Abstract
Contraction (retraction) of the blood clot is a part of the clotting process driven by activated platelets attached to fibrin. The aim of this work was to reveal the pathogenic importance of contraction of clots and thrombi in venous thromboembolism (VTE). We investigated the kinetics of clot contraction in clots made from the blood of 55 patients with VTE not receiving antiplatelet and anticoagulant medications. In addition, we studied the ultrastructure of ex vivo venous thrombi, as well as the morphology and functionality of isolated platelets. Thrombi from VTE patients contained compressed polyhedral erythrocytes, a marker for clot contraction in vivo . The extent and rate of contraction of in vitro clots were reduced by 2-fold in clots from the blood of VTE patients compared to healthy controls. The contraction of clots from the blood of patients with pulmonary embolism was significantly impaired compared to that of those with isolated venous thrombosis, suggesting that less compacted thrombi may be prone to embolization. The reduced ability of clots to contract correlated with continuous platelet activation followed by their partial refractoriness to stimulation. Morphologically, 75% of platelets from VTE patients were spontaneously partially activated (with filopodia) compared to only 21% of those from healthy controls. At the same time, platelets from VTE patients showed a 1.4-fold reduction in activation markers expressed in response to chemical activation when compared to platelets from healthy individuals. The results obtained suggest that the impaired contraction of thrombi resulting from platelet dysfunction is an underappreciated pathogenic mechanism in VTE that may regulate the obstructiveness and embologenicity of venous thrombi. Furthermore, an assay for clot contraction may have diagnostic and prognostic value for venous thromboembolism. The work was supported by the Program for Competitive Growth at Kazan Federal University.
Published Version
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