Acute coronary insufficiency due to pulmonary embolism

Abstract

A study of forty-one consecutive fatal cases of pulmonary embolism confirmed by autopsy showed that acute coronary insufficiency is an important factor in determining the electrocardiographic and myocardial effects following embolism of the pulmonary artery. The electrocardiographic pattern of “acute cor pulmonale” (deep S 1 and Q 3, depressed RS-T in Lead I, elevated RS-T in Lead III and T 3 inversion) occurred in only a minority of cases. In the majority the electrocardiographic changes were those characteristic of acute coronary insufficiency, namely, RS-T depression and T wave inversion in one or more leads and often in all leads. Antecedent hypertensive or arteriosclerotic heart disease and cardiac hypertrophy were important predisposing factors of acute coronary insufficiency. The classical cor pulmonale pattern was seen more often in patients with previously normal hearts. When the electrocardiogram prior to the embolism was very abnormal, the electrocardiographic changes were usually those of coronary insufficiency or, less often, atypical in character. Furthermore, the presence of marked left axis deviation made the development of the cor pulmonale pattern less likely. Right ventricular dilatation was not regularly associated with either “cor pulmonale” or “coronary insufficiency” electrocardiogram. The pattern of coronary insufficiency was often noted in patients with marked dilatation of the chambers of the right side of the heart, a fact which suggests that coronary insufficiency and right ventricular strain may occur simultaneously following massive embolism of the pulmonary artery. Changes indicative of myocardial necrosis or infarction resulting from acute coronary insufficiency were found in ten cases or 24 per cent. In three of these cases there were gross changes in the myocardium and in seven cases histologic changes. Acute occlusion of a coronary artery was not seen in any of the hearts. The most frequent sites of necrosis were the subendocardial layer of the left ventricle and the papillary muscles. The anterior and posterior walls of the left ventricle were involved with equal frequency. The right ventricle was involved in only one case, emphasizing the greater deleterious effect of pulmonary embolism on the left ventricle. Acute myocardial changes were found in cases with electrocardiograms indicative of cor pulmonale as frequently as in cases with electrocardiographic signs of acute coronary insufficiency. Coronary insufficiency following embolism of the pulmonary artery is caused by diminished coronary blood flow and myocardial anoxia which result from systemic shock, right ventricular dilatation, anoxemia and possible reflex vasoconstriction. The pathologic physiology and relative importance of these factors are discussed.