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Updated: Mar 11, 2026

Deep Vein Thrombosis Induced by Stasis in Mice Monitored by High Frequency Ultrasonography
Published on: April 13, 2018
New findings on venous thrombogenesis
James R Byrnes, Alisa S Wolberg1
1Alisa S. Wolberg, Ph. D., Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, 819 Brinkhous-Bullitt Building, CB #7525, Chapel Hill, NC 27599-7525, United States, Phone: (919) 962-8943, Fax: (919) 966-6718,
Insights
Venous thrombosis (VT) is a major cause of cardiovascular death. Understanding its complex mechanisms, involving blood clotting and vessel function, is key to developing new treatments.
Area of Science:
- Cardiovascular Science
- Hematology
- Thrombosis Research
Background:
- Venous thrombosis (VT) is the third leading cause of cardiovascular death globally, with complications like pulmonary embolism causing significant disability.
- VT arises from a complex interplay of genetic and acquired risk factors, including blood group, age, cancer, and hormone use.
- The underlying pathophysiology, known as Virchow's Triad, involves abnormalities in blood coagulability, vessel function, and blood flow, but remains incompletely understood.
Purpose of the Study:
- To explore the multifaceted mechanisms contributing to venous thrombosis formation and stability.
- To identify potential new therapeutic targets by elucidating the pathophysiology of VT.
- To highlight the need for further research into VT mechanisms, especially in the context of aging.
Main Methods:
- Review of epidemiologic studies in humans.
- Analysis of findings from animal models.
- Integration of biochemical and biophysical investigation data.
Main Results:
- VT pathogenesis involves multiple components including coagulation pathways, endothelial cells, leukocytes, red blood cells, platelets, and microvesicles.
- Blood rheology and stasis-induced vascular cell changes also contribute to VT.
- Virchow's Triad components (coagulability, vessel function, flow) are central to VT development.
Conclusions:
- A comprehensive understanding of VT mechanisms requires integrating data from various research disciplines.
- Further characterization of VT formation and stability, particularly in aging populations, is crucial.
- Elucidating these mechanisms may pave the way for novel therapeutic strategies against venous thrombosis.
Abstract:
Venous thrombosis (VT) is the third most common cause of cardiovascular death worldwide. Complications from VT and pulmonary embolism are the leading cause of lost disability-adjusted life years. Risks include genetic (e.g., non-O blood group, activated protein C resistance, hyperprothrombinemia) and acquired (e.g., age, surgery, cancer, pregnancy, immobilisation, female hormone use) factors. Pathophysiologic mechanisms that promote VT are incompletely understood, but involve abnormalities in blood coagulability, vessel function, and flow (so-called Virchow's Triad). Epidemiologic studies of humans, animal models, and biochemical and biophysical investigations have revealed contributions from extrinsic, intrinsic, and common pathways of coagulation, endothelial cells, leukocytes, red blood cells, platelets, cell-derived microvesicles, stasis-induced changes in vascular cells, and blood rheology. Knowledge of these mechanisms may yield new therapeutic targets. Characterisation of mechanisms that mediate VT formation and stability, particularly in aging, are needed to advance understanding of VT.
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