Biochemical markers of cardiac damage: From traditional enzymes to cardiac-specific proteins

Abstract

Measurement of cardiac markers in blood has been the mainstay for diagnosis of acute myocardial infarction for nearly 50 years. The field has evolved from measurement of enzyme activity to mass concentrations of proteins using automated non-isotopic immunoassays. With changing clinical practices, cardiac markers are now needed to detect the presence of minor myocardial infarction in patients with unstable angina. Outcome studies have shown that patients with increased troponin are at high short-term risk for death and AMI. Recent developments involve the use of cardiac markers to select the most appropriate therapy for patients with acute coronary syndromes. The success of new cardiac markers such as troponin is due to their high cardiac specificity and the existence of assays with low detection limits. Traditional enzymes such as CK and CK-MB are thought to be released only in situations of irreversible myocardial necrosis. In the case of cardiac troponin, clinical observations and animal studies suggest that cytosolic free troponin may be released in reversible ischemia in addition to irreversible cell damage. The IFCC S-SCM has recommended use of two cut-off concentrations for cardiac troponin to differentiate normal from minor myocardial injury and AMI. A low cut-off may detect reversible ischemic events in some cases.