Vascular Endothelial Dysfunction and Immunothrombosis in the Pathogenesis of Atrial Fibrillation

Autor: Gabriel D. Dungan MD, Bulent Kantarcioglu MD, Ameer Odeh MD, Debra Hoppensteadt PhD, Fakiha Siddiqui BDS, Luke Rohde BS, Jawed Fareed PhD, Mushabbar A. Syed MD
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Clinical and Applied Thrombosis/Hemostasis, Vol 30 (2024)
Druh dokumentu: article
ISSN: 1938-2723
10760296
DOI: 10.1177/10760296241296138
Popis: Atrial Fibrillation (AF) induces proinflammatory processes which incite vascular endothelial activation and dysfunction. This study seeks to examine the potential relationship between various endothelial, inflammatory, thrombotic, and renin-angiotensin-system (RAS) biomarkers in AF patients. Blood samples were from AF patients (n = 110) prospectively enrolled in this study prior to their first AF ablation. Control plasma samples (n = 100) were used as reference. All samples were analyzed for endothelial (NO, ICAM-1, VEGF, TF, TFPI, TM, Annexin V), inflammatory (IL-6, TNFα, CRP), thrombotic (vWF, tPA, PAI-1, TAFI, D-dimer), and RAS (Renin, Ang-II) biomarkers using ELISA methods. Biomarker average comparisons and Spearman correlations were performed. AF patients showed varying levels of biomarker increase compared to controls. We observed a significant decrease of Ang-II in the AF population relative to controls when stratified for the use of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin II receptor blocker (ARB) upon study enrollment. AF patients showed statistically significant correlations between the following biomarkers: TNFα vs IL-6 (r s = 0.317, p = .004), ICAM-1 vs TNFα (r s = 0.527, p = .012), Annexin V vs VEGF (r s = 0.620, p
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