Coronary artery disease is the leading cause of death in North America and Europe. Each year in the United States, approximately one million people are admitted to hospitals with the diagnosis of acute myocardial infarction (MI), and another 200,000–300,000 die before reaching the hospital. Overall mortality is about 40%.
Recent advances in the understanding of the pathogenesis of MI indicate that the inciting event is most often coronary artery occlusion due to atherosclerotic plaque rupture followed by thrombosis. The majority of “culprit” lesions occlude less than 50% of the arterial lumen prior to the event. The thin, unstable fibrous cap overlying a lipid-laden core fissures at a weak point, exposing blood in the lumen to the plaque’s underlying thrombogenic contents. Platelet adhesion immediately occurs, followed by platelet aggregation and fibrin crosslinking. Once the thrombus is formed, blood flow in the artery stops and the myocardium in that arterial territory begins to die. The amount of that territory which can be rescued from necrosis is directly related to the rapidity with which reperfusion is established.
KeywordsMyocardial Infarction Arterial Territory Total Creatine Kinase Atherosclerotic Plaque Rupture Left Ventricular Regional Wall
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