The diagnosis of myocardial infarction has conventionally relied on the presence of chest pain or typical ST segment and T wave abnormalities on the 12 lead electrocardiogram (ECG) and a rise in the serum concentrations of cardiac muscle enzymes. Whereas most patients with ST segment elevation also invariably have high serum cardiac muscle enzyme values, indicating myocardial damage, a considerable proportion of patients with less specific ST segment changes may not have increased cardiac muscle enzymes, and in the past have been diagnosed as having either stable angina or non-cardiac chest pain. Cardiac troponin T (cTnT) and troponin I (cTnI) are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin. The cardiac forms of these regulatory proteins are coded by specific genes and theoretically have the potential of being unique to the myocardium. Indeed, cTnI has not been identified outside the myocardium.¹ Cardiac troponin T is expressed to a small extent in skeletal muscle; however, the current cTnT assay does not identify skeletal troponins.²

“Cardiac troponin T and troponin I are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin”

The measurement of serum cTnI and cTnT is superior in terms of sensitivity and specificity to cardiac muscle enzyme measurements in the identification of cardiac muscle damage.³ Raised cardiac troponin concentrations are now accepted as the standard biochemical marker for the diagnosis …