Metabolism of the Heart in Failure

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Abstract
Investigations of the 3 phases of cardiac metabolism (energy production, energy conservation and energy utilization) have shown marked differences in the underlying mechanisms of heart failure. Thus, in failure with prolonged overload of the myocardium as occurs with hypertension, valvular heart disease, and arteriosclerotic heart disease (group I), an abnormality of energy utilization seems most likely. In the diverse situations with heart failure considered under group II, there appears to be a defect in energy production or conservation. In anemia, myocardial failure results in insufficient transport of oxygen for substrate metabolism, while in hyperthyroidism uncoupling of oxidative phosphorylation may lead to failure of energy conservation. In beriberi heart disease, a deficiency of thiamine pyrophosphate (cocarboxylase) produces a breakdown of certain specific decarboxylation reactions that appear to interfere with normal myocardial energy production. In hemorrhagic shock and myocardial infarction, general or localized anoxia leads to defective energy production. Spontaneous failure occurring in the heart-lung preparation is in all likelihood the result of diminished catecholamine and cholinergic substances of the perfusion fluid. It is apparent from this review that no common denominator exists as a cause of heart failure. Rather at the base of the uniform dynamic manifestations of this condition are multifarious disturbances in energy production, conservation, and utilization.