Biochemical studies of energy production in the failing human heart.

Abstract

The defective myocardial performance responsible for the syndrome of congestive heart failure has been considered for many years to involve a biochemical abnormality. However, identification of this abnormality remains to be achieved. Muscle cell function is basically a process by which chemical energy is transformed into the mechanical work of myofibrillar shortening and force development. The presence of a biochemical abnormality in the failing cardiac muscle must therefore be sought either in the mechanism of energy production or in the mechanism of energy utilization by the contractile system. The present report is a study of energy production in the failing human heart. Considerable evidence has accumulated to indicate that myocardial extraction of oxygen and of oxidizable substrates is not diminished in patients with congestive heart failure (1-3). These studies have not, however, provided evidence that the final supply of chemical energy to the contractile apparatus is normal. ATP, the immediate source of chemical energy utilized by muscle (4), is formed within the mitochondrion during the oxidation of substrates by the process of oxidative phosphorylation. The completeness with which the process of phosphorylation is coupled to that of oxidation determines whether or not the energy liberated in the oxidation of substrates becomes available for useful mechanical work by the contractile apparatus. A number of toxic agents have been shown to be capable of uncoupling electron transport and phosphorylation, both in vitro (5)

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@article{Chidsey1966BiochemicalSO, title={Biochemical studies of energy production in the failing human heart.}, author={Charles A. Chidsey and Eugene C. Weinbach and Peter E. Pool and Andrew G. Morrow}, journal={The Journal of clinical investigation}, year={1966}, volume={45 1}, pages={40-50} }