European Heart Journal (2002) 23, 586–588
Letters to the
Editor
doi:10.1053/euhj.2001.3058, available online at http://www.idealibrary.com onMaintainance of sinus rhythm after electrical cardioversion of persistent atrial fibrillation
I read with interest the article by Plewan et al.[1]that compared head-to-head the efficacy of sotalol vs biso-prolol in the maintenance of sinus rhythm after electrical cardioversion of persistent atrial fibrillation. Their study failed to show any benefit of sotalol over bisoprolol during a follow-up period of 1 year, and showed more adverse effects with sotalol, principally due to pro-arrhythmia. Several considerations have to be made, however, before ban-ning sotalol indefinitely from our therapeutic arsenal against atrial fibrillation.
The first point concerns efficacy. The dose of sotalol was 80 mg b.i.d, which has been shown to be no more effective than placebo for maintaining sinus rhythm in a randomized placebo-controlled dose-response study[2]. In that study, the optimal dose of sotalol was suggested to be 120 mg b.i.d. Therefore the dose of sotalol may have been too low to show any benefit over bisoprolol.
The second issue concerns pro-arrhythmia with sotalol, with an inci-dence of torsades de pointes of 3·1%. The majority of patients had structural heart disease, with a mean left ven-tricular ejection fraction of around 40%. About a third of the patients had coronary artery disease. In a trial using d-sotalol in patients with a left ventricular ejection fraction of 40% or less and with either a recent myocar-dial infarction or symptomatic heart failure with a remote myocardial infarction, administration of d-sotalol was associated with increased mor-tality as compared to placebo, presum-ably due to arrhythmias[3]. Therefore proarrhythmia in the study may have been reduced by excluding patients with a depressed left ventricular function and ischaemic heart disease.
H. BURRI
Cardiology Service, University Hospital of Geneva, Geneva, Switzerland
References
[1] Plewan A, Lehmann G, Ndrepepa G
et al. Maintenance of sinus rhythm after
electrical cardioversion of persistent atrial fibrillation. Sotalol vs bisoprolol. Eur Heart J 2001; 22: 1504–10. [2] Benditt DG, Williams JH, Jin J et al.
Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and/ or atrial flutter. d,l-Sotalol Atrial Fibrillation/Flutter Study Group. Am J Cardiol 1999; 8: 270–7.
[3] Waldo AL, Camm AJ, deRuyter H
et al. Effect of d-sotalol on mortality in
patients with left ventricular dysfunc-tion after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol. Lancet 1996; 348(9019): 7–12.
doi:10.1053/euhj.2001.3118, available online at http://www.idealibrary.com on
A reply
We are very grateful for the interest in our study[1]and the discussion follow-ing publication.
We do not agree with Dr Burri’s suggestion that an 80 mg dose of sota-lol b.i.d. would be too low to show any benefit over a pure beta-blocker for maintenance of sinus rhythm after cardioversion of atrial fibrillation. In our trial we demonstrated a significant prolongation of QT and QTc intervals (Table 2; Fig. 2) as a variable of the class-III properties of sotalol at a daily dosage of 160 mg[1]. Furthermore, another placebo-controlled study showed a significant benefit for main-taining sinus rhythm after paroxysmal supraventricular arrhythmias, starting at 80 mg b.i.d.[2]. At a first glance the trial of Benditt et al.[3]seems to be in contrast to these findings. But there was a dose reduction in 20% of all patients in this study to a single 80, 120 and 160 mg daily dose of sota-lol. Taking this fact into account, sotalol was efficient at a mean daily dosage of approximately 200 mg. With respect to this mean, the sotalol dos-age given to the patients of Benditt et al. might be in accordance with our results.
We agree with Dr Burri, that an underlying structural heart disease with depressed left ventricular func-tion increases the risk of proarrythmia
under sotalol. We found an incidence for torsade de pointes tachycardia of 3·1%, in accordance with other pub-lications, with a range from 2–5% depending on the severity of con-comitant heart disease[4]. Astonish-ingly both patients in our trial with torsade de pointes tachycardia suf-fered from arterial hypertension, but had normal left ventricular func-tion. Therefore, excluding ‘high-risk’ patients with proarrhythmia would not have reduced the incidence of adverse effects under sotalol in our study.
Finally our findings are supported by a study ofSteeds et al.[5]who found no difference in control of paroxysmal atrial fibrillation between a dosage of sotalol 160 mg and atenolol 50 mg, although there was improvement com-pared to baseline prior to treatment with either substance.
A. PLEWAN
German Heart Center and 1. Medizinische Klinik, Klinikum rechts der Isar, Technische Universita¨t Mu¨nchen, Munich, Germany
References
[1] Plewan A, Lehmann G, Ndrepepa G et
al. Maintenance of sinus rhythm after
electrical cardioversion of persistent atrial fibrillation: sotalol vs bisoprolol. Eur Heart J 2001; 22: 1504–10. [2] Wanless RS, Anderson K, Joy M,
Joseph SP. Multicenter comparative study of the efficacy and safety of sota-lol in the prophylactic treatment of patients with paroxysmal supraven-tricular tachyarrythmias. Am Heart J 1997; 133: 441–6.
[3] Benditt DG, Williams JH, Jim J et al. Maintenance of sinus rhythm with oral d,l-sotalol therapy in patients with symptomatic atrial fibrillation and/or flutter. D,l-Sotalol Atrial Fibrillation/ Flutter Group. Am J Cardiol 1999; 84: 270–7.
[4] Roden RM. Risks and benefits of anti-arrhythmic therapy. N Engl J Med 1994; 331: 785–91.
[5] Steeds RP, Birchall AS, Smith M, Channer KS. An open label, random-ized, crossover study comparing sotalol and atenolol in the treatment of symp-tomatic paroxysmal atrial fibrillation. Heart 1999; 82: 170–5.
doi:10.1053/euhj.2001.3013, available online at http://www.idealibrary.com on
Interference of two common European digital cellular phones with
implantable cardioverter-defibrillators