Cardiac hypertrophy is often characterized by abnormalities in myocardial perfusion, including decreased coronary reserve, increased minimal coronary vascular resistance, underperfusion of the subendomyocardium during conditions of high oxygen demand and increased risk of infarction in the presence of coronary occlusion. Two major anatomic variables may cause these perfusion deficits. First, the coronary resistance vessels may not grow in proportion to the magnitude of the cardiac enlargement. Second, the luminal diameter of resistance vessels may become reduced as a consequence of medial hypertrophy, hyperplasia or fibrosis. A luminal narrowing coupled with a lack or inadequate numeric proliferation of resistance vessels can markedly limit maximal myocardial perfusion.
However, not all models of cardiac hypertrophy are characterized by perfusion abnormalities. A substantial growth of arterioles and capillaries has been documented in exercise- and thyroxine-induced left ventricular hypertrophy. Moreover, at least in some models, angiogenesis occurs when the duration of the ventricular hypertrophy is sufficient. The hypothesis that coronary angiogenesis is stimulated by increased blood flow or prolongation of diastole appears to have support from a number of experimental studies. However, the cascade of events underlying angiogenesis and the numerous variables that characterize the various models of hypertrophy are complex and require elucidation.
