scholarly journals Structural features of the lower limb deep vein remodeling as a morphologic component in the pathogenesis of pulmonary thromboembolism in cancer patients

2019 ◽  
Vol 25 (4) ◽  
pp. 11-16
Author(s):  
P.Ya. Bodnar
Keyword(s):  
Pulmonary Embolism ◽  
Endothelial Cells ◽  
Lower Extremity ◽  
Retrospective Analysis ◽  
Cancer Patients ◽  
Thrombus Formation ◽  
Vascular Wall ◽  
Structural Features ◽  
Vasa Vasorum ◽  
Deep Vein

Oncological patients are at high risk of developing thromboembolic complications, which is a manifestation of a complex set of symptoms – cancer. At the same time, the analysis of the literature shows that the question of the involvement of structural changes of the vascular wall in the pathogenesis of possible primary thrombus formation in cancer patients remains open. The aim of the study – to study the structural features of remodeling of the deep vein of the lower extremity as a morphological link of pathogenesis of pulmonary embolism in cancer patients. Retrospective analysis of 54 protocols of autopsy of deaths from cardiopulmonary shock caused by pulmonary embolism in 2014-2018 was performed. In parallel, all patients were determined the number of free-circulating endothelial cells in the citrate blood by Hladovez J. method, in modification of Sivak V.V. and co-authors (2007). Statistical processing of digital data was performed using the software “Excel” and “STATISTICA” 6.0. In retrospective analysis of autopsy protocols, the highest proportion of pulmonary embolism was report in patients with cancer of the uterus and colon. Morphological changes of the deep vein of the lower extremities in cancer patients were manifested by endothelium desquamation and circular and focal muscular-fibrous hyperplasia of the intima, which caused disturbances of laminar flow of blood; muscular-fibrous atrophy with neovascularization of the middle membrane and sclerosis of vasa vasorum vessels of adventitia. The process of remodeling was also manifest by the inflammatory transformation of the vascular wall, the formation of obstructing and floating blood clots with their subsequent organization, vascularization and recanalization. The cause of intimal thickening, atrophy, and sclerosis with midbrain neovascularization is most likely a hypoxic mechanism of activation of transforming connective tissue growth factors that stimulate collagenogenesis and neoangiogenesis. Desquamation of endothelial cells can also be considered as a significant contributor to thrombus formation. Endothelial cells have a protective function aimed at eliminating damage to the vascular wall by thrombus formation and the development of fibrous intima hyperplasia. In addition, tumor cells are themselves capable of producing excess platelet growth factor, which causes intima proliferation. So, a component of pathomorphogenesis of pulmonary artery thromboembolism in cancer patients is a complex structural reconstruction of the wall of the deep vein of the lower extremity, which causes the development of its thrombosis. Deep vein remodeling in cancer patients is characterized by endothelial cell desquamation, intima and middle-membrane thickening and sclerosis in combination with vasa vasorum fibrous degeneration and perforant vein thrombosis. In response to hemodynamic disorders, compensatory remodeling develops: the combination of leiomyocyte atrophy with their hypertrophy and neovascularization of the middle membrane.

Venous Thromboembolism

2017 ◽  
Author(s):  
Guillermo A. Escobar ◽  
Peter K. Henke ◽  
Thomas W. Wakefield
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Venous Thromboembolism ◽  
Lower Extremity ◽  
The United States ◽  
Laboratory Evaluation ◽  
Individual Risk ◽  
Vein Thrombosis ◽  
Clinical Scenarios ◽  
Deep Vein

Deep vein thrombosis (DVT) and pulmonary embolism (PE) comprise venous thromboembolism (VTE). Together, they comprise a serious health problem as there are over 275,000 new VTE cases per year in the United States, resulting in a prevalence of one to two per 1,000 individuals, with some studies suggesting that the incidence may even be double that. This review covers assessment of a VTE event, initial evaluation of a patient suspected of having VTE, medical history, clinical presentation of VTE, physical examination, laboratory evaluation, imaging, prophylaxis against perioperative VTE, indications for immediate intervention (threat to life or limb), indications for urgent intervention, and management of nonemergent VTE. Figures show a modified Caprini score questionnaire used at the University of Michigan to determine individual risk of VTE and the indicated prophylaxis regimen; Wells criteria for DVT and PE; phlegmasia cerulea dolens secondary to acute left iliofemoral DVT after thigh trauma; compression duplex ultrasonography of lower extremity veins; computed tomographic angiogram of the chest demonstrating a thrombus in the pulmonary artery, with extension into the right main pulmonary; management of PE according to Wells criteria findings; management of PE with right heart strain in cases of massive or submassive PE; treatment of DVT according to clinical scenario; a lower extremity venogram of a patient with May-Thurner syndrome and its subsequent endovascular treatment; and various examples of retrievable vena cava filters (not drawn to scale). Tables list initial clinical assessment for VTE, clinical scenarios possibly benefiting from prolonged anticoagulation after VTE, indications for laboratory investigation of secondary thrombophilia, venous thromboembolic risk accorded to hypercoagulable states, and Pulmonary Embolism Rule-out Criteria Score to avoid the need for D-dimer in patients suspected of having PE.   This review contains 11 highly rendered figures, 5 tables, and 167 references. Key words: anticoagulation; deep vein thrombosis; postthrombotic syndrome; pulmonary embolism; recurrent venous thromboembolism; thrombophilia; venous thromboembolism; PE; VTE; DVT 

