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Interview With Dr. Quintiliano H. de Mesquita, Who Developed the Myogenic Theory of Myocardial Infarction
Q.: Professor Mesquita, what led you to the Myogenic Theory and the cardiotonics as anti-infarction drugs? A. : The Myogenic Theory of Myocardial Infarction was evolved through the traditional induction method, having its starting point in the inefficiency of the anticoagulants in the prevention and treatment of infarction. It has been strengthened by the successive reports of clinical conditions which cause infarction and do not conform to Herrick’s Thrombogenic Theory. It has also been propelled by the anatomo-pathological findings of the dissident group that indicate coronary thrombosis as a consequence and not as cause of acute myocardial infarction and most of all by the ever increasing literature on angiographically normal coronaries or pervious aorto-coronary anastomosis, coinciding with acute myocardial infarction. In clinical practice, the findings of angiographically normal coronaries or else stenotic, but pervious in direct correspondence with the infarcted myocardial area, only increases the misgivings as regards Herrick’s original concept. Besides, the MI observed in the perioperative period of aorto-coronary anastomosis, or else in a prolonged period, has been very properly called paradoxical myocardial necrosis because it happens in areas of marked revascularization and showing pervious anastomosis. The reciprocal is also true; the absence of infarction is noticed in myocardial sites dependent on an artery with a total atherosclerotic obstruction. This fact represents the late condition of natural evolution of the atherosclerotic coronariopathy with the installation of the progressive segmentary myocardial disease, frequently reported very much earlier before the process of a clinical infarctioning picture. According to the myogenic theory, there is no difference between the natural history of a chronic coronariopathy which winds up in an infarction or cardiac insufficiency; the variable lies in the direction only in the extension of the failing area which is limited to only one myocardial segment in the first case, being generalized in the other case. Q. : Professor Mesquita, why the cardiologists in general have afraid to use cardiotonics in MI treatment? A. : Experimental pharmacological studies have been responsible for the absolute contraindication of cardiotonics for acute myocardial infarction, as a result of their possible damaging action, with the increase of contractility and of oxygen consumption under conditions of a smaller oxygen supply. Spreading such concepts generated a ban against cardiotonics on the administration in the acute myocardial infarction. Nevertheless, in clinical practice the use of cardiotonics show absence of complications and a low mortality rate. These features oppose each other, but they are significant and sound, because the therapeutic results have consecrated them and should awaken the researchers to them. A better placement of the cardiotonics has been lately reported as concerns experimental infarction and chronic coronariopathy, by means of critical studies where the cardiotonics have a beneficial action with their effect characterized by an increase in contractility both in the ischemic and the non-ischemic segments, without a higher oxygen consumption owing to the participation of other counterbalancing mechanisms. Thus, the taboo concerning the use of cardiotonics in acute infarction of the myocardium is showed merely as a prejudice which does not correspond to facts. More information at: Myogenic Theory of Myocardial Infarction
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