Elsevier

Progress in Cardiovascular Diseases

Volume 47, Issue 3, November–December 2004, Pages 177-188
Progress in Cardiovascular Diseases

Troponins in acute coronary syndromes

https://doi.org/10.1016/j.pcad.2004.07.004Get rights and content

Abstract

Cardiac troponins have replaced creatine kinase-MB as the preferred biomarker for establishing the diagnosis of myocardial infarction (MI). Expert recommendations set the diagnostic decision-limit for each assay at the 99th percentile of troponin levels in an apparently healthy reference population, which due to a lack of standardization, will vary depending upon the manufacturer. Among patients presenting with an acute coronary syndrome (ACS), even low-level elevations of cardiac troponin T or I correlate with higher risk of death and recurrent ischemic events compared to patients with levels of troponin below the decision limit. Renal failure does not appear to diminish the prognostic value of troponins among patients with a high clinical probability of ACS. Moreover, patients with elevated levels of troponin derive the most benefit from more intense medical therapy with antithrombin and antiplatelet medications, as well as an early invasive management strategy. Whereas cardiac troponins are extremely specific for myocardial necrosis, they do not discriminate between ischemic and nonischemic etiologies of myocardial injury. Clinicians must, therefore, determine whether a patient’s presenting symptoms are consistent with ACS. Combining troponin with other cardiac biomarkers may offer complimentary information on the underlying pathobiology and prognosis in an individual patient. Future generations of troponin assays may detect specific posttranslational modifications of troponins that may increase the analytic sensitivity for myocardial damage and offer insight into the timing and mechanism of myocardial injury.

Section snippets

Detection of myocardial injury

The most common substrate of ACS is an unstable atherosclerotic plaque that ruptures or erodes, thereby exposing the highly procoagulant contents of the atheroma core and precipitating the acute thrombotic obstruction of the culprit coronary artery.7, 8 The severity of occlusion determines, in part, whether the distal myocardium remains only ischemic, with recovery after reperfusion, or becomes necrotic from prolonged cellular hypoxia. Myocyte necrosis and associated cell membrane disruption

Diagnostic application of cardiac troponin

The diagnosis of an acute MI (AMI) has traditionally been made on the basis of fulfilling two of the three World Health Organization criteria: (1) typical symptoms of ischemia, (2) elevated levels of CK-MB, or (3) typical ECG changes resulting in Q waves. However, approximately half of patients presenting with cardiac ischemic syndromes and not meeting this definition for MI may have an elevated serum concentration of cardiac troponin indicative of myocardial necrosis.1 As such, the

Non-ST elevation acute coronary syndromes

Hamm et al9 first showed that among patients with unstable angina (normal CK-MB) those with elevated levels of cTnT were at significantly higher risk of in-hospital mortality. Since then, a highly consistent database composed of more than 15 studies has emerged confirming the strong association between cardiac troponin and the risk of death or recurrent ischemic events among patients presenting with Non-ST elevation acute coronary syndromes (NSTE ACS). In aggregate, these studies indicate a

Application of troponin for therapeutic decision making

In addition to providing prognostic information, cardiac troponin has also been shown to be valuable for individualizing therapy. Initial investigations regarding the interaction of troponin and specific therapies was guided, at least in part, by insights into the pathobiology underlying low-level troponin elevation.41 Angiographic studies supported the hypothesis that embolization of platelet aggregates into the distal coronary artery is responsible for microinfarction and impaired

Analytic advances

Advances in understanding regarding the biology of troponins and their degradation and modification both within and outside the cardiac myocyte are likely to guide future improvements in the analytic performance of assays for troponin. Furthermore, it is possible that products of troponin modification may be used to determine the time course of myocardial injury, more accurately describe the severity of myocardial cellular damage, or even define the mechanism of cellular injury (see page 00).

Summary

Cardiac troponin has replaced CK-MB as the preferred cardiac biomarker for diagnosis and risk assessment in suspected ACS. When integrated with the clinical history, physical examination, and ECG, testing for cardiac troponin substantially improves the clinician’s ability to assess risk and guide therapeutic decision making. Patients presenting with ACS and elevated levels of troponin are most likely to derive substantial benefit from treatment with LMWHs, glycoprotein IIb/IIIa inhibitors, and

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