The performance of the hypertrophied and failing myocardium has been analyzed in the isolated heart muscle from experimental animals, intact ventricle of experimental animals, and now the intact ventricle of conscious man. It is apparent there are characteristic intrinsic depressions of contractility in the hypertrophied heart in which circulatory compensation is maintained. These depressions are found in the overtly failing heart to a greater degree. The basic abnormality appears to be a decrease in the intensity of the active state of the contractile elements within the myocardial fibers. This decrease in the intensity of active state is not associated with any changes in the duration of active state and does not appear to be associated with any changes in the resting tension characteristics of the muscle. The basic decrease in intensity of active state in hypertrophied and failing heart muscle finds expression in the decrease in the maximum intrinsic velocity of shortening (Vmax) and in decreased rate of ventricular pressure rise (dP/dt). This basic decrease in intrinsic contractile element performance is compensated for by a number of mechanisms in order to maintain circulatory performance despite decreased function of cardiac muscle. When the ventricle is chronically stressed by an abnormal load, there is a rapid response to increase the total muscle mass. This increase in muscle mass operating in conjunction with the Frank-Starling mechanism, and an increased sympathetic stimulation, maintains overall circulatory compensation despite depression of the intrinsic contractile state of each unit of myocardium. As the intrinsic contractile state of each unit of myocardium becomes more severely depressed, there is a more extensive fall in the maximum velocity of shortening, a further decrease in maximal isometric force, a decrease in the rate of force development, and also the sympathetic nerve support of cardiac contractility becomes impaired. At some point, circulatory compensation can no longer be maintained despite maximal utilization of the compensatory mechanisms provided by the Frank-Starling mechanism and the increases in muscle mass; overt congestive heart failure then ensues with a fall in cardiac output.