ArticleMolecular medicine reports2017
Prognostic implications and procoagulant activity of phosphatidylserine exposure of blood cells and microparticles in patients with atrial fibrillation treated with pulmonary vein isolation.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Phosphatidylserine-blocking nanoparticles inhibit thrombosis without increased bleeding in mice.Journal of thrombosis and haemostasis : JTH · 2025Article
- Phosphatidylserine-Exposing Annexin A1-Positive Extracellular Vesicles: Potential Cancer Biomarkers.Vaccines · 2023Article
- Extracellular Vesicles in Atrial Fibrillation-State of the Art.International journal of molecular sciences · 2022Review
- Regulation and functions of membrane lipids: Insights fromBBA advances · 2022Review
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to evaluate the procoagulant effects of phosphatidylserine (PS) exposure on blood cells and microparticles (MPs), and examine its role in predicting early recurrence atrial fibrillation (ERAF) in patients with atrial fibrillation (AF) treated with pulmonary vein isolation (PVI). Blood samples were obtained from 40 healthy controls and 56 patients with AF at baseline (prior to PVI), and 0, 1 h, 1 day, 3 days and 7 days following PVI. The exposure of PS (PS+) to blood cells (platelets, erythrocytes and leukocytes) and MPs was detected using flow cytometry. The procoagulant activity was evaluated by coagulation time, and the formation of factor Xa (FXa) and thrombin. In addition, independent factors associated with PS+ blood cells and MPs, and significant predictors of ERAF following PVI were investigated by statistical analyses. The numbers of PS+ blood cells and MPs were significantly increased by PVI (P<0.01). A significant decrease in coagulation time, and increases in FXa and thrombin were exhibited in the PS+ blood cells and MPs from patients with AF treated with PVI, whereas these alterations were inhibited by either lactadherin or anti‑tissue factor (P<0.01). The maximum power of the PVI was significantly associated with platelet‑derived MPs, and high‑sensitivity C‑reactive protein (hs‑CRP) was closely associated with leukocyte‑derived MPs and endothelial‑derived MPs (EMPs) (P<0.01). In addition, hs‑CRP and EMPs >355/µl were identified as independent predictors of ERAF (P<0.05). The increased numbers of PS+ platelets, erythrocytes, leukocytes and MPs contributed to the procoagulant state of AF, and hs‑CRP and EMPs were able to predict ERAF following PVI.
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Registered trials
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