Elevated Cardiac Troponin Measurements in Critically Ill Patients

Abstract
Cardiac troponin (cTn) I and T are regulatory proteins that control the calcium-mediated interaction of actin and myosin, producing myocardial contraction.1 Injury to myocardial cells results in cTn release into blood, which can be detected using commercially available immunoassays. The specificity and sensitivity of cTn for detecting myocardial necrosis is substantially superior to other biomarkers, and myocardial infarction was redefined in 2000 by a joint European Society of Cardiology/American College of Cardiology (ESC/ACC) Committee, based on the detection of elevated cTn measurements in the appropriate clinical setting.2