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Ventricular fibrillation (VF) is a fatal cardiac arrhythmia during which different parts of the heart do not beat together, and the heart cannot pump. There are about 300,000 sudden cardiac deaths associated with VF alone in the United States each year. On a wider scale, VF remains the leading cause of death among industrialized nations. The implantation of an automatic cardioverter-defibrillator is presently the most successful treatment of patients with uncontrollable VF. Such a device is designed to restore the heart to its normal rhythm via a large electrical shock that terminates any turbulent electrical activity. Drug therapies, in contrast, are aimed to control fibrillation in a less invasive and more cost-effective way by preventing its occurrence. They are thus in principle more desirable if they can be made equally effective as implantable devices. Antifibrillatory drugs, however, have so far remained largely unreliable and unsuccessful. Clinical trials to date, such as the Cardiac Arrhythmia Suppression Trial (1) where the death rate was higher among treated patients than those given placebo, have epitomized the danger of empirical drug therapies. The experimental findings of Garfinkel et al. (2) in this issue of PNAS point to a promising new direction for antifibrillatory drug development that is based on recent advances in our understanding of cardiac fibrillation. Those authors demonstrate that VF can be suppressed by pharmacologically altering the electrophysiology of cardiac cells in a specific way that prevents wave-breaking instabilities, namely by flattening the action potential duration restitution curve discussed below. The stabilizing effect of flattening restitution has been predicted on the basis of computer simulations of cardiac activation (3, 4). Experimental findings in support of this prediction were recently reported by Riccio et al. (5) who showed that the calcium channel blocker verapamil, observed previously to have an antifibrillatory effect (6 …

New paradigm for drug therapies of cardiac fibrillation