dofetilide was effective in converting AF, preventing its recurrence, and reducing the risk of hospitalization for worsening heart failure in patients with congestive heat failure and left ventricular dysfunction, without affecting mortality.…”

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“…The recognition that VT occurring in a structurally normal heart is potentially curable by radiofrequency catheter ablation (RFA), and that VT in the setting of structural heart disease is also amenable to effective treatment by RFA 40 .…”