Is atrial fibrillation an inflammatory disorder?

I read with great interest the excellent review on the influence of inflammation in the pathogenesis of atrial fibrillation (AF) by Boos et al.1 As the authors have demonstrated, there is compelling evidence supporting the role of inflammation in the pathogenesis of this arrhythmia. I was surprised, however, to find no mention of the possible efficacy of beta-blockers with anti-inflammatory properties in this respect. Carvedilol, in particular, is a slightly beta 1-selective beta-blocker, which also possesses alpha 1-blocking and antioxidant properties.2 Indeed, part of its reported beneficial effects on ventricular remodelling effects and coronary microcirculation has been attributed to its antioxidant activities.2 Recently, we have provided evidence that carvedilol is probably more efficient than bisoprolol in the prevention of AF recurrences in an unselected patient population.3 In our study, 90 patients undergoing cardioversion of persistent AF were randomized to bisoprolol 5–10 mg once daily or carvedilol 12.5–25 mg twice daily. By intention-to-treat analysis, 23 (46%) patients in the bisoprolol group and 17 (32%) patients in the carvedilol group relapsed into AF, during the 1 year of total follow-up period (P=0.486). Patients treated with carvedilol had a 14% (hazard ratio=0.86) lower risk to relapse to AF when compared with patients on bisoprolol group. This issue deserves closer attention, particularly when discussing the limitations of current anti-arrhythmic drugs as far as their anti-inflammatory action is concerned.