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Plasma Levels of Soluble CD146 Reflect the Severity of Pulmonary Congestion Better Than Brain Natriuretic Peptide in Acute Coronary Syndrome

P. Kubena, M. Arrigo, J. Parenica, E. Gayat, M. Sadoune, E. Ganovska, M. Pavlusova, S. Littnerova, J. Spinar, A. Mebazaa, . ,

. 2016 ; 36 (4) : 300-5.

Language English Country Korea (South)

Document type Journal Article

BACKGROUND: Acute heart failure negatively affects short-term outcomes of patients with acute coronary syndrome (ACS). Therefore, reliable and non-invasive assessment of pulmonary congestion is needed to select patients requiring more intensive monitoring and therapy. Since plasma levels of natriuretic peptides are influenced by myocardial ischemia, they might not reliably reflect congestion in the context of ACS. The novel endothelial biomarker, soluble CD146 (sCD146), presents discriminative power for detecting the cardiac origin of acute dyspnea similar to that of natriuretic peptides and is associated with systemic congestion. We evaluated the performance of sCD146 for the assessment of pulmonary congestion in the early phase of ACS. METHODS: One thousand twenty-one consecutive patients with ACS were prospectively enrolled. Plasma levels of sCD146, brain natriuretic peptide (BNP), and high-sensitive troponin T were measured within 24 hr after the onset of chest pain. Pulmonary congestion on chest radiography was determined and classified in three groups according to the degree of congestion. RESULTS: Nine hundred twenty-seven patients with ACS were analyzed. Ninety-two (10%) patients showed signs of pulmonary edema on chest radiography. Plasma levels of sCD146 reflected the radiological severity of pulmonary congestion. Higher plasma levels of sCD146 were associated with the worse degree of pulmonary congestion. In contrast to BNP, sCD146 levels were not affected by the level of troponin T. CONCLUSIONS: The novel endothelial biomarker, sCD146, correlates with radiological severity of pulmonary congestion in the early phase of ACS and, in contrast to BNP, is not affected by the amount of myocardial cell necrosis.

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$a Kubena, Petr $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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$a BACKGROUND: Acute heart failure negatively affects short-term outcomes of patients with acute coronary syndrome (ACS). Therefore, reliable and non-invasive assessment of pulmonary congestion is needed to select patients requiring more intensive monitoring and therapy. Since plasma levels of natriuretic peptides are influenced by myocardial ischemia, they might not reliably reflect congestion in the context of ACS. The novel endothelial biomarker, soluble CD146 (sCD146), presents discriminative power for detecting the cardiac origin of acute dyspnea similar to that of natriuretic peptides and is associated with systemic congestion. We evaluated the performance of sCD146 for the assessment of pulmonary congestion in the early phase of ACS. METHODS: One thousand twenty-one consecutive patients with ACS were prospectively enrolled. Plasma levels of sCD146, brain natriuretic peptide (BNP), and high-sensitive troponin T were measured within 24 hr after the onset of chest pain. Pulmonary congestion on chest radiography was determined and classified in three groups according to the degree of congestion. RESULTS: Nine hundred twenty-seven patients with ACS were analyzed. Ninety-two (10%) patients showed signs of pulmonary edema on chest radiography. Plasma levels of sCD146 reflected the radiological severity of pulmonary congestion. Higher plasma levels of sCD146 were associated with the worse degree of pulmonary congestion. In contrast to BNP, sCD146 levels were not affected by the level of troponin T. CONCLUSIONS: The novel endothelial biomarker, sCD146, correlates with radiological severity of pulmonary congestion in the early phase of ACS and, in contrast to BNP, is not affected by the amount of myocardial cell necrosis.
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$a Parenica, Jiri $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic. International Clinical Research Center-Department of Cardiovascular Disease, University Hospital St Anne's, Brno, Czech Republic.
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$a Gayat, Etienne $u INSERM UMR-S 942, Paris, France. Department of Anesthesiology and Critical Care Medicine, AP-HP, Saint Louis Lariboisière University Hospitals, Paris, France. Université Paris Diderot, PRES Sorbonne Paris Cité, France.
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$a Pavlusova, Marie $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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$a Littnerova, Simona $u Institute of Biostatistics and Analyses, Faculty of Medicine, Masaryk University, Brno, Czech Republic.
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$a Spinar, Jindrich $u Department of Internal Medicine and Cardiology, University Hospital Brno, Brno, Czech Republic. Faculty of Medicine, Masaryk University, Brno, Czech Republic. International Clinical Research Center-Department of Cardiovascular Disease, University Hospital St Anne's, Brno, Czech Republic.
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