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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 cTnT and cTnI almost always imply a poor prognosis. This article attempts to highlight the differential diagnosis of elevated cTn according to the various aetiologies of myocyte damage (table 1).
WHAT ARE CARDIAC TROPONINS?
The troponin complex consists of three subunits—troponin C, troponin I, and troponin T—and is located on the myofibrillar thin (actin) filament of striated (skeletal and cardiac) muscle (fig 1). The cardiac isoforms troponin T and I are only expressed in cardiac muscle. Hence, cardiac troponin T (cTnT) and I (cTnI) are more specific than creatine kinase (CK) values for myocardial injury and, because of their high sensitivity, they may even be elevated when CK-MB concentrations are not. The cTn complex regulates excitation–contraction coupling in the heart. Cardiac troponin C (cTnC), a calcium (Ca2+) binding 18-kD-protein, regulates the activation of the actin filaments. cTnI (∼23 kD) inhibits contraction in the absence of Ca …