EDUCATION IN HEART

General cardiology

Differential diagnosis of elevated troponins

Susanne Korff, Hugo A Katus, Evangelos Giannitsis

Department of Medicine III, University of Heidelberg, Germany

Correspondence to:
Correspondence to:
Dr P D Evangelos Giannitsis
Abteilung Innere Medi-zin III, Medizinische Klinik, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany; evangelos.giannitsis@med.uni-heidelberg.de

Keywords: scute coronary syndrome; cardiac troponins; cardiac troponin I; cardiac troponin T

The first 150 words of the full text of this article appear below.

In the year 2000, the European Society of Cardiology and the American College of Cardiology Committee jointly redefined myocardial infarction (MI) by an elevation of cardiac troponin T (cTnT) or I (cTnI) in conjunction with clinical evidence of myocardial ischaemia.¹ Since then, cTnT and cTnI have replaced creatine kinase-MB (CK-MB) as the preferred biochemical markers for the diagnosis of MI. The decision for including cardiac troponins (cTn) in the diagnostic pathway was made because of the high sensitivity of cTn for detection of even small amounts of myocardial necrosis. An elevation of cTn indicates the presence of, but not the underlying reason for, myocardial injury. Hence, besides acute myocardial infarction (AMI), there is a myriad of potential diseases with troponin release, including acute pulmonary embolism, heart failure, myocarditis, and end stage renal disease. But regardless of what the release mechanism into the blood from cardiac myocytes is, elevated . . . [Full text of this article]

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