Abstract
The population incidence of sudden cardiac arrest (SCA) and sudden cardiac death have not changed appreciably during the decades of improvement in general outcomes from cardiovascular diseases, but the age, clinical circumstances, and pathophysiologic mechanisms have. The epidemiology and pathophysiology of SCA are linked, in that mechanisms of SCA can be modeled based on substrate and expression characteristics. The goal for the future is to expand pathophysiologic and epidemiologic interactions to achieve strong individual risk prediction, to complement the limits of application of population risk data to individuals.