Morten Mørk1, Jan J Andreasen2, Lars H Rasmussen3, Gregory Y H Lip4, Shona Pedersen5, Rikke Bæk6, Malene M Jørgensen7, Søren R Kristensen8. 1. Department of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Aalborg AF Study Group, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; EVsearch.dk, Denmark. Electronic address: morten.moerk@rn.dk. 2. Department of Cardiothoracic Surgery, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Søndre Skovvej 15, 9000 Aalborg, Denmark; Aalborg AF Study Group, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark. Electronic address: jja@rn.dk. 3. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 15, 9000 Aalborg, Denmark; Aalborg AF Study Group, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark. Electronic address: lhr@adm.aau.dk. 4. Department of Clinical Medicine, Aalborg University, Søndre Skovvej 15, 9000 Aalborg, Denmark; Institute of Cardiovascular Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK. Electronic address: G.Y.H.Lip@bham.ac.uk. 5. Department of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Søndre Skovvej 15, 9000 Aalborg, Denmark; EVsearch.dk, Denmark. Electronic address: shp@rn.dk. 6. Department of Clinical Immunology, Aalborg University Hospital, Urbansgade 32, 9000 Aalborg, Denmark; EVsearch.dk, Denmark. Electronic address: rikke.baek@rn.dk. 7. Department of Clinical Immunology, Aalborg University Hospital, Urbansgade 32, 9000 Aalborg, Denmark; EVsearch.dk, Denmark. Electronic address: maljoe@rn.dk. 8. Department of Clinical Biochemistry, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; Department of Clinical Medicine, Aalborg University, Søndre Skovvej 15, 9000 Aalborg, Denmark; Aalborg AF Study Group, Aalborg University Hospital, Hobrovej 18-22, 9000 Aalborg, Denmark; EVsearch.dk, Denmark. Electronic address: srk@rn.dk.
Abstract
BACKGROUND: The risk of thrombus formation in the left atrial appendage (LAA) in patients with atrial fibrillation (AF) may result from blood stasis, local endocardial changes, and/or changed blood composition. Extracellular vesicles (EVs), especially subtypes exposing tissue factor (TF), have procoagulant capacity. We hypothesized that blood concentrations of TF-bearing EVs and other procoagulant biomarkers are elevated in AF patients, particularly in the LAA lumen. METHODS: From 13 AF patients and 12 controls a venous blood sample was drawn prior to cardiac surgery. Intraoperatively, venous blood and blood directly from the LAA was drawn. Plasma levels of EVs, including TF- and cell type specific antigen-bearing EVs, were measured using a protein microarray platform. Plasma levels of TF, von Willebrand factor (vWF), cell free deoxyribonucleic acid (cf-DNA), procoagulant phospholipids (PPLs), and total submicron particles were also evaluated. RESULTS: Significantly higher EV levels, including a several-fold higher median level of TF-bearing EVs were measured in AF patients compared with controls. Median concentrations of TF and vWF were approximately 40% and 30% higher, respectively, in the AF group than in the control group, while no significant differences in levels of cf-DNA, PPLs, or total submicron particles were observed. No significant differences in levels of any of the measured analytes were observed between intraoperative venous and LAA samples. CONCLUSIONS: Increased plasma concentrations of TF in AF patients are accompanied and probably at least partly explained by increased levels of TF-bearing EVs, which may be mechanistically involved in increased thrombogenicity in AF patients. Crown
BACKGROUND: The risk of thrombus formation in the left atrial appendage (LAA) in patients with atrial fibrillation (AF) may result from blood stasis, local endocardial changes, and/or changed blood composition. Extracellular vesicles (EVs), especially subtypes exposing tissue factor (TF), have procoagulant capacity. We hypothesized that blood concentrations of TF-bearing EVs and other procoagulant biomarkers are elevated in AFpatients, particularly in the LAA lumen. METHODS: From 13 AFpatients and 12 controls a venous blood sample was drawn prior to cardiac surgery. Intraoperatively, venous blood and blood directly from the LAA was drawn. Plasma levels of EVs, including TF- and cell type specific antigen-bearing EVs, were measured using a protein microarray platform. Plasma levels of TF, von Willebrand factor (vWF), cell free deoxyribonucleic acid (cf-DNA), procoagulant phospholipids (PPLs), and total submicron particles were also evaluated. RESULTS: Significantly higher EV levels, including a several-fold higher median level of TF-bearing EVs were measured in AFpatients compared with controls. Median concentrations of TF and vWF were approximately 40% and 30% higher, respectively, in the AF group than in the control group, while no significant differences in levels of cf-DNA, PPLs, or total submicron particles were observed. No significant differences in levels of any of the measured analytes were observed between intraoperative venous and LAA samples. CONCLUSIONS: Increased plasma concentrations of TF in AFpatients are accompanied and probably at least partly explained by increased levels of TF-bearing EVs, which may be mechanistically involved in increased thrombogenicity in AFpatients. Crown
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