Journal
THROMBOSIS RESEARCH
Volume 133, Issue 5, Pages 936-944Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2014.02.023
Keywords
Antiphospholipid Syndrome; Anticardiolipin; Fibrinolysis; Turbidimetry
Categories
Funding
- Swedish Heart-Lung Foundation
- Swedish Research council
- Swedish Rheumatism Association
- King Gustaf V 80th Birthday Fund
- Swedish Society of Medicine
- Alex and Ake Wiberg Foundation
- Alex and Eva Wallstoms Foundation
- Foundation in memory of Clas Groschinsky
- Karolinska Institutet Foundations
- Stockholm County Council
- Karolinska Institutet
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Objective: The antiphospholipid syndrome (APS) is defined by persistent antiphospholipid antibodies together with thrombosis and/or pregnancy morbidity. We investigated the tightness of fibrin clot and fibrinolytic function in plasma samples from APS patients compared with two control groups. Material and Methods: APS patients (n = 49), healthy controls (HC) (n = 19) and warfarin-treated nonAPS thrombosis controls (nonAPS-TC) (n = 39) were investigated. Fibrin permeability was assessed as the permeability coefficient (Ks) by a flow measurement technique. Additionally, clot density and fibrinolytic function was analysed by a turbidimetric clotting and lysis assay. Fibrin structure was visualised using scanning electron microscopy. Finally, the number of cell-derived microparticles (MPs) in the samples were correlated to fibrin permeability Results and Conclusions: The Ks value was lower in samples from APS-patients compared to HC and nonAPS-TC (p < 0.0001 for both) indicating a less permeable fibrin clot in APS patients. Scanning electron microscopy images confirmed compact fibrin with smaller intrinsic pores and thinner fibers in samples from APS patients as compared to HC. Prolonged fibrinolysis (clot lysis) times were present in the subgroup of APS patients with previous arterial thrombosis (n = 15) as compared to HC and to nonAPS-TC (all p-values < 0.05). In conclusion, tighter fibrin clots were formed in plasma from APS patients compared with healthy controls and warfarin treated patients with thrombosis of nonAPS origin. This new observation presents a possible mechanism contributing to the thrombotic predisposition of APS patients. Impaired fibrinolysis, selectively present among APS patients with previous arterial thrombosis, may further aggravate the pro-thrombotic state in this APS subgroup. (C) 2014 Elsevier Ltd. All rights reserved.
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