Cardiac troponin: friend of the cardiac physician, foe to the cardiac patient?

Troponin, an important regulatory protein of the thin filament (actin) of striated muscle, is a complex of 3 subunits: C, T, and I. Troponin T and I isoforms from the heart are structurally different from the corresponding forms found in skeletal muscle. Because of this distribution, the measurement of cardiac troponin T and I isoforms is superior to other serum biomarkers of cardiac disease such as creatine kinase (CK)-MB and myoglobin because these proteins are released in patients with skeletal muscle disease or injury, as well as the heart. Recently, the European Society of Cardiology (ESC) and American College of Cardiology (ACC) have redefined acute myocardial infarction (AMI) to be predicated on the finding of increased concentrations of cardiac troponin in the clinical context of myocardial ischemia.1 These and other clinical practice guidelines2–4 have led to a steady decline in the use of CK-MB and myoglobin as diagnostic laboratory tests for MI. Because there is a high tissue content of troponin within myocytes, measurement of troponin T and I has become important for risk stratification of patients for short-term adverse events (cardiac death, MI, readmission for recurrent ischemia, and need for revascularization).