Ischemic heart disease is the leading cause of morbidity and mortality in western countries. According to the data from the American Heart Association, coronary artery disease causes about one of every six deaths in the United States. Each year, an estimated 785,000 Americans will have a new coronary attack, about 470,000 will have a recurrent attack, and an additional 195,000 will have a silent fi rst myocardial infarction. Thus, approximately every 25 s, an American will have a coronary event; approximately every minute, someone will die of one . The pathophysiological process underlying most ischemic heart disease is atherosclerosis of coronary arteries. Atheroma formation, with or without thrombus, can lead to stenosis in coronary arteries, resulting in a reduction in coronary blood flow and oxygen supply. A sudden and significant reduction in coronary blood flow, most commonly from rupture of plaques in the coronary arteries, can cause myocardial infarction. A large number of cardiomyocytes die, and cardiac muscles in the infarcted area lose their striations. The death of cardiomyocytes invokes the recruitment of inflammatory cells at the infarct border, which remove the necrotic cell debris by phagocytosis . As a result, the infarct area becomes thin and non-contractile and may lead to infarct rupture, which accounts for 15�30 % of deaths in the fi rst week after infarction [3, 4].
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