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Published on: May 24, 2020
Interrelationship between venous and arterial thrombosis
1Department of Vascular Diseases, Ljubljana University Medical Centre, Ljubljana, Slovenia - pavel.poredos@kclj.si.
Insights
Arterial and venous thrombosis share similar inflammatory pathways and risk factors, challenging the view of them as distinct diseases. Atherosclerosis may increase venous thrombosis risk, highlighting a significant link between these conditions.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Inflammation Research
Background:
- Arterial and venous thrombosis were historically considered separate diseases.
- Emerging evidence suggests shared pathogenetic mechanisms and risk factors.
- Atherothrombosis is increasingly recognized as a chronic inflammatory condition.
Purpose of the Study:
- To challenge the traditional view of distinct arterial and venous thrombosis mechanisms.
- To explore the shared etiopathogenetic pathways, particularly inflammation.
- To investigate the link between atherothrombosis and venous thromboembolism risk.
Main Methods:
- Review of pathophysiological studies and clinical evidence.
- Analysis of common risk factors for arterial and venous thrombosis.
- Examination of the role of inflammation in thrombogenesis.
Main Results:
- Coagulation and platelet activation are implicated in both arterial and venous thrombogenesis.
- Inflammation is identified as a fundamental mechanism linking arterial and venous thromboembolic disease.
- Shared risk factors include age, metabolic syndrome, hypercholesterolemia, and thrombophilia.
- Patients with atherosclerosis show increased risk for venous thromboembolism.
Conclusions:
- Arterial and venous thrombosis share closely interrelated etiopathogenetic mechanisms, primarily inflammation.
- Atherosclerosis may directly contribute to venous thrombosis development.
- Common risk factors underscore the interconnectedness of these vascular diseases.
Abstract:
In the past, arterial and venous thrombosis have been accepted as two completely different diseases. Recently, the thesis of two separate pathogenetic mechanisms of venous and arterial thrombosis has been challenged by accumulation of evidence which suggest that patients with atherothrombosis are at increased risk for venous thrombosis. Pathophysiological studies indicated that etiopathogenetic mechanisms of both diseases are similar and that coagulation and platelet activation participate in both venous and arterial thrombogenesis. Inflammation most probably represents the basic etiopathogenetic mechanism of arterial as well as venous thromboembolic disease, being a common mechanism through which different risk factors trigger thrombus formation in both veins and arteries. Atherothrombosis is accepted as a chronic inflammatory disease and the association between circulating inflammatory markers and venous thromboembolism also indicates an involvement of the inflammatory process in venous thrombosis. During inflammation, there is an increase in the production of procoagulant factors, a down-regulation of the anticoagulant mechanisms and an inhibition of the endogenic fibrinolytic activity. In line with the arguments which support the link between arterial and venous thrombosis is also the recognition that different risk factors are common in both diseases, such as age, metabolic syndrome, hypercholesterolemia and thrombophilia. A relation was also found between subjects with preclinical or clinical atherosclerotic disease and venous thromboembolism. These findings indicate close interrelationship between arterial atherothrombotic and venous thromboembolic disease. It could mean that atherosclerosis may induce venous thrombosis or that these two diseases have common risk factors which promote the development of both diseases.
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