Chiara Caselli1, Concetta Prontera2, Riccardo Liga2, Michiel A De Graaf2, Oliver Gaemperli2, Valentina Lorenzoni2, Rosetta Ragusa2, Martina Marinelli2, Silvia Del Ry2, Daniele Rovai2, Daniela Giannessi2, Santiago Aguade-Bruix2, Alberto Clemente2, Jeroen J Bax2, Massimo Lombardi2, Rosa Sicari2, José Zamorano2, Arthur J Scholte2, Philipp A Kaufmann2, Juhani Knuuti2, S Richard Underwood2, Aldo Clerico2, Danilo Neglia2. 1. From the CNR, Institute of Clinical Physiology, Pisa, Italy (C.C., M.M., S.D.R., D.R., D.G., R.S., D.N.); Fondazione Toscana G. Monasterio, Pisa, Italy (C.P., A.C., M.L., A.C., D.N.); Cardio-Thoracic and Vascular Department, University Hospital of Pisa, Italy (R.L.); Leiden University Medical Center, Leiden, The Netherlands (M.A.D.G., J.J.B., A.J.S.); University Hospital Zurich, Zurich, Switzerland (O.G., P.A.K.); Scuola Superiore Sant'Anna, Pisa, Italy (V.L., R.R., A.C.); Hospital Universitario Vall d'Hebron, Barcelona, Spain (S.A.-B.); University Alcala, Hospital Ramón y Cajal, Madrid, Spain (J.Z.); University of Turku and Turku University Hospital, Turku, Finland (J.K.); and Imperial College London, United Kingdom (S.R.U.). chiara.caselli@ifc.cnr.it. 2. From the CNR, Institute of Clinical Physiology, Pisa, Italy (C.C., M.M., S.D.R., D.R., D.G., R.S., D.N.); Fondazione Toscana G. Monasterio, Pisa, Italy (C.P., A.C., M.L., A.C., D.N.); Cardio-Thoracic and Vascular Department, University Hospital of Pisa, Italy (R.L.); Leiden University Medical Center, Leiden, The Netherlands (M.A.D.G., J.J.B., A.J.S.); University Hospital Zurich, Zurich, Switzerland (O.G., P.A.K.); Scuola Superiore Sant'Anna, Pisa, Italy (V.L., R.R., A.C.); Hospital Universitario Vall d'Hebron, Barcelona, Spain (S.A.-B.); University Alcala, Hospital Ramón y Cajal, Madrid, Spain (J.Z.); University of Turku and Turku University Hospital, Turku, Finland (J.K.); and Imperial College London, United Kingdom (S.R.U.).
Abstract
OBJECTIVE: Circulating levels of high-sensitivity cardiac troponin T (hs-cTnT) and N terminal pro brain natriuretic peptide (NT-proBNP) are predictors of prognosis in patients with coronary artery disease (CAD). We aimed at evaluating the effect of coronary atherosclerosis and myocardial ischemia on cardiac release of hs-cTnT and NT-proBNP in patients with suspected CAD. APPROACH AND RESULTS: Hs-cTnT and NT-proBNP were measured in 378 patients (60.1±0.5 years, 229 males) with stable angina and unknown CAD enrolled in the Evaluation of Integrated Cardiac Imaging (EVINCI) study. All patients underwent stress imaging to detect myocardial ischemia and coronary computed tomographic angiography to assess the presence and characteristics of CAD. An individual computed tomographic angiography score was calculated combining extent, severity, composition, and location of plaques. In the whole population, the median (25-75 percentiles) value of plasma hs-cTnT was 6.17 (4.2-9.1) ng/L and of NT-proBNP was 61.66 (31.2-132.6) ng/L. In a multivariate model, computed tomographic angiography score was an independent predictor of the plasma hs-cTnT (coefficient 0.06, SE 0.02; P=0.0089), whereas ischemia was a predictor of NT-proBNP (coefficient 0.38, SE 0.12; P=0.0015). Hs-cTnT concentrations were significantly increased in patients with CAD with or without myocardial ischemia (P<0.005), whereas only patients with CAD and ischemia showed significantly higher levels of NT-proBNP (P<0.001). CONCLUSIONS: In patients with stable angina, the presence and extent of coronary atherosclerosis is related with circulating levels of hs-cTnT, also in the absence of ischemia, suggesting an ischemia-independent mechanism of hs-cTnT release. Obstructive CAD causing myocardial ischemia is associated with increased levels of NT-proBNP.
OBJECTIVE: Circulating levels of high-sensitivity cardiac troponin T (hs-cTnT) and N terminal pro brain natriuretic peptide (NT-proBNP) are predictors of prognosis in patients with coronary artery disease (CAD). We aimed at evaluating the effect of coronary atherosclerosis and myocardial ischemia on cardiac release of hs-cTnT and NT-proBNP in patients with suspected CAD. APPROACH AND RESULTS: Hs-cTnT and NT-proBNP were measured in 378 patients (60.1±0.5 years, 229 males) with stable angina and unknown CAD enrolled in the Evaluation of Integrated Cardiac Imaging (EVINCI) study. All patients underwent stress imaging to detect myocardial ischemia and coronary computed tomographic angiography to assess the presence and characteristics of CAD. An individual computed tomographic angiography score was calculated combining extent, severity, composition, and location of plaques. In the whole population, the median (25-75 percentiles) value of plasma hs-cTnT was 6.17 (4.2-9.1) ng/L and of NT-proBNP was 61.66 (31.2-132.6) ng/L. In a multivariate model, computed tomographic angiography score was an independent predictor of the plasma hs-cTnT (coefficient 0.06, SE 0.02; P=0.0089), whereas ischemia was a predictor of NT-proBNP (coefficient 0.38, SE 0.12; P=0.0015). Hs-cTnT concentrations were significantly increased in patients with CAD with or without myocardial ischemia (P<0.005), whereas only patients with CAD and ischemia showed significantly higher levels of NT-proBNP (P<0.001). CONCLUSIONS: In patients with stable angina, the presence and extent of coronary atherosclerosis is related with circulating levels of hs-cTnT, also in the absence of ischemia, suggesting an ischemia-independent mechanism of hs-cTnT release. Obstructive CAD causing myocardial ischemia is associated with increased levels of NT-proBNP.
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