• S H Hohnloser, A van de Loo, and F Baedeker.
• Department of Cardiology, University Hospital, Freiburg, Germany.
• J. Am. Coll. Cardiol. 1995 Oct 1; 26 (4): 852-8.

ObjectivesThis study compared the efficacy and safety of sotalol and quinidine for conversion and prevention of recurrent atrial fibrillation.BackgroundAtrial fibrillation is the most common arrhythmia. Pharmacologic therapy has been advocated for both immediate restoration of sinus rhythm and prevention of recurrent atrial fibrillation. Quinidine is the therapeutic mainstay for both purposes, but its safety has recently been questioned. Although sotalol has been used successfully to maintain sinus rhythm after direct current cardioversion, its efficacy in pharmacologically reverting atrial fibrillation has not been examined.MethodsFifty consecutive patients with persistent atrial fibrillation were randomized to receive quinidine or sotalol for up to 7 days to restore sinus rhythm. Patients were followed up for 6 months.ResultsQuinidine was more effective than sotalol in terminating atrial fibrillation (60% vs. 20%, p = 0.009). When nonresponders to drug therapy underwent subsequent direct current cardioversion, total conversion rates in the quinidine and sotalol groups were comparable (88% vs. 68%, p = 0.17), as was the efficacy of the two drugs in preventing recurrent atrial fibrillation. Side effects necessitating drug discontinuation were more often observed with quinidine. No patient receiving sotalol but four patients receiving quinidine had drug-associated arrhythmia (torsade de pointes in three patients, sustained ventricular tachycardia in one patient). Precordial QT dispersion determined on the surface electrocardiogram (ECG) increased with quinidine (mean +/- SD 34 +/- 9 vs. 44 +/- 16 ms, p = 0.02), indicating enhanced inhomogeneity in ventricular repolarization. There was no change in QT dispersion in patients receiving sotalol (36 +/- 18 vs. 40 +/- 17 ms, p = 0.44).ConclusionsQuinidine is more effective than sotalol in terminating atrial fibrillation but is associated with more side effects. The proarrhythmic risk may be related to quinidine's propensity to increase disparity in ventricular repolarization. This risk warrants careful ECG monitoring during the 1st 4 to 7 days of therapy. Because most proarrhythmic effects occurred shortly after restoration of sinus rhythm, observation should continue > or = 2 to 3 days after sinus rhythm is reestablished.

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