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Editorial
November 21, 2001

Troponins in Acute Coronary SyndromesMore TACTICS for an Early Invasive Strategy

Author Affiliations

Author Affiliations: Department of Cardiovascular Medicine and C5 (Cleveland Clinic Cardiovascular Coordinating Center), The Cleveland Clinic Foundation, Cleveland, Ohio.

JAMA. 2001;286(19):2461-2462. doi:10.1001/jama.286.19.2461

Cardiac isoforms of troponin I (cTnI) and T (cTnT) are highly sensitive and specific markers of myocardial injury. Elevations of either of these proteins in the setting of an acute coronary syndrome (ACS) identify patients with a several-fold increased risk of death in subsequent weeks.1 The prognostic importance of these markers likely stems from their ability to detect microscopic amounts of myocardial necrosis that result from a severe epicardial stenosis or distal embolization of friable atherothrombotic debris overlying the unstable coronary plaque.2 As such, troponin-positive patients often have complex coronary lesion morphology with intracoronary thrombus,3 and understandably derive particular benefit from platelet glycoprotein (Gp) IIb/IIIa inhibitors46 as well as low-molecular-weight heparins.7

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