The role of ET-1 in acute myocardial infarction is both beneficial and detrimental. ET-1 seems to play an important role in causation of myocardial infarction, in postinfarct scar formation, in left ventricular remodeling, and in prognosis of myocardial infarction. ET-1 is a causative factor in stenosis of atherosclerotic coronary arteries, contributing to the pathophysiology of the acute myocardial infarction. In an angiographic human study,12intracoronary delivery of an ET-A receptor blocker resulted in a marked 21% dilatation of stenotic coronary arteries at 60 min, compared to 7% dilatation of angiographically smooth epicardial coronary arteries. After myocardial infarction, the physiologic role of ET-1 is in stabilization of scarring and is likely due to a combination of its inflammatory, proliferative, and fibrotic effects, the characteristics necessary for healing of myocardial infarction. ET-1 is a chemotactic factor for macrophages, and it stimulates neutrophil adhesions. After a myocardial infarction, ET-1 levels in the infracted area are many-fold higher than those in healthy myocardium, which suggests the favorable effects of ET-1 in scar healing and stabilization. ET-1 promotes myocardial fibrosis by enhancing cardiac fibroblast proliferation, adhesion molecule expression, and extracellular matrix deposition, and therefore, plays a role in postinfarct remodeling after acute myocardial infarction. At the same time, elevated plasma levels of ET-1 early after myocardial infarction may cause vasoconstriction of coronary and systemic arteries, further increasing the afterload and myocardial ischemia causing scar expansion. These deleterious vascular effects seems to predominate, as it has been noted in studies using animal ischemia-reperfusion models that the ET-receptor blockade has either favorable effects on myocardial infarction size, incidence of arrhythmia, and myocardial function, or has no effect.13–18 In humans, a significant correlation has been observed between the transcardiac extraction of ET-1 in the acute phase of myocardial infarction and the left ventricular ejection fraction and left ventricular end-diastolic volume index after 1 month, indicating a possible strong role of ET-1 in evolution of infarct and postinfarct ventricular remodeling.19Similarly, in a human study,20 plasma levels of ET-1 measured after myocardial infarction were found to be a strong predictor of 1-year survival independent of clinical and biochemical variables previously associated with a poor prognosis.