Abstract

It was the purpose of this study to determine what factors are responsible for the development of chronic congestive failure in chronic coronary disease and myocardial fibrosis. The clinical and post-mortem records of 100 unselected cases were studied. The overwhelming majority were in, or gave a history of, congestive failure. Varying degrees of vascular and myocardial damage were common to the entire series, but the vast majority of those in congestive failure had definite and in most instances advanced cardiac hypertrophy. There were but three exceptions to this rule. The group not in failure had nonhypertrophied or, in a few cases, slightly hypertrophied hearts. The characteristic feature of the chronic congestive phase of chronic coronary artery disease is the presence of cardiac hypertrophy. The genesis of cardiac hypertrophy in relation to muscle damage is discussed. The view is accepted that increased initial fiber tension rather than increased work is the stimulus for generalized cardiac hypertrophy. Contraction with increased initial tension compensates for inadequate contractility. Myocardial disease by diminishing contractile power calls forth increased initial fiber tension and may, according to the above theory, be the cause of generalized cardiac hypertrophy. Application of this concept to the question of cardiac hypertrophy in coronary artery disease is not sufficiently supported, however, by clinical experience. Since the data in the literature are contradictory on this point, it is necessary to study further the causal relationship of chronic coronary artery disease to generalized cardiac hypertrophy by following patients whose blood pressure figures and heart size are known before and after the onset of the disease. Our present belief is that in the majority of cases generalized and advanced cardiac hypertrophy is caused by hypertension, present or antecedent, and not by vascular and myocardial damage. Diminished blood supply and severe muscle damage produce loss of contractility and may cause failure without leading to fiber hypertrophy. The striking predominance of hypertrophied hearts of the group in failure, however, indicates that it is work under long standing increased fiber tension irrespective of the cause, and the eventual loss of contractile power of the hypertrophied fiber, that leads to chronic congestive failure. Congestive failure in chornic arteriosclerotic heart disease is—like that of other types of heart disease—overwhelmingly the failure of the hypertrophied heart. (Table II.)

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