Troponins in acute coronary syndromes
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
References (69)
- et al.
Validation of the thrombolysis in myocardial infarction (TIMI) risk score for unstable angina pectoris and non-ST-elevation myocardial infarction in the TIMI III registry
Am J Cardiol
(2002) - et al.
ACC/AHA guideline update for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction—summary articleA report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina)
J Am Coll Cardiol
(2002) Biology of troponins
Progress in Cardiovascular Diseases
(2004)- et al.
European Society of Cardiology and American College of Cardiology guidelines for redefinition of myocardial infarctionHow to use existing assays clinically and for clinical trials
Am Heart J
(2002) - et al.
Clinical performance of three cardiac troponin assays in patients with unstable coronary artery disease (a FRISC II substudy)
Am J Cardiol
(2002) - et al.
Cardiac troponins in renal insufficiencyReview and clinical implications
J Am Coll Cardiol
(2002) - et al.
A classification of unstable angina revisited
Circulation
(2000) Evidence-based risk stratification to target therapies in acute coronary syndromes
Circulation
(2002)Troponins in patients with acute coronary syndromesBiologic, diagnostic, and therapeutic implications
Cardiovascular Toxicology
(2002)- et al.
The future of cardiac biomarkersMoving toward a multimarker approach
Circulation
(2002)