Two myocardial processes are initiated by acute myocardial infarction: hypertrophy of residual myocardium and a change in left ventricular chamber dimension. The sequence of these events appears to be critically dependent on the size of the infarct and its distensibility, on the load placed on the myocardium, on the metabolic state of adjacent and remote myocardium, and on the degree of activation of tissue hormone systems. Hypertrophy may occur transversely (concentric) or longitudinally (eccentric). The chamber may enlarge because of cell lengthening or slippage or because of infarct expansion. An increase in radius of curvature intensifies wall stress and metabolic demands, whereas increased wall thickness moderates stress. In a canine experimental model of acute regional myocardial necrosis, hypertrophy and dilatation appear to have a different time course, and both may be attenuated by pharmacologic intervention with either an angiotensin‐converting enzyme (ACE) inhibitor or a nitrate. The relative contributions of load reduction, hormone inhibition, and the metabolic effect of pharmacologic intervention need further study. Targeting therapy to the prevention of detrimental ventricular remodeling may be a rational approach but one that needs clinical confirmation.
- angiotensin‐conveiting enzyme inhibitors
- myocardial infarction