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A number of 65 heart malformations, taken from intraoperatory biopsies at different degrees of congestive heart failure were histological, histoenzymological and electronmicroscopical analyzed. It was followed the pathogenesis of the lesions determined by the hemodynamic and hypoxic intracardiac disorders. These hadn't specificity and were disseminated in different evaluative degrees, being predominant in certain myocardial areas. Initially, cardiomyocytes hypertrophical changes appear, and also changes of the edematous matrix. Then, the nuclear lesions, the apoptosis processes and the hypoxic alterations increased to cytolysis. In succession, after the matrix edema was organized, immune lesions and myocardial sclerosis processes appeared. Out of the various lesions, we mention: the sarcoplasmatic fuchsinophilia and alcianophilia, the glycogenic depletion, the decrease of SDH, LDH reactions, the increase of the cytolitic enzymes, especially of the kathepsine B. Out of the ultrastructural changes, we mention: the mitochondrial, sarcotubular lesions and, the lysosomial activations, the interstitial organelles, including the natriuretic granules, synthesized in the ventricular myocytes, details regarding the matrix changes with tendency to fibrosclerosis.

In this paper, an attempt was made to describe the alterations of the myocardial energy metabolism following moderate stenoses of aorta or pulmonary artery. Biochemical investigations regarding the main high energy phosphates and a large series of dehydrogenases in the myocardium of the overloaded ventricles have revealed the following facts: (1) the myocardial CP-CPK system appears to be more labile than the myocardial AMP-ATP system in response to a ventricular overload; (2) the changes in the amounts of myocardial high energy phosphates seem to be more important in the right chronic cardiac overload than in the left one; (3) before the overloaded ventricle becomes insufficient, the myocardial dehydrogenase system elicits no alteration, suggesting that the oxidative phosphorylation is not affected; (4) there is a closer relationship between the coronary flow and pressure and the myocardial energy metabolism than that existing between this metabolism and the tension of the myocardial fibres following a persistent increase in the systemic arterial resistance.