venous thrombosis/hypoxia

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Genome-Wide Expression Analysis Suggests Hypoxia-Triggered Hyper-Coagulation Leading to Venous Thrombosis at High Altitude.

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Venous thromboembolism (VTE), a multi-factorial disease, is the third most common cardiovascular disease. Established genetic and acquired risk factors are responsible for the onset of VTE. High altitude (HA) also poses as an additional risk factor, predisposing individuals to VTE; however, its

Deep venous thrombosis: The valve cusp hypoxia thesis and its incompatibility with modern orthodoxy.

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The valve cusp hypoxia thesis (VCHT) of the aetiology of deep venous thrombosis (DVT) was adumbrated in this journal in 1977 and fully articulated in 2008, the original hypothesis having been strongly corroborated by experiments published in 1981 and 1984. It presents a unitary account of the

Activation of NLRP3 inflammasome complex potentiates venous thrombosis in response to hypoxia.

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Venous thromboembolism (VTE), caused by altered hemostasis, remains the third most common cause of mortality among all cardiovascular conditions. In addition to established genetic and acquired risk factors, low-oxygen environments also predispose otherwise healthy individuals to VTE. Although

The sequestration and margination of platelets and leucocytes in veins during conditions of hypokinetic and anaemic hypoxia: potential significance in clinical postoperative venous thrombosis.

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Lesions apparently similar to the white part of natural and experimental thrombi were found in the veins of animals starved of oxygen by "hypokinetic" and "anaemic" means: in contrast to this, no comparable lesions were seen in animals exposed to "arterial" hypoxia. The interpretation of these

Hemorrhagic cerebral white matter: infarction with cerebral deep venous thrombosis and hypoxia.

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Postmortem examination of the brain of a 5-week-old boy disclosed extensive thrombosis of the deep venous system and widespread necrosis of the cerebral parenchyma. As is characteristic of this uncommon form of cerebrovascular disease, malacia was present in the central gray matter but was only

Hypoxia, such as encountered at high altitude, promotes deep vein thrombosis in mice.

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Deep Vein Thrombosis and Pulmonary Embolism in a Mountain Guide: Awareness, Diagnostic Challenges, and Management Considerations at Altitude.

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High intensity exercise is associated with several potentially thrombogenic risk factors, including dehydration and hemoconcentration, vascular trauma, musculoskeletal injuries, inflammation, long-distance travel, and contraceptive usage. These are well documented in case reports of venous

Deep Vein Thrombosis in Patients with Pulmonary Embolism: Prevalance, Clinical Significance and Outcome.

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OBJECTIVE Deep venous thrombosis (DVT) and pulmonary embolism (PE) are considered as similar disease entities representing different clinical manifestations. The objectives of this study were: 1) to determine the prevalence and outcome of DVT in patients with PE; 2) to identify additional risk

To what extent might deep venous thrombosis and chronic venous insufficiency share a common etiology?

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According to the valve cusp hypoxia hypothesis (VCHH), deep venous thrombosis is caused by sustained non-pulsatile (streamline) venous blood flow. This leads to hypoxemia in the valve pockets; hypoxic injury to the inner (parietalis) endothelium of the cusp leaflets activates the elk-1/egr-1

Experimental Validation of Methods for Prophylaxis against Deep Venous Thrombosis: A Review and Proposal.

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The experimental procedure by which the valve cusp hypoxia (VCH) hypothesis of the etiology of deep venous thrombosis (DVT) was confirmed lends itself to testing of methods of prophylaxis. Similar animal experiments could end the present exclusive reliance on statistical analysis of data from large

Hypoxia Induces a Prothrombotic State Independently of the Physical Activity.

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Hypoxia (oxygen deprivation) is known to be associated with deep vein thrombosis and venous thromboembolism. We attempted to get a better comprehension of its mechanism by going to high altitude, thereby including the potential contributing role of physical activity. Two groups of 15 healthy

Association between acute hypobaric hypoxia and activation of coagulation in human beings.

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The risk of venous thrombosis is thought to be increased by flying. In a study of 20 healthy male volunteers who were suddenly exposed to a hypobaric environment similar to that encountered within aeroplane cabins, markers of activated coagulation transiently Increased by two-fold to eight-fold. We

Hypoxia primes endotoxin-induced tissue factor expression in human monocytes and endothelial cells by a PAF-dependent mechanism.

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Tissue factor (TF) is a glycoprotein which acts as a trigger of the coagulation cascade. TF expression may be induced at the surface of monocytes and endothelial cells by several stimuli including bacterial endotoxin (LPS) and cytokines (IL 1 beta, TNF alpha) and there is a large body of evidence

Refractory hypoxemia in a 23-year-old patient with Budd-Chiari syndrome.

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Antiphospholipid syndrome is an autoimmune disorder characterized by a hypercoagulable state, leading to arterial and venous thrombosis. We present a 23-year-old patient, suspected of having Budd-Chiari syndrome due to antiphospholipid syndrome, who developed severe and progressive hypoxemia,

Incidence of Deep Vein Thrombosis among non-ICU Patients Hospitalized for COVID-19 Despite Pharmacological Thromboprophylaxis

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We thank Dr. Thachil for his interesting comment regarding our article (1). Indeed, we agree that the precise contribution of various risk factors to the development of venous thromboembolism (VTE) in COVID-19 patients remains to be fully elucidated. In this context, it is possible that also

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