Damage of the Heart Muscle Cell 95 



HEART FAILURE 



In congestive cardiac failure due to valvular disease with de- 

 creased cardiac output, the coronary blood flow and myocardial 

 oxygen usage are unchanged. Carbohydrate and fatty acid extrac- 

 tion are but slightly reduced and there is no alteration in oxi- 

 dative metabolism. There is, however, some evidence of a biochemi- 

 cal defect in the contractile mechanism itself. The molecular weight 

 of cardiac myosin for normal dogs is about 225,000, for dogs in 

 valvular cardiac failure about 750,000. Probably some abnormality 

 of myosin aggregation prevents the formation of an acto-myosin 

 with normal contraction properties (Olson et ah, 1956) . Acto-myo- 

 sin preparations from failing heart muscle of man show reduced 

 contractility (Kaks and Bing, 1958) . 



In thyrotoxicosis, with high-output cardiac failure, there is a 

 greatly increased total oxygen consumption, increased coronary 

 blood flow and augmented oxygen usage (Rowe et al., 1956) . But 

 the threshold for glucose extraction by the muscle cells is raised, the 

 extraction efficiency for pyruvate and lactate is reduced. Hence de- 

 pendence upon fatty acid catabolism for energy becomes more and 

 more imperative in hyperthyroidism. Myosin abnormality has 

 not been demonstrated. 



Myocardial anoxia is extremely severe in ventricular fibrilla- 

 tion. Cardiac output and coronary flow are greatly reduced and 

 metabolism of the heart muscle is much altered (Bing) . Glucose, 

 pyruvate, lactate and potassium loss from the muscle is considerable 

 and quite likely certain co-enzymes such as ATP are maintained 

 in their phosphorylated form only as long as active oxidation is 

 assured. When it fails the co-enzymes break down and the process 

 becomes irreversible. 



Response of the heart muscle to ischaemia obviously is not uni- 

 form. The classical response with lactic acid production in the 

 muscle by way of the usual glycolytic mechanism is obtained only 

 in its severest form, as with ventricular fibrillation. When ischaemia 

 is moderate the metabolic defect may be confined to the level of the 

 co-enzyme co-carboxylase. 



