Strenuous exercise/ultraвЂђendurance athletesДў6% (cTnT), 9% (cTnI) 23% (cTnT), 32% (cTnI) Global wall stretch, hypoxaemia, systemic hypoperfusion, coronary malperfusion Global wall stretch, degradation of contractile protein and cellular injury due to oxidative stress and neurohumoral factorsДҐ2% (cTnT в©ѕ0.02вЂ…ng/ml) вЂ“55% (cTnT в©ѕ0.1вЂ…ng/ml) Several possible reasons including coronary and nonвЂђcoronary cardiac origin prolonged renal elimination nonвЂђdialysable, intact cTnT differences to cTnI may be related to higher affinity to dialysis membrane, unstable molecule (fragments), smaller protein Variable, depending on cutвЂђoff 99 th centile/10% CV/ROC: 82%/53%/20% for cTnT and 6%/1%/0.4% for cTnI Variable, depending on cutвЂђoff 32% at cTnT >0.1вЂ…ng/ml вЂ“ 50% at cTnT >0.01вЂ…ng/ml Myocardial infarction, incomplete cardioprotection, reperfusion injury, direct surgical trauma Side branch occlusion, coronary dissection, bulky devices causing transient ischaemia and microembolisms Thrombotic occlusion of coronary artery (STEMI), microembolisation (NSTEMI) This article attempts to highlight the differential diagnosis of elevated cTn according to the various aetiologies of myocyte damage (table 1 вЂ‹ 1 ).ДЄlpert JS. But regardless of what the release mechanism into the blood from cardiac myocytes is, elevated cTnT and cTnI almost always imply a poor prognosis. 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. An elevation of cTn indicates the presence of, but not the underlying reason for, myocardial injury.

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. 1 Since then, cTnT and cTnI have replaced creatine kinaseвЂђMB (CKвЂђMB) as the preferred biochemical markers for the diagnosis of MI. 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.

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