Lipoprotein-associated phospholipase A2 levels, endothelial dysfunction and arterial stiffness in patients with stable coronary artery disease. (25th November 2020)

• Record Type: Journal Article
• Authors: Mourouzis, K; Siasos, G; Oikonomou, E; Zaromitidou, M; Tsigkou, V; Antonopoulos, A.S; Bletsa, E; Stampouloglou, P.K; Vlassis, K; Vavouranakis, M; Tousoulis, D
• Is Part Of: European heart journal. Volume 41:(2020)Supplement 2
• Publication Date: 2020-11-25
• Subjects: Chronic Ischemia; Cardiology -- Periodicals; Heart -- Diseases -- Periodicals; 616.12005
• DOI: 10.1093/ehjci/ehaa946.1264
• Languages: English
• ISSNs: 0195-668X

Abstract

Abstract: Background: Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has inflammatory and atherogenic actions in the vascular wall. We investigate the impact of high Lp-PLA2 levels on endothelial function and arterial stiffness on patients with coronary artery disease (CAD). Methods: We enrolled 374 consecutive patients with stable CAD (mean age 61±11 years). Endothelial function was evaluated by flow-mediated dilation (FMD) and reflected waves with augmentation index (AIx) of the central aortic pressure. Serum levels of Lp-PLA2 were measured with ELISA. Results: In the studied population the median values of Lp-PLA2 levels was 125 (96–152) μg/L. There was no difference between subjects with Lp-PLA2 levels above and below 125μg/L concerning classical risk factors for CAD. Importantly, subjects with Lp-PLA2 values ≥125μg/L had significantly impaired FMD (4.44±2.19% vs. 4.89±2.07%, p=0.04) and AIx values (25.21±8.70% vs. 23.06±9.47%, p=0.03), compared to participants with lower Lp-PLA2 serum levels. A linear regression analysis revealed that Lp-PLA2 ≥125μg/L negatively relates to impaired FMD [b=−0.54 (95% CI: −1.05 to −0.02), p=0.04] and AIx values [b=2.14 (95% CI: 0.18–4.01), p=0.03] independently of cofounders. Conclusions: Elevated Lp-PLA2 relates to endothelial dysfunction and arterial stiffness in CAD patients. These findings highlight the significant role of Lp-PlA2 in the process of atherosclerosis. Funding Acknowledgement: Type of funding source: None