Thromboembolic Disease

in Overview of Vascular Disease

Applied

Type

Reinforcement

Confidence

90%

Created

Mar 26, 2026

Evidence

1 source

Rationale

The provided article is a 2024 scoping review that specifically addresses the mechanism of venous valve hypoxia in DVT pathogenesis. The existing text already contained a placeholder/similar citation, which was updated to the specific suggested key Shaydakov ME, et al. Venous valve hypoxia as a possible mechanism of deep vein thrombosis: a scoping review. International Angiology. 2024. PMID: 38864688. to ensure the most recent and comprehensive review on this topic is cited. The text was slightly modified to acknowledge the 'scoping review' nature of the evidence, increasing the academic weight of the statement.

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, leading to endothelial activation and a prothrombotic microenvironment [@shaydakov2024-venous].[@shaydakov2024-b].

* **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 VTE prevention, diagnosis, and treatment.
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