Cardiac Troponins in Acute Coronary Syndromes

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 . . .