Energy requirements of contraction and relaxation: implications for inotropic stimulation of the failing heart.

It is likely that the myocardium in the patient with congestive heart failure is unable to provide enough chemical energy to meet its mechanical requirements. If this interpretation is correct, inotropic stimulation, by increasing energy utilization, could contribute to the progressive myocardial cell death that characterizes end-stage cardiac hypertrophy. This deterioration could be delayed by the depressed myocardial contractility in the chronically overloaded heart, which reduces myocardial energy utilization, and delayed by changes in the expression of myosin isoforms that improve cardiac efficiency. An important goal of therapy in congestive heart failure, therefore, may be to reduce energy expenditure by unloading the failing heart and, in some cases, by administration of negative inotropic drugs.