Thromboembolic Disease

in Overview of Vascular Disease

Applied

Type

Reinforcement

Confidence

85%

Created

Mar 27, 2026

Evidence

1 source

Rationale

The provided article is a scoping review that specifically investigates venous valve hypoxia as a mechanism for DVT. The existing text already contained a reference to this concept (using a different citation key); this update ensures the content is supported by the specific peer-reviewed source provided and clarifies the physiological process of endothelial activation in the valve pocket.

Evidence

Shaydakov ME et al. Venous valve hypoxia as a possible mechanism of deep vein thrombosis: a scoping review. International Angiology. 2024. PMID: 38864688.
Verified source
PubMedDOI

Content Changes

Virchow's triad — endothelial injury, venous stasis, and hypercoagulability — remains the conceptual framework for understanding the pathogenesis of deep vein thrombosis (DVT) [@rutherford2018-rutherford]. Recent evidence from a scoping review suggests that venous stasis may trigger thrombus formation through venous valve hypoxia, particularly within the valve pockets where oxygen tension is lowest,lowest leading[@shaydakov2024-e]. This localized hypoxia leads to endothelial activation and the development of a prothrombotic microenvironment [@shaydakov2024-b].[@shaydakov2024-e].

* **Acquired risks:** trauma, surgery, malignancy, immobility, oral contraceptives, pregnancy.
* **Inherited thrombophilia:** Factor V Leiden, prothrombin gene mutation, protein C/S deficiency.

> **See Also:** [[venous thromboembolism (VTE)|Ch. 12: Venous Thromboembolism]] for comprehensive VTEvenous thromboembolism (VTE) prevention, diagnosis, and treatment.
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