Beta-blocker treatment is an established therapy for heart failure. It provides an additional reduction in mortality due to a decrease in sudden death and heart failure worsening related death [1]. However, beta-blockers are not a homogeneous group of agents and not all tested drugs have demonstrated a favorable effect on mortality [2]. Carvedilol, bisoprolol and metoprolol have all improved the prognosis in controlled clinical trials, although there are pharmacological differences between them. Metoprolol and bisoprolol are selective for beta1-adrenergic receptors while carvedilol blocks also beta2and alfa1-adrenergic receptors and has antioxidant, anti-endothelin and antiproliferative properties. In addition, carvedilol has been associated with a further significant reduction in mortality and sudden death as compared with metoprolol, showing that different betablockers may have different effects [3]. Thus, results of clinical trials suggest that by reducing sudden death, betablockers must have some antiarrhythmic properties. On the other hand, there is overwhelming evidence about the inefficacy or even harm of antiarrhythmic agent’s (other than beta-blockers) in heart failure, guided or not by electrophysiological testing or Holter monitoring [4, 5]. On the contrary, beta-blockers have certain in vitro and in vivo electrophysiologic effects that can help to explain their antiarrhythmic properties. The beta-blocker carvedilol has multiple pharmacological actions, targeting membrane adrenoreceptors, ion channels and reactive oxygen species. Carvedilol-induced changes in atrial and ventricular action potential have been demonstrated in experimental studies and are due to its modulating effects on a variety of ion channels and currents. At a concentrations similar to those achieved in the clinical setting, carvedilol has a potent IKr blocking effect and a moderate ICa blocking effect. These actions may result in a moderate prolongation of the action potential duration, with minimal reverse frequency dependence, resembling those of amiodarone [6, 7]. The electrophysiologic effects of antiarrhythmic drugs in patients are variable and complex and depend on many factors, including the clinical scenario. For instance, differences in the cellular metabolism and intraand extracellular ionic milieu, in circulating catecholamines and autonomic tone, in the passive membrane properties, in fiber orientation, etc., can alter the effects of the drug. Therefore, it is clear that the electrophysiologic actions of a given drug during an electrophysiologic study cannot completely explain their antiarrhythmic or proarrhythmic effects during long term administration. Nonetheless, the knowledge of how the drug modify ionic conductance in normal and diseased tissue helps us to better understand the clinical effects of the drug. The paper of Kanoupakis et al [8] in this issue of the journal is remarkable because it provides interesting data on the elctrophysiological mechanisms supporting the antiarrhythmic effect of carvedilol when administered for a 2 months period in heart failure patients. The authors conducted a prospective randomized placebo-controlled trial studying the electrophysiological effects of a high oral dose of carvedilol in a subset of patients with chronic heart failure. Patients underwent an electrophysiological study previous and after chronic carvedilol administration. As compared with basal measurements, carvedilol increased all conduction times and the atrial and ventricular effective refractory periods without significant changes in repolarization Cardiovasc Drugs Ther (2008) 22:163–164 DOI 10.1007/s10557-008-6104-0