Contraction (retraction) of the blood clot is a part of the clotting process driven by activated platelets attached to fibrin that can potentially modulate the obstructiveness and integrity of thrombi. 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 the blood of 55 patients with VTE. 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 were reduced by twofold in clots from the blood of VTE patients compared with healthy controls. The contraction of clots from the blood of patients with pulmonary embolism was significantly impaired compared with that of those with isolated venous thrombosis, suggesting that less compacted thrombi are prone to embolization. The reduced ability of clots to contract correlated with continuous platelet activation followed by their partial refractoriness. Morphologically, 75% of platelets from VTE patients were spontaneously activated (with filopodia) compared with only 21% 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 with healthy individuals. The results obtained suggest that the impaired contraction of thrombi is an underappreciated pathogenic mechanism in VTE that may regulate the obstructiveness and embologenicity of venous thrombi.

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This consensus statement of Russian experts is based on a review of the relevant literature on the prevalence, diagnosis, and treatment of non-thrombotic and post-thrombotic venous obstruction, as well as management of patients after venous stenting. In the Part 1 we discussed the clinical manifestations of venous obstruction, the role of duplex ultrasound scan, CT venography, MR venography, direct venography, and intravascular ultrasound scan, as well as typical findings obtained by using these methods. The authors mentioned the functional assessment of venous outflow in healthy subjects and in those with obstruction and changes in them after the intervention. In conclusion, the authors formulated the suggestions for clinical recommendations on the diagnosis of chronic venous obstruction.

Introduction: Pelvic congestion syndrome (PCS) may be effectively managed with conservative treatment in certain patients. Treatment with venoactive drugs is common, but supportive data are limited. This study evaluated the clinical efficacy of micronized purified flavonoid fraction (MPFF) in women with PCS. Methods: In a single-blind, placebo-controlled study, women with duplex ultrasound diagnosis of pelvic varicose veins (PVV) and PCS were randomized to MPFF 1000 mg once daily or placebo for 2 months. Clinical manifestations of PCS were evaluated at baseline and end of treatment (M2) using three assessment tools: disease-specific quality of life (QoL) Pelvic Varicose Vein Questionnaire (PVVQ), Pelvic Venous Clinical Severity Score (PVCSS), and the Visual Analog Scale (VAS) for the main symptoms of the disease.

Aim. To study the effect of the blood components on clot contraction dynamics in vitro.Methods. The original method based on the optical detection of changes in the blood clot volume over time was used. Whole blood, as well as reconstructed samples using washed platelets, erythrocytes, purified fibrinogen, platelet-poor and platelet-rich plasma were studied.Results. Blood clot contraction has a non-linear kinetics, reflecting the complexity of the underlying mechanisms. Platelets increase the blood clot contraction, while the red blood cells have an inhibitory effect. Blocking the fibrin and platelets interaction using the RGDS peptide, an integrin αIIbβ3 antagonist, reduces the extent and rate of clot contraction. The exogenous Ca2+ is not required for contraction, but its addition stabilizes clots by inhibiting the erythrocytes. Thrombin has a dose-dependent effect and increases the rate and extent of contraction. In blood samples of patients taking warfarin, blood clot contraction was delayed.Conclusion. The blood clot contraction is a process which depends on many factors, including the blood cell composition, amount of fibrinogen, the endogenous thrombin activity and platelets interaction with fibrin; understanding the mechanisms of the blood clot contraction could form the basis for the development of novel approaches to the hemostatic disorders treatment.

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