The role of cardiac troponin in the recent redefinition of acute myocardial infarction.

Abstract

1. Alan HB Wu, PhD[⇑][1] 1. is at Hartford Hospital, Hartford CT 1. Address for correspondence: Alan HB Wu PhD, Department of Pathology and Laboratory Medicine, Hartford Hospital, 80 Seymour St, Hartford CT 06102. (860) 545-5221, (860) 545-3733 (fax). awu{at}harthosp.org 1. Describe the structure and function of the three troponin proteins. 2. Explain the release of cardiac troponins following an acute myocardial infarction. 3. Discuss the clinical utility of troponin T versus troponin I. 4. Describe the impact of troponin assays on the redefinition of acute myocardial infarction. 5. Explain the issues surrounding lower cutoff concentrations for troponin assays. Troponin is a complex of three proteins (troponins T, I, and C) that bind to the thin filament (actin) of striated muscle. Its major regulatory function is to bind calcium and regulate muscle contraction. Following injury to muscle cells (heart or skeletal muscles) the intact troponin complex along with free troponin subunits are released into blood. Although troponin is found in both skeletal muscles and the myocardium, the amino acid sequences for cardiac troponin T (cTnT) and I (cTnI) isoforms are significantly different from their skeletal muscle counterparts. This is not the case for troponin C, where the subunits from these tissues are identical. Commercial assays have been constructed for measurement of cTnT and cTnI in blood that have been shown to have high specificity for cardiac disease. These assays also have high sensitivity, because the tissue concentrations of cardiac troponin T and I are higher than for other cardiac markers such as myoglobin and creatine kinase. Moreover, the normal concentrations of these cardiac proteins are much lower than for myoglobin and CK, as these proteins are also released from normal skeletal muscle turnover.1 Following acute myocardial infarction (AMI), cardiac troponins are released into blood from two subcellular pools. The initial rise within the first six hours after disease onset is due to the free cytosolic pool, estimated to be about 6% to 8% for cTnT and 3% to 4% for cTnI.2 There is a second, continual increase of cardiac troponin that is due to the gradual breakdown of myofibrils… ABBREVIATIONS: AMI = acute myocardial infarction; cTnI = cardiac troponin I; cTnT = cardiac troponin T. 1. Describe the structure and function of the three troponin proteins. 2. Explain the release of cardiac troponins following an acute myocardial infarction. 3. Discuss the clinical utility of troponin T versus troponin I. 4. Describe the impact of troponin assays on the redefinition of acute myocardial infarction. 5. Explain the issues surrounding lower cutoff concentrations for troponin assays. [1]: #corresp-1