Cardiac hypertrophy is commonly present in patients with chronic coronary artery disease, and may play an important role in determining the severity of the disease. Several studies have indicated that cardiac hypertrophy reduces the cardiac reserve, possibly rendering the myocardium more susceptible to ischemic injury. The hypothesis of the proposed study is that the reduced cardiac reserve in cardiac hypertrophy is due to morphologic changes in the vascular bed which compromise the vascular capacity relative to the increased mass. Furthermore, hypertrophy due to different hemodynamic causes such as high or low aortic end diastolic pressure overload, or volume overload, may produce different morphologic changes in the vascular system of hypertrophied hearts. Specific aims of the study are 1) to determine the extent of functional compromise of the cardiac flow reserve in models of hypertrophy associated with high and low aortic end-diastolic pressure (afterload) and volume overload, 2) to evaluate the additional effect of chronic subtotal coronary artery stenosis in these models, and 3) to quantitatively evaluate structural changes in the coronary vascular system in these models. Cardiac hypertrophy will be induced in dogs with perinephritic hypertension (high end-diastolic aortic pressure), progressive aortic stenosis (normal end-diastolic aortic pressure), and complete heart block (volume overload). Subtotal coronary artery stenosis will be produced in the left coronary arteries in some dogs to evaluate the effect of hypertrophy on the lesions of chronic coronary artery stenosis. Vascular morphology will be evaluated in perfusion fixed hearts using morphometric and stereologic techniques at the light and electron microscopic level to compare changes in the large epicardial vessles, intramyocardial small arteries and arterioles, and capillaries. Both functional and morphologic evaluation will be done in the same animal and should provide information relative to the possible increased susceptibility of hypertrophied myocardium due to several different causes to ischemic myocardial damage.