Prevention effect of orally active heparin derivative on deep vein thrombosis

2006 ◽  
Vol 96 (08) ◽  
pp. 149-153 ◽  
Author(s):  
Sang Kim ◽  
Dong Lee ◽  
Choong Kim ◽  
Hyun Moon ◽  
Youngro Byun
Keyword(s):  
Pulmonary Embolism ◽  
Deep Vein Thrombosis ◽  
Venous Thrombosis ◽  
Thrombus Formation ◽  
Sprague Dawley ◽  
Vein Thrombosis ◽  
Sprague Dawley Rats ◽  
Acid Conjugate ◽  
Deep Vein ◽  
Orally Active

SummaryThe use of heparin as the most potent anticoagulant for the prevention of deep vein thrombosis and pulmonary embolism is nevertheless limited, because it is available to patients only by parenteral administration. Toward overcoming this limitation in the use of heparin, we have previously developed an orally active heparin-deoxycholic acid conjugate (LMWH-DOCA) in 10% DMSO formulation. The present study evaluates the anti-thrombogenic effect of this orally active LMWH-DOCA using a venous thrombosis animal model with Sprague-Dawley rats. When 5 mg/kg of LMWH-DOCA was orally administered in rats, the maximum anti-FXa activity in plasma was 0. 35 ± 0. 02, and anti-FXa activity in plasma was maintained above 0. 1 IU/ml [the minimum effective anti-FXa activity for the prevention of deep venous thrombosis (DVT) and pulmonary embolism (PE)] for five hours. LMWH-DOCA (5 mg/kg, 430 IU/kg) that was orally administered reduced the thrombus formation by 56. 3 ± 19. 8%;on the other hand, subcutaneously administered enoxaparin (100 IU/kg) reduced the thrombus formation by 36. 4 ± 14. 5%. Also, LMWH-DOCA was effectively neutralized by protamine that was used as an antidote. Therefore, orally active LMWH-DOCA could be proposed as a new drug that is effective for the longterm prevention of DVT and PE.

Embolismo pulmonar agudo en pacientes con neumonía por SARS-COV2. Serie de Casos. [Acute Pulmonary Embolism in patients with SARS-COV2 pneumonia. Cases report]

2021 ◽  
Vol 40 (03) ◽  
Author(s):  
Olmedo Villarreal ◽  
Lizeth Pinilla ◽  
Sabrina Trejos
Keyword(s):  
Pulmonary Embolism ◽  
Acute Pulmonary Embolism ◽  
Scoring Systems ◽  
Vascular Wall ◽  
Average Hospital ◽  
Vein Thrombosis ◽  
Thrombotic Complications ◽  
Deep Vein ◽  
Hospital General

