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Coronary angiographic findings in patients with clinical unstable angina according to cardiac troponin I and T concentrations in serum
Authors:Panteghini Mauro  Cuccia Claudio  Pagani Franca  Turla Claudia  Bonetti Graziella  Bonini Elena
Affiliation:Laboratorio Analisi Chimico Cliniche 1, Azienda Ospedaliera Spedali Civili and Universitá, Brescia, Italy. panteghi@bshosp.osp.unibs.it
Abstract:CONTEXT: Elevated cardiac troponin levels have been reported to identify unstable angina patients at high risk. OBJECTIVE: To examine the relation of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels to findings of coronary angiography in these patients. METHODS: Samples for troponin estimation were taken every 4 hours throughout the first 48 hours after admission before angiography in 34 patients with primary unstable angina. Patients were considered to be troponin positive if the marker was increased (>0.04 microg/L for cTnT and >0.03 microg/L for cTnI) in at least one sample collected. RESULTS: An increased troponin (I or T) concentration was documented in 14 patients (41.2%). Twelve patients (35.3%) had elevations of both markers, whereas the remaining 2 patients had elevations of cTnI or cTnT alone. Patients with or without increased troponin levels did not differ with respect to degree of coronary disease at angiography. However, patients with elevated troponin concentrations had more complex lesion characteristics. In 69% of patients with increased cTnI levels and in 77% of patients with increased cTnT levels, type B2 or C lesions were documented with presence of ulcerated plaques and thrombus formation. In contrast, only 23% of the patients with elevated cTnI or cTnT levels had type A lesions compared with 71% of patients with negative troponin concentrations. CONCLUSIONS: Patients with unstable angina who have significant release of cTnI and/or cTnT have evidence of more complex lesions on coronary angiography, supporting the hypothesis that both troponins might be used without distinction as surrogate markers for microembolization from thrombus formation on a disrupted plaque.
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