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QJM Advance Access published online on August 12, 2006
QJM, doi:10.1093/qjmed/hcl070
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© The Author 2006. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: Journals.permissions@oxfordjournals.org

Review

The aetiology of deep venous thrombosis

P.C. Malone and P.S. Agutter 1 *

1 From the Theoretical and Cell Biology Consultancy, Glossop, UK

* To whom correspondence should be addressed.
P.S. Agutter, E-mail: tcbc26{at}btopenworld.com


  Abstract

Most ideas about the pathogenesis of deep venous thrombosis (DVT) are dominated by a 'consensus model' first articulated around 1962. This model invokes ‘Virchow's triad’ and attributes thrombogenesis in veins to some combination of ‘hypercoagulability’, ‘stasis’ and ‘intimal injury’. This arose as a by-product of studies on the mechanisms of haemostasis and bleeding diatheses that were at best only indirectly relevant to thrombosis, and there are reasons for doubting the causal significance of ‘hypercoagulability’ and ‘stasis’ in the aetiology of DVT. Proponents of the consensus model make little reference to a substantial literature, mostly historical, that: (a) emphasizes the significance of the venous valve pockets (VVP) and blood rheology in DVT pathogenesis; and (b) describes morphological features specific to venous thrombi that a valid aetiological model must explain. This literature provides the basis for an alternative hypothesis of DVT aetiology, published some 30 years ago, which has been experimentally corroborated and is compatible with recent cell and molecular biological studies of the venous endothelium. We review this alternative hypothesis, considering its potential value for future research on DVT and embolism, and its significance for clinical practice.


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