Cardiac Troponins in Acute Coronary Syndromes

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Abstract
Acute coronary syndromes have a common pathophysiologic mechanism. A coronary atherosclerotic plaque ruptures and a mural or occlusive thrombus forms, impairing or interrupting the perfusion of myocardial tissue.1 Consequently, the clinical spectrum in patients arriving at the hospital with ischemic chest pain at rest ranges from unstable angina, due to the partial occlusion of a coronary vessel, to acute myocardial infarction, due to complete occlusion. In the absence of specific electrocardiographic changes, such as the development of new Q waves, only serial measurements of serum levels of cardiac enzymes, usually creatine kinase and its myocardial MB isoenzyme, can differentiate unstable . . .