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There is increasing awareness of the limitations of standard biochemical markers of cardiac damage in patients with acute coronary syndromes. A desire to improve sensitivity and specificity has led to the search for markers uniquely expressed by the myocardium. The cardiac troponins T and I (cTnT and cTnI) have been found to have excellent sensitivity and specificity and are superior to creatine kinase-MB (CK-MB) as indicators of myocardial necrosis.1 Using cTnT or cTnI as a diagnostic marker, the positivity rate in studies has varied from 20–48%, with death and acute myocardial infarction (MI) varying from 11–30% in 28 months follow up.2-4 These variations are largely caused by differences in risk among the populations studied and differing lengths of follow up.
Troponins have proven useful for the diagnosis and subsequent risk stratification of patients presenting with acute chest pain.5 6 A raised troponin concentration may also identify those who are most likely to benefit from additional therapeutic measures.7 Nevertheless, is cTnT superior to cTnI?
Biochemistry and release kinetics
The troponin complex is situated on the thin filament of the striated muscle contractile apparatus and consists of troponin T (39 kD), troponin I (26 kD), and troponin C (18 kD), each coded by a separate gene.8 Specific cardiac and skeletal muscle isoforms are expressed in cardiac and skeletal striated muscle in adults. Troponins are mainly bound to the myofibrils, although 6–8% of cTnT and 2.8–4.1% of cTnI is cytosolic.9 This affects release kinetics. There is rapid early release of cytosolic cTnT after ischaemic injury, followed by more prolonged release of myofibrillar troponin, resulting in a biphasic release pattern. As cTnI has a smaller cytosolic pool, release is likely to be monophasic. Concentrations of both begin to rise in the 4–8 hours following injury and peak at 12–24 hours.7-9 cTnT may remain raised …
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