Line Pourtau1, Jean Marc Sellal2, Romaric Lacroix3, Philippe Poncelet4, Olivier Bernus5, Gisèle Clofent-Sanchez6, Mélèze Hocini7, Michel Haïssaguerre8, Françoise Dignat-George9, Frédéric Sacher10, Paquita Nurden11. 1. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France. Electronic address: line.pourtau@ihu-liryc.fr. 2. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Bordeaux University Hospital (CHU), Electrophysiology and Ablation Unit, 33600 Pessac, France; Centre Hospitalier Régional Universitaire (CHRU) de Nancy, département de cardiologie, 54500 Vandœuvre-lès-Nancy, France. Electronic address: jeanmarc.sellal@free.fr. 3. VRCM, UMR-S1076, Aix -Marseille Université, INSERM, UFR de Pharmacie, 13385 Marseille, France; Department of Haematology and Vascular Biology, CHU Conception, AP-HM, 13385 Marseille, France. Electronic address: romaric.lacroix@univ-amu.fr. 4. Research & Technology Department, BioCytex, 13010 Marseille, France. Electronic address: philippe.poncelet@biocytex.fr. 5. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France. Electronic address: olivier.bernus@ihu-liryc.fr. 6. Univ Bordeaux, CNRS, Centre de Résonance Magnétique des Systèmes Biologiques, U5536, 33076 Bordeaux, France. Electronic address: gisele.clofent-sanchez@rmsb.u-bordeaux2.fr. 7. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; Bordeaux University Hospital (CHU), Electrophysiology and Ablation Unit, 33600 Pessac, France. Electronic address: meleze.hocini@chu-bordeaux.fr. 8. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; Bordeaux University Hospital (CHU), Electrophysiology and Ablation Unit, 33600 Pessac, France. Electronic address: michel.haissaguerre@chu-bordeaux.fr. 9. VRCM, UMR-S1076, Aix -Marseille Université, INSERM, UFR de Pharmacie, 13385 Marseille, France; Department of Haematology and Vascular Biology, CHU Conception, AP-HM, 13385 Marseille, France. Electronic address: francoise.dignat-george@univ-amu.fr. 10. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France; Univ. Bordeaux, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; INSERM, Centre de recherche Cardio-Thoracique de Bordeaux, U1045, 33000 Bordeaux, France; Bordeaux University Hospital (CHU), Electrophysiology and Ablation Unit, 33600 Pessac, France. Electronic address: frederic.sacher@chu-bordeaux.fr. 11. IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac, France. Electronic address: paquita.nurden@gmail.com.
Abstract
BACKGROUND: Thrombotic risk constitutes a major complication of atrial fibrillation (AF). Platelets and microparticles (MPs) are important for hemostasis and thrombosis, however their participation during AF is not well known. The aim of this study was to characterize platelet function and MPs procoagulant and fibrinolytic activity in AF patients and to determine the effects of an acute-AF episode. METHODS: Blood was collected from paroxysmal (21) and persistent (16) AF patients referred for AF catheter ablation. Ten patients in sinus rhythm for 10days were induced in AF allowing comparisons of left atrium samples before and after induction. Platelet aggregation with ADP, TRAP, collagen, and ristocetin was studied. Platelet surface expression of PAR-1, αIIbβ3, GPIb and P-selectin were evaluated by flow cytometry, and MPs-associated procoagulant and fibrinolytic activity levels were determined by functional assays. RESULTS: A specific reduction in platelet aggregation to TRAP, activating the thrombin receptor PAR-1, was found in all AF patients. No differences in platelet receptor expression were found. Yet, after acute-induced AF, the platelet response was improved. Furthermore, a significant decrease of left atrium tissue factor-dependent procoagulant activity of MPs was observed. CONCLUSION: Acute episodes of AF results in a decrease in MPs-associated tissue factor activity, possibly corresponding to consumption, which in turn favors coagulation and the local production of thrombin. A decreased platelet basal aggregation to TRAP may result from PAR1 desensitization, whereas the improved response after an induced episode of AF suggests activation of coagulation and PAR1 re-sensitization.
BACKGROUND:Thrombotic risk constitutes a major complication of atrial fibrillation (AF). Platelets and microparticles (MPs) are important for hemostasis and thrombosis, however their participation during AF is not well known. The aim of this study was to characterize platelet function and MPs procoagulant and fibrinolytic activity in AFpatients and to determine the effects of an acute-AF episode. METHODS: Blood was collected from paroxysmal (21) and persistent (16) AFpatients referred for AF catheter ablation. Ten patients in sinus rhythm for 10days were induced in AF allowing comparisons of left atrium samples before and after induction. Platelet aggregation with ADP, TRAP, collagen, and ristocetin was studied. Platelet surface expression of PAR-1, αIIbβ3, GPIb and P-selectin were evaluated by flow cytometry, and MPs-associated procoagulant and fibrinolytic activity levels were determined by functional assays. RESULTS: A specific reduction in platelet aggregation to TRAP, activating the thrombin receptor PAR-1, was found in all AFpatients. No differences in platelet receptor expression were found. Yet, after acute-induced AF, the platelet response was improved. Furthermore, a significant decrease of left atrium tissue factor-dependent procoagulant activity of MPs was observed. CONCLUSION: Acute episodes of AF results in a decrease in MPs-associated tissue factor activity, possibly corresponding to consumption, which in turn favors coagulation and the local production of thrombin. A decreased platelet basal aggregation to TRAP may result from PAR1 desensitization, whereas the improved response after an induced episode of AF suggests activation of coagulation and PAR1 re-sensitization.
Authors: Grzegorz Procyk; Dominik Bilicki; Paweł Balsam; Piotr Lodziński; Marcin Grabowski; Aleksandra Gąsecka Journal: Int J Mol Sci Date: 2022-07-08 Impact factor: 6.208
Authors: Andreas Zietzer; Baravan Al-Kassou; Paul Jamme; Verena Rolfes; Eva Steffen; Marko Bulic; Mohammed Rabiul Hosen; Philip Roger Goody; Vedat Tiyerili; Sebastian Zimmer; Jan Wilko Schrickel; Alexander Sedaghat; Bernardo S Franklin; Nikos Werner; Georg Nickenig; Felix Jansen Journal: Clin Res Cardiol Date: 2021-06-01 Impact factor: 5.460