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  • Chest discomfort, usually described as “pressure,” “dull,” “squeezing,” or “aching.”
  • Characteristic electrocardiographic changes.
  • Elevated biomarkers, such as troponin.
  • Imaging may show new regional wall motion abnormality with preserved wall thickness.
  • The elderly, women, and diabetics may have atypical presentation.

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Acute myocardial infarction (MI) is a clinical syndrome that results from occlusion of a coronary artery, with resultant death of cardiac myocytes in the region supplied by that artery. Depending on the distribution of the affected coronary artery, acute MI can produce a wide range of clinical sequelae, varying from a small, clinically silent region of necrosis to a large overwhelming area of infarcted tissue resulting in cardiogenic shock and death. About 1.2 million people experience MI in the United States each year; every minute, one American will die of coronary artery disease.

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The risk of having an acute MI increases with age, male gender, smoking, dyslipidemia, diabetes, hypertension, abdominal obesity, a lack of physical activity, low daily fruit and vegetable consumption, alcohol overconsumption, and psychosocial index. As much as 90% of the risk of acute MI has been attributed to the modifiable risk factors. The diagnostic criteria for acute MI are listed in Table 5–1.

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Table Graphic Jump Location
Table 5–1. ESC/ACC Definition of Myocardial Infarction. 
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A prolonged imbalance between myocardial oxygen supply and demand leads to the death of myocardial tissue. Coronary atherosclerosis is an essential part of the process in most patients. Ischemic heart disease seems to progress through stages of fatty-streak deposition in coronary arteries to development of fibro-fatty plaque, which then increases in size until it causes luminal obstruction, leading to exertional angina (see Chapter 3). However, at any stage in this process, the atherosclerotic lesion may erode, ulcerate, fissure, or rupture, thereby exposing subendothelial vessel wall substances to the circulating blood. Procoagulant factors (such as tissue factor) reside within the plaque itself and, in the absence of counterbalancing antithrombotic factors (eg, heparin, tissue-factor-inhibitor) and fibrinolytic activities (tissue plasminogen activator ...

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