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More TACTICS for an Early Invasive Strategy

Martin J. Quinn, MD,PhD; David J. Moliterno, MD

JAMA. 2001;286:2461-2462.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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 inhibitors^4-6 as well as low-molecular-weight heparins.⁷

In this issue of THE JOURNAL, Morrow and colleagues⁸ present the results of their prespecified subanalysis of cTnI or cTnT levels obtained at the time of randomization in the Treat Angina . . . [Full Text of this Article]

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

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