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M ajor advances in cardiovascular therapeutics generally have resulted from elucidation of pathogenetic mechanisms. For example, delineation of the role of thrombosis as the proximate cause of acute transmural myocardial infarction was seminal in the evolution of coronary thrombolysis as primary treatment.1 Similarly, recognition of the importance of afterload as a determinant of ventricular performance led ultimately to the extensive use of vasodilators in modern treatment of congestive heart failure.2 An association between impairment in left ventricular pump function and the extent of antecedent myocardial infarction was delineated soon after the dynamic nature of infarction and the dependence of its evolution on an imbalance between myocardial oxygen requirements and myocardial oxygen supply had been established.3 Ventricular tachycardia, which may occur more frequently when pump dysfunction is present, can precipitate derangements leading to cardiac death including hemodynamic impairment, augmentation of myocardial oxygen requirements, and impaired coronary perfusion secondary to hypotension and elevation of left ventricular diastolic pressure. Ventricular tachycardia may be presaged by distinct electrophysiological alterations such as late potentials.4 However, these important associations do not fully clarify the basis for the strength of the association between impairment of ventricular function and sudden cardiac death. Several factors may be involved, including heightened sympathetic neural activation and extensive regional conduction delay and block predisposing to reentrant ventricular tachycardias, as well as numerous other phenomena. In fact, multiple etiologies may apply even in a single instance, including alterations of membrane ion channels, fluctuations in global and regional autonomic function, and G protein-mediated effects among others.

Arrhythmogenesis and ventricular dysfunction after myocardial infarction. Is anomalous cellular coupling the elusive link?