Fibrinolytic Deficit and Platelet Activation in Atrial Fibrillation and Their Postablation Modulation

Author:

Otto Abigail1ORCID,Fareed Jawed2,Liles Jeffrey1,Statz Stephen1,Walborn Amanda1,Rowe Timothy1,Jabati Sallu1,Hoppensteadt Debra2,Syed Mushabar A.3

Affiliation:

1. Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA

2. Department of Pathology, Loyola University Medical Center, Maywood, IL, USA

3. Department of Cardiology, Loyola University Medical Center, Maywood, IL, USA

Abstract

This study aims to examine the effects of atrial fibrillation (AF) on the expression of the cellular mediators plasminogen activator inhibitor 1 (PAI-1) and CD40 ligand (CD40-L). Additionally, the effect of catheter ablation on the levels of the aforementioned biomarkers was also examined. In this prospective study, plasma samples were collected from patients with AF at baseline prior to ablation and at 1 and 3 months postablation. There was a statistically significant increase in CD40-L at baseline in patients with AF compared to control ( P = .0034). There was a statistically significant decrease in CD40-L levels postablation at both 1 month ( P < .0001) and 3 months ( P < .0001) compared to baseline. Baseline levels of PAI-1 were elevated compared to the control group (mean 19.55 ± 2.17 ng/mL vs 4.85 ± 0.41 ng/mL) and a statistically significant decrease in circulating PAI-1 levels 1 month postablation ( P = .05) was noted compared to preablation levels. These data suggest that inflammation plays an important role in the pathogenesis of AF and that these cellular mediators are modulated by catheter ablation.

Publisher

SAGE Publications

Subject

Hematology,General Medicine

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