A neurophysiologic mechanism for stress-induced cardiac arrhythmias is proposed based on the integration of two bodies of research that have until now developed independently: the role of hemispheric specialization in the mediation of emotional arousal and the role of a lateralized imbalance in sympathetic input to the heart in cardiac arrhythmogenesis. The specific hypothesis is that individuals who manifest more lateralized frontal lobe activity during emotional arousal may concomitantly generate more lateralized sympathetic input to the heart and be at increased risk for fatal cardiac arrhythmias. The theoretical background for the hypothesis is presented, empirical support for the hypothesis is reviewed, and implications for empirical research are discussed.