Coronary microvascular angiogenesis during cardiac enlargement is variable and dependent upon several factors including age, model, and duration of cardiac hypertrophy. We, and others, have documented coronary angiogenesis in several models of cardiac enlargement and in several species. Although growth of the coronary vasculature occurs during hypertension, it usually fails to compensate for the magnitude of hypertrophy. Substantial growth may occur, however, after a long period of time. In some other models of cardiac hypertrophy (excess thyroxine hormone, exercise training, and volume overload) capillary angiogenesis is greater and may occur more rapidly. An examination of a variety of models and interventions (e.g., increased myocardial perfusion, bradycardia) suggests that mechanical factors (stretch, shear stress and wall tension) associated with increases in (A) capillary perfusion, (B) diastolic interval, or (C) diastolic ventricular chamber filling may provide an initiating stimulus for capillary angiogenesis during cardiac enlargement.