<p>El síndrome respiratorio agudo severo coronavirus 2 (SARS-COV-2) descrito en Wuhan, China a finales del 2019, ha causado más de 9 millones de infecciones en el mundo, y más de 480 mil muertes. En Panamá se han reportado más de 28 mil casos, y más de 500 muertes por COVID-19. Se ha observado un alto riesgo de complicaciones trombóticas, probablemente como consecuencia del daño vascular asociado con la infección viral y la inflamación severa, con la contribución patógena de las plaquetas que interactúan con la pared vascular y los leucocitos. Describimos 3 casos de pacientes hospitalizados en un hospital general en la provincia de Panamá, República de Panamá. Dos hombres y una mujer, edad promedio 40.6 años, estadía hospitalaria promedio de 35.3 días; ingresados con diagnóstico de neumonía por SARS-COV-2, niveles elevados de dimero D (&gt; 5 ug/mL), riesgo bajo calculado para embolia pulmonar. Encontrando embolia pulmonar aguda en las ANGIO tomografía y en un caso acompañado de trombosis venosa profunda. Todos recibían dosis profiláctica de heparina de bajo peso molecular. Se necesitan algoritmos para identificar a aquellos susceptibles de desarrollar complicaciones trombóticas y enfermedades graves, determinar el papel de los biomarcadores y sistemas de puntuación para estratificar el riesgo.</p><p><strong>Abstract</strong></p><p>The severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) described in Wuhan, China in late 2019, has caused more than 9 million infections worldwide, and more than 480 thousand deaths. In Panama, more than 28 thousand cases have been reported, and more than 500 deaths from COVID-19. A high risk of thrombotic complications has been observed, probably as a consequence of vascular damage associated with viral infection and severe inflammation, with the pathogenic contribution of platelets that interact with the vascular wall and leukocytes. We describe 3 cases of patients hospitalized in a general hospital in the province of Panama, Republic of Panama. Two men and one woman, average age 40.6 years, average hospital stay of 35.3 days; admitted with a diagnosis of SARS-VOC-2 pneumonia, elevated levels of dimer D (&gt; 5 ug / mL), calculated low risk for pulmonary embolism. Finding acute pulmonary embolism on ANGIO tomography and in one case accompanied by deep vein thrombosis. All received prophylactic doses of low molecular weight heparin. Algorithms are needed to identify those susceptible to developing thrombotic complications and serious diseases, determine the role of biomarkers and scoring systems to stratify risk.</p>

Development of Venous Thromboembolic Events in Cancer Patients with Elevated Levels of Tissue Factor-Bearing Microparticles

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3832-3832
Author(s):  
Jeffrey Zwicker ◽  
Howard A. Liebman ◽  
Donna Neuberg ◽  
Kenneth Bauer ◽  
Furie Barbara ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Cancer Patients ◽  
Tissue Factor ◽  
Thrombus Formation ◽  
P Value ◽  
Prospective Clinical Study ◽  
Thromboembolic Events ◽  
Increased Risk ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic

Abstract Cancer cells shed procoagulant vesicles containing tissue factor, and these tissue factor-bearing microparticles (TFMP) may play a role in thrombus formation in vivo. Using impedance-based flow cytometry to quantify microparticles and a high affinity monoclonal antibody specific for tissue factor, we previously demonstrated the presence of tissue factor-bearing microparticles in platelet-poor plasma in cancer patients. In this case control study, tissue factor-bearing microparticles represented a 4-fold risk factor for venous thromboembolic events (VTE) in cancer patients with acute VTE compared to age, stage, sex, diagnosis-matched controls with cancer but without acute VTE. To further assess the relationship between tissue factor-bearing microparticles and VTE, we performed a retrospective analysis of deep venous thrombosis or pulmonary emboli diagnosed in cancer patients initially enrolled without evidence of VTE. All radiographic reports for the cancer-no VTE group in the 2 years following enrollment were analyzed by a reviewer blinded to microparticle status. Only documented evidence of a new proximal extremity deep vein thrombosis or pulmonary embolism was included in the analysis. The TFMP and no-TFMP groups did not differ significantly for age, sex, active cancer treatment, smoking status, diabetes, or the presence of metastatic disease at time of enrollment. Sixteen of the 60 patients in this group had measurable tissue factor-bearing microparticles, 4 (4/16; 25%) of which subsequently developed radiographic evidence of VTE within 12 months of enrollment. No thrombotic events were recorded among the 44 patients without detectable tissue factor-bearing microparticles within the initial 12 months; however, one patient developed a pulmonary embolism 17 months following enrollment. Identifying death without VTE as a competing risk, the one-year estimate of the rate of VTE in cancer patients with detectable tissue factor-bearing microparticles was 34.8%; among the same group without detectable tissue factor-bearing microparticles, the 1-year rate was 0% (Log Rank p-value=0.002). The presence of tissue factor-bearing microparticles in cancer patients initially thrombosis-free predicted a 7-fold increased risk of thrombosis over cancer patients who were negative for tissue factor-bearing microparticles (OR 7.00, 95% CI 0.85–82.74, P=0.02). These tissue factor-bearing microparticles appear to be derived from the underlying malignancy since samples analyzed from patients with pancreatic cancer demonstrated co-expression of both tissue factor and MUC-1, a transmembrane glycoprotein overexpressed in epithelial malignancies. These data further support the role of tissue factor-bearing microparticles in the pathogenesis of cancer-associated thrombosis and as a biomarker for the prediction of cancer patients at risk of thrombosis. A prospective clinical study, currently being initiated, is required to evaluate this biomarker for the prediction of VTE risk in cancer patients and the utility of thromboprophylaxis in patients with elevated numbers of tissue factor-bearing microparticles.

