To the Editor:

The two modalities of cardioversion for converting atrial fibrillation, chemical and electrical, have never been compared in a randomized study. Nonetheless, the experience acquired in clinical practice and the results of numerous studies have generated enough evidence for a consensus that electrical cardioversion is more effective than chemical cardioversion, especially when atrial fibrillation lasts more than one week.1 It also seems clear that electrical cardioversion is very safe, in spite of requiring deep sedation, and rarely needs prolonged hospital monitoring. This cannot be said of chemical cardioversion. Antiarrhythmic drugs often produce cardiovascular side effects, particularly after the first doses, and these side effects can occur at any time. Although all antiarrhythmics can produce potentially mortal ventricular arrhythmias, the antiarrhythmics with class III effect do so most often. From 1% to 5% of treated patients develop polymorphic tachycardia. In the case of quinidine, this effect so is well known that it has already become part of the history of medicine.2 The administration of a loading dose of quinidine to convert atrial fibrillation has such a pronounced proarrhythmic effect that it is advised against in recent guidelines for clinical practice on atrial fibrillation3 (class IIb indication). Authors understand that we now have better alternatives. In a publication reporting the findings of a registry of 1152 consecutive patients treated with electrical or chemical cardioversion to convert atrial fibrillation, 6 cardiac deaths occurred among 570 patients under the age of 65 years. All the deaths were sudden and associated with the administration of quinidine in high doses (1000-2000 mg/day).4

Given this background, it is easy to understand our surprise when we read the article by Valencia Martín et al,5 whose conclusions undermine the certainties of 50 years of accumulated evidence. The authors conclude, literally: «Both therapeutic modalities (electrical cardioversion and pharmacological cardioversion with quinidine) are valid and the decision to choose one or the other one will depend on the experience of the cardiologist.» This conclusion is supported by a non-randomized, retrospective study, to mention only one of its limitations. They detected a single episode of torsades de pointes, of unknown consequences for the patient, which meant that the incidence was 1.16%, which is lower than has been reported in the literature. It is possible that this finding could be explained by the fact that patients did not undergo continuous electrocardiographic control, which would seem to be mandatory, and that less symptomatic cases passed unnoticed. To our knowledge, the effect on the QT interval was not controlled either. The elevated effectiveness reported for quinidine is also notable, since it is much higher than would be expected in a population of patients with sustained arrhythmia for such a long time (mean 58 weeks). In contrast, the effectiveness of electrical cardioversion would have been greater if an alternative paddle configuration on the chest and/or a second 360-J shock had been used.

For these reasons, we think that the conclusion reached by the authors is venturesome considering that it contradicts numerous studies and clinical practice guidelines, and magnifies the role that quinidine now has in cardioversion for atrial fibrillation.