Troponins in patients with acute coronary syndromes: biologic, diagnostic, and therapeutic implications.

The cardiac troponins have expanded the spectrum of detectable myocardial injury and enhanced the clinician's ability to identify patients with acute coronary syndromes who are at higher risk for death or recurrent ischemic events. Based on available data, it appears most likely that any reliably detected troponin elevation results from myocyte necrosis. This notion has served as the basis for the recent revision of diagnostic criteria for acute myocardial infarction based on cardiac troponin. Nevertheless, further research is necessary to conclusively refute the possibility that the release of cardiac troponins may also occur in the setting of reversible myocyte injury resulting from cellular ischemia. Such an investigation establishing biologic correlates of troponin elevation is likely to prove valuable in guiding diagnostic terminology as well as in therapy. For example, clinical research finding cardiac troponin elevation to be predictive of intracoronary thrombus and distal microvascular obstruction has been important to the evaluation of troponins for targeting powerful antiplatelet and antithrombin therapies. Whether related to irreversible or reversible injury, the cardiac troponins have blurred the traditional boundaries between unstable angina and myocardial infarction and have evolved as powerful tools for risk stratification and therapeutic decision-making.