Thromboembolic Disease

in Overview of Vascular Disease

Applied

Type

Reinforcement

Confidence

95%

Created

Mar 26, 2026

Evidence

1 source

Rationale

The provided article is a scoping review that specifically investigates venous valve hypoxia as a mechanism for deep vein thrombosis. Since the existing text already described this mechanism, the new citation was added to reinforce the evidence base. The existing structure and abbreviations (DVT, VTE) were preserved as per instructions.

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-b].[@shaydakov2024-b; @shaydakov2024-c].

* **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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