Myocardial Oxygen Consumption in Patients with Idiopathic Dilated Cardiomyopathy: Effects of Vasodilating and Inotropic Agents

Abstract

Idiopathic dilated cardiomyopathy is a myocardial disease of unknown origin. Several causal factors are discussed. One hypothesis involves energy depriviation in the failing myocardium, and a number of arguments exist for such an energy-starving situation [22, 23]. These include the following: (a) In some studies investigating the energy state of hypertrophied and failing myocardium, a reduced content of high energy phosphates was reported [5, 39]. However, these findings were not confirmed by others [33, 34]. (b) In the failing human myocardium, a reduction in myofibrillar ATPase activity [1, 25, 30] and a shift of the isoenzyme pattern of lactate dehydrogenase [36] has been observed. Both changes may be interpreted in terms of adaptation to energy depletion; reduced myofibrillar ATPase activity is associated with more economical tension development, as shown in mammalian myocardium [2, 15, 16] and in human myocardium [14], and the shifts in the isoforms of the lactate dehydrogenase are indicators of anaerobic glycolysis [36]. (c) A reduction in capillary density may lead to increased diffusion distances [4]. (d) A reduced ratio of mitochondria and myofibrillar volumes indicates a mismatch between the number of ATP synthesizing sites and the number of ATP consuming sites [4, 31]. (e) Reduced coronary reserve has been observed in patients with dilated cardiomyopathy using the dipyridamole test [28, 29, 32].