Galectin-3 binding protein, coronary artery disease and cardiovascular mortality

• Verfasst von: Gleißner, Christian A. [VerfasserIn]
• Verfasst von: Erbel, Christian [VerfasserIn]
• Verfasst von: Linden, Fabian [VerfasserIn]
• Verfasst von: Domschke, Gabriele [VerfasserIn]
• Verfasst von: Akhavanpoor, Mohammadreza [VerfasserIn]
• Verfasst von: Helmes, Christian Michael [VerfasserIn]
• Verfasst von: Dösch, Andreas [VerfasserIn]
• Verfasst von: Kleber, Marcus E. [VerfasserIn]
• Verfasst von: Katus, Hugo [VerfasserIn]
• Verfasst von: März, Winfried [VerfasserIn]
• Titel: Galectin-3 binding protein, coronary artery disease and cardiovascular mortality
• Titelzusatz: insights from the LURIC study
• Verf.angabe: Christian A. Gleissner, Christian Erbel, Fabian Linden, Gabriele Domschke, Mohammadreza Akhavanpoor, Christian M. Helmes, Andreas O. Doesch, Marcus E. Kleber, Hugo A. Katus, Winfried Maerz
• E-Jahr: 2017
• Jahr: 23 March 2017
• Umfang: 9 S.
• Fussnoten: Gesehen am 01.08.2018
• Titel Quelle: Enthalten in: Atherosclerosis
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1970
• Jahr Quelle: 2017
• Band/Heft Quelle: 260(2017), Seite 121-129
• ISSN Quelle: 1879-1484
• DOI: doi:10.1016/j.atherosclerosis.2017.03.031
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Atherosclerosis
• Sach-SW: Biomarker
• Sach-SW: Coronary artery disease
• Sach-SW: Inflammation
• K10plus-PPN: 1577926838

Abstract

Background and aims Galectin-3 binding protein (Gal-3BP) has been associated with inflammation and cancer, however, its role in coronary artery disease (CAD) and cardiovascular outcome remains unclear. Methods Gal-3BP plasma levels were measured by ELISA in 2922 individuals from the LURIC study (62.7 ± 10.6 years, 62.7% male). All-cause and cardiovascular mortality was assessed by Kaplan-Meier analysis and Cox proportional hazards regression. Causal involvement of Gal-3BP was tested for by Mendelian randomization. Gal-3BP effects on human monocyte-derived macrophages were assessed in vitro. Results During 8.8 ± 3.0 years, 866 individuals died, 654 of cardiovascular causes. There was a significant increase in all-cause and cardiovascular mortality with increasing Gal-3BP quintiles. After thorough adjustment, all-cause mortality remained significantly increased in the fifth Gal-3BP quintile (HRQ5 1.292 (1.030-1.620), p = 0.027); cardiovascular mortality remained increased in Gal-3BP quintiles two to five (HRQ51.433 (1.061-1.935, p = 0.019). Gal-3BP levels were not associated with diagnosis and extent of coronary artery disease. In addition, Mendelian randomization did not show a direct causal relationship between Gal-3BP levels and mortality. Gal-3BP levels were, however, independently associated with markers of metabolic and inflammatory distress. In vitro, Gal-3BP induced a pro-inflammatory response in human monocyte-derived macrophages. Adding Gal-3BP levels to the ESC score improved risk assessment in patients with ESC SCORE-based risk >5% (p = 0.010). Conclusions In a large clinical cohort of CAD patients, Gal-3BP levels are independently associated with all-cause and cardiovascular mortality. The underlying mechanisms may likely involve metabolic and inflammatory distress. To further evaluate the potential clinical value of Gal-3BP, prospective studies are needed.