Dynamic left ventricular outflow tract obstruction induced by pericardial tamponade during acute anterior myocardial infarction

Abstract

evidence that diffuse coronary vasoconstriction can occur in the early minutes of acute myocardial infarction. In animal models, severe coronary stenoses with associated endothelial injury commonly cause cyclic reductions in coronary blood flow that are related to platelet aggregation and leukocyte and red blood cell accumulation at the stenotic site.3 Local platelet activation at these sites may cause vasoconstriction of large epicardial coronary arteries, which can be relieved with specific inhibitors of thromboxane A2 and serotonin but not with nitroglycerin or diltiazem.‘j It is attractive to speculate that platelet activation caused a similar sequence of events in our patient. Although the observations in our patient suggest that dynamic coronary vasoconstriction may play an important role in the early pathogenesis of acute infarction, several limitations leave some important questions unanswered. It would have been interesting to have observed the effects of intracoronary nitroglycerin on arterial patency immediately after demonstrating the right coronary occlusion. However, the hemodynamic collapse exhibited by the patient mandated definitive therapeutic measures. Furthermore, it would have been interesting to have obtained simultaneous aortic and coronary sinus samples for measurements of transcardiac levels of potential platelet mediators such as serotonin. Again, the urgency of the situation prohibited appropriate investigative preparations. Clinical studies with specific inhibitors of thromboxane AZ, serotonin, and other possible mediators of coronary tone may offer further insights into the pathophysiology of the early moments of acute myocardial infarction, and may provide more effective preventive and therapeutic measures for the treatment of acute ischemic syndromes.