Abstract

Sudden cardiac death remains a major public health problem in the United States. Ventricular fibrillation (VF) is the most common arrhythmia that directly leads to sudden cardiac death. However, the mechanisms of VF are unclear. Recently,1 2 different types of VF have been demonstrated in isolated, perfused rabbit hearts linked to the electrical restitution properties of the heart (ie, the dynamic dependence of action potential duration [APD] or conduction velocity [CV] on the previous diastolic interval). Type I (fast) VF is associated with a steep APD restitution, flat CV restitution, and multiple wandering wavelets. Type II (slow) VF is associated with flat APD restitution, broad CV restitution, decreased excitability, and spatiotemporal periodicity in activation maps. Our goal in this article is to explain how this new knowledge about the 2 types of VF can account for seemingly contradictory experimental findings by different investigators, and to speculate on the relevance to patient care. In normal hearts, physiological triggers such as premature ventricular contractions (PVCs) usually do not have the ability to generate an initial wavebreak causing sustained ventricular reentry. If such an event occurs, however, practically all normal hearts can fibrillate.2 In contrast, physiological triggers can sometimes induce wavebreak, initiating reentry in diseased hearts, as a result of increased structural and electrophysiological heterogeneity caused by the disease. Wiggers et al2 reported that VF occurred in 4 distinct stages visible by cinematography. The first (tachysystolic) stage lasts no more than a few seconds, characterized by either a single spiral wave or a figure-of-eight reentry.3 A second premature stimulus given during the protective zone can terminate this reentry and prevent the induction of VF.4 The second (convulsive incoordination) stage lasts for 15 to 40 seconds. Multiple wavelets and organized reentry coexist.5,6 The third (tremulous incoordination) stage lasts …

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