Myocardial Infarction, Experimental Cardiac Necroses, and Potassium

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MYOCARDIAL INFARCTION, EXPERIMENTAL CARDIAC NECROSES, AND POTASSIUM PLINIO PRIORESCHI* I. Myocardial Infarction It has been said that the development of a scientific problem passes through four stages: (i) formulation; (2) oversimplification; (3) anarchy; and (4) solution [1]. The problem of human myocardial infarction passed through stage 2 when everybody was happy with the explanation that the syndrome was produced by a sudden occlusion ofa branch ofa coronary artery with subsequent acute ischemia and necrosis ofthe area supplied by the occluded vessel. A little uncertainty persisted on the mechanism ofthe sudden occlusion (although thrombosis was thought to be responsible in most cases), but the general explanation was there and everybody was confident that the details would be worked out later. In the meantime the anticoagulants were extensively used because they were thought to prevent the thrombosis . Stage 3 started a few years ago. It is difficult in retrospect to pinpoint exactly when it started, but at a certain moment some disturbing evidence began to accumulate and the simplistic explanation became obviously inadequate . The almost invariable association ofcoronary atherosclerosis and acute myocardial infarction is not questioned. Troubles begin when we assume that a thrombotic occlusion developing in the damaged vessel is ultimately responsible for the necrosis. In the first place it has been emphasized [2, 3] that very often the occlusion can be found in coronarles that were already so narrowed by the atherosclerotic process that "the observer frequently cannot help wondering what difference the minimal added insult might have made." * Department ofPharmacology, Queen's University, Kingston, Ontario, Canada. This work was supported by the Ontario Heart Foundation and the Medical Research Council ofCanada. 369 In the second place the low incidence ofcoronary thromboses in carefully examined infarcted hearts induced several authors to suggest that the thrombosis could be the consequence and not the cause of the infarct. Spain and Bradess [4], in a study of568 cases, found thrombotic occlusionin 16 per cent ofthehearts ofpatients who survived less than one hour after the infarction, 37 per cent in those who survived 1-24 hours, and 54 per cent in those who survived one or more days. They suggested that "thrombosis occurs as a secondary manifestation" ofthe infarction. Branwood and Montgomery [5] found thrombotic occlusion in 13 out of61 hearts with recent infarcts. They concluded that "the thrombosis found at post-mortem in coronary arteries is sometimes not the cause but the terminal event in an established recent infarct." Ehrlich and Yuuji Shinohara [6] in 38 hearts with recent infarcts found arterial thrombosis in 50 per cent, but only in 26 per cent did the thrombosis totally occlude the lumen. They concluded: "it may be necessary to reassess traditional concepts ofthe significance of recent thrombosis in the coronary arteries of hearts with recent infarcts. The term 'infarct' . . . may be in erroneous application to many lesions of the myocardium which possibly have resulted from as yet obscure mechanisms." These observations shake the very foundations of the classic pathogenetic theory ofmyocardial infarction. Problems related to the pathogenesis and therapy ofangina pectoris are also disturbing. Although there seems to be no doubt that this syndrome results from ischemia of the myocardium [7] some experiments have shown that the resting coronary blood flow per unit weight of heart muscle is normal in patients with angina and that in such patients, during exercise, the coronary flow increases as much as it does in the normal person [8-10]. In addition, although there seems to be no doubt that coronary vasodilators are effective in the treatment of coronary insufficiency , some experiments have shown that nitroglycerine, beside increasing oxygen consumption of the myocardium [11], does not increase coronary blood flow in patients with angina [12]; nor does erythrol tetranitrate [13]. In fact some authors have concluded that nitroglycerine and other coronary dilators are of no value at all in the relief of anginal pain or that they are not better than placebos [14-17]. On the other hand it has been pointed out that adenosine triphosphate (ATP) and Hydralazine increase coronary flow but are considered ineffective or even harm370 Plinio Prioreschi · Myocardial Infarction Perspectives in Biology and Medicine · Spring 19 ful in the treatment of angina pectoris [18-20]. Rowe...

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