This investigation primarily deals with a systematic study and definition of the performance and efficiency characteristics of the stable hypertrophied myocardium in vivo, it metabolic aspects and interaction with the rest of the circulation, and the transition between stable hypertrophy and failure. Models of stable left ventricular hypertrophy have been developed in dogs, rabbits, and rats, to study the various above-mentioned aspects as they pertain to the selectively hypertrophied left ventricular chamber. These studies indicate that the stable hypertrophied myocardium performs similarly to the normal myocardium in terms of its physiological and biochemical characteristics. However, its coronary blood flow per unit myocardial mass is decreased, and the oxygen extraction on its part is increased. When stressed, it derives its increased oxygen demand by primarily increasing its coronary blood flow. The volume-overloaded, non-failing left ventricle appears to have a somewhat decreased functional reserve than the pressure-overloaded left ventricle. Although total myocardial blood flow is decreased per unit mass in stable hypertrophy, its distribution through various areas of the myocardium is similar to that of the normal heart. Cardiac beta-adrenergic mechanisms do not appear to play an important role in the development of hypertrophy. The continuing thrust of the investigation in the coming grant period is aimed at futher definition of the physiological characteristics of the stable hypertrophied left ventricle in the conscious intact animal with and without the physiologic stress of exercise. Alterations in regional myocardial blood flow, performance characteristics, and metabolic functions induced by cardiopulmonary bypass are being investigated, as well as the comparative protective effect of various methods of myocardial preservation during surgery. These studies are aimed at better understanding of the physiology and biochemical alterations in stable hypertrophy in order to better define the optimal timing and the role of corrective surgery for lesions which are accompanied by a rather long stage of stable hypertrophy, and to outline the best methods of myocardial preservation during such corrective procedures.