Abstract

Atrial fibrillation (AF) frequently complicates heart failure (HF), and vice versa, and—when found together—for clinicians they form an insufferable odd couple. Once AF appears, HF can worsen and stroke rate increases. Therefore, prediction and prevention of AF may be desirable goals. Secondary prevention using conventional rhythm control measures is, however, difficult to achieve and has not shown survival benefit.1,2 In high-risk patients primary prevention of AF using non-antiarrhythmic drugs such as angiotension-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and statins may be useful because of their secondary antiarrhythmic effects.3,4 The ancillary study of GISSI-HF by Maggioni et al. found that compared with placebo rosuvastatin reduces the incidence of AF in patients with HF.5 This substudy is very interesting and the first to report the effects of a statin compared with placebo on the incidence of AF in a stable HF population. Unfortunately, the antiarrhythmic effect is not large and the question remains of whether suppressing AF in HF patients is beneficial or only kills the messenger. This GISSI-HF substudy mainly concerned primary prevention since patients with AF on the pre-randomization ECG were excluded and eventually only ∼15% of study patients had had paroxysmal AF before inclusion. However, one must bear in mind that many patients with HF may have asymptomatic or otherwise unrecognized AF episodes, and these were not checked before randomization. Even so, the question is whether it was reasonable to exclude patients with previous AF. In addition, a related question is whether the endpoint should have been incidence of new AF. In stead, development of or progression to non-self-terminating (i.e. persistent) AF would have been a …

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