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Q J Med 2002; 95: 199-210
© 2002 Association of Physicians

Review

Peripheral vascular disease and Virchow's triad for thrombogenesis

A. Makin, S.H. Silverman and G.Y.H. Lip

From the Haemostasis Thrombosis and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, UK


   Introduction
 
Peripheral vascular disease (PVD), with its symptomatic manifestation, intermittent claudication, is associated with significant morbidity and mortality,1–3 and is an important cause of clinic visits and hospitalizations.4 Many patients with PVD sustain cardiovascular complications, such as heart attacks and strokes,5 which represent the main causes of death in this condition, rather than PVD per se.2,6 Further, emergency treatment is commonly required in this condition due to thrombosis of the affected artery. Indeed, the ‘costs’ of peripheral artery occlusion resulting in critical leg ischaemia have been estimated at $500–1000 per million per year, with a mortality of about 20% per year in these patients.7

While it would be convenient to treat PVD as a single entity, this is not the case, as several almost distinct processes can be identified. The development of the atherosclerotic plaque is the obvious initial process, eventually progressing in severity and leading to intermittent claudication. The next . . . [Full Text of this Article]


   Virchow's triad and the complications of peripheral vascular disease
 

   Abnormal blood flow
 

   Blood constituents
 
Fibrinogen
Fibrin degradation products
Plasminogen activator inhibitