title: Risk stratification and therapeutic decision making in patients with acute coronary syndrome--the role of cardiac troponin T.
abstract: Patients with chest pain represent an inhomogeneous group with greatly varying severity of coronary artery disease and cardiac risk. The proper selection of different treatment strategies in these patients requires reliable risk assessment. Patients with definitive myocardial infarction: in patients with ST-segment elevation on ECG, a positive troponin T (cTnT) on admission identifies a group of patients having a threefold higher mortality rate than patients with a negative cTnT test. The differences in risk based on cTnT are found for patients treated with thrombolytic as well as mechanical recanalization therapy. These differences in mortality based on admission cTnT may be explained by more severe coronary artery disease, worse left ventricular function, and less efficient microvascular reperfusion in the cTnT-positive patients. Patients with rest angina: in patients with angina at rest, a positive cTnT value on admission identifies a subgroup having a threefold higher cardiac event rate than cTnT-negative patients. The cTnT-positive patients seem to benefit from treatment with low molecular weight heparin and fibrinogen receptor antagonists, while cTnT-negative patients do not. The differences in risk and response to therapy may be due to more severe coronary artery disease, more critical coronary artery stenoses, and a higher rate of intracoronary thrombus formation in the cTnT-positive versus negative patients. Low risk chest pain patients: in low risk chest pain patients, (i.e. no rest angina, no ECG-changes) cTnT-positive patients on admission have a twofold higher cardiac event rate than cTnT-negative patients. The proper treatment strategy for the low risk cTnT-positive patients remains to be determined. Troponin T versus troponin 1: many of the findings on cTnT also relate to troponin I. However, there is a high interassay variability of troponin I assays, which has to be taken into consideration.
authors.affiliation: Med. Klinik II, Universität zu Lübeck, Germany.
authors.forename: F
authors.initials: F
authors.lastname: Hartmann
authors.forename: E
authors.initials: E
authors.lastname: Giannitsis
authors.forename: V
authors.initials: V
authors.lastname: Kurowski
authors.forename: N
authors.initials: N
authors.lastname: Frey
authors.forename: M
authors.initials: M
authors.lastname: Kampmann
authors.forename: H A
authors.initials: HA
authors.lastname: Katus
mesh_terms: D000787:Angina Pectoris / Q000378:metabolism; D015415:Biomarkers / Q000097:blood*; D006801:Humans; D009203:Myocardial Infarction / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D012307:Risk Factors; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D019210:Troponin I; D020107:Troponin T