The risk of recurrent venous thromboembolism in patients with unprovoked symptomatic deep vein thrombosis and asymptomatic pulmonary embolism

2006 ◽  
Vol 95 (03) ◽  
pp. 562-566 ◽  
Author(s):  
Gema Díaz ◽  
Elena Marín ◽  
Rafael Vidal ◽  
Antonio Sueiro ◽  
Roger Yusen ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Lower Extremity ◽  
Vitamin K Antagonist ◽  
First Episode ◽  
Oral Vitamin ◽  
Antagonist Therapy ◽  
Vein Thrombosis ◽  
Recurrent Venous Thromboembolism ◽  
Deep Vein

SummaryPatients with a first episode of symptomatic pulmonary embolism (PE) havea higher risk of recurrent venous thromboembolism (VTE) than patients with a first episode of proximal lower extremity deep vein thrombosis (DVT). Patients with symptomatic DVT and silent PE may havea different risk of VTE recurrence than patients that have symptomatic DVT without PE. Therefore, it was the aim of this prospective cohort study to compare the risk of recurrent symptomaticVTE in patients with proximal lower extremity DVT and silent PE to the risk in patients that only have proximal lower extremity DVT. Ninty-one consecutive outpatients presenting to the emergency department of a university hospital subsequently hospitalised with a first episode of unprovoked symptomatic proximal lower extremity DVT, and without new pulmonary symptoms were included. Standard initial treatment consisted of intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin for 5–7 days, overlapped with oral vitamin-K antagonist therapy, with long-term oral vitamin-K antagonist therapy (goal INR 2.5 [2.0–3.0]). Study endpoints were: symptomatic recurrent DVT, new PE, and recurrent PE, evaluated by standard objective testing. At enrolment, 28 of 91 (31%) patients with DVT had silent PE. In the patients with DVT and silent PE, there were 3 VTE recurrences during 20 person-years of follow-up, while there were no VTE recurrences during 61 person-years of follow-up in the patients with isolated DVT. The Kaplan-Meier estimated VTE recurrence rate at 1 year after the diagnosis of DVT was 11% (95% CI: 2–28%) for patients with symptomatic DVT and silent PE, compared to 0% in patients with isolated symptomatic DVT (p = 0.0045). In patients with a first episode of unprovoked symptomatic acute proximal lower extremity DVT, the risk of recurrent VTE was significantly higher in those with silent PE compared to those without PE.

scholarly journals Effect of miR-495 on lower extremity deep vein thrombosis through the TLR4 signaling pathway by regulation of IL1R1

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Ke-Cheng Tang ◽  
Zhi-Peng Yang ◽  
Qiu Zeng ◽  
Jing Wang ◽  
Feng Guo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Deep Vein Thrombosis ◽  
Lower Extremity ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Lower Limbs ◽  
Tlr4 Signaling ◽  
Vein Thrombosis ◽  
Tlr4 Signaling Pathway ◽  
Deep Vein

Lower extremity deep vein thrombosis (LEDVT), a common peripheral vascular disease caused by a blood clot in a deep vein is usually accompanied by swelling of the lower limbs. MicroRNAs (miRs) have been reported to play roles in LEDVT. We aimed to investigate the effect of miR-495 on LEDVT via toll-like receptor 4 (TLR4) signaling pathway through interleukin 1 receptor type 1 (IL1R1). LEDVT mouse model was established, and the femoral vein (FV) tissues were collected to detect expressions of miR-495, IL1R1, and TLR4 signaling-related genes. The expressions of both CD31 and CD34 (markers for endothelial progenitor cells) in the FV endothelial cells as well as the proportion of CD31+/CD34+ cells in peripheral blood were measured in order to evaluate thrombosis. The effect of miR-495 on cell viability, cell cycle, and apoptosis was analyzed. IL1R1 was confirmed as the target gene of miR-495. Besides, inhibiting the miR-495 expression could increase IL1R1 expression along with activating the TLR4 signaling pathway. The total number of the leukocytes along with the ratio of weight to length of thrombus in the FV tissue showed an increase. The overexpression of miR-495 could promote FV endothelial cell viability. By injecting agomiR-495 and antagomiR-495 in vivo, the number of leukocytes in the FV tissues and the ratio of weight to length of thrombus were significantly decreased in the mice injected with the overexpressed miR-495, and the IL1R1/TLR4 signaling pathway was inhibited. Collectively, overexpressed miR-495 directly promotes proliferation while simultaneously inhibiting apoptosis of FV endothelial cells, alleviating FV thrombosis by inhibiting IL1R1 via suppression of TLR4 signaling pathway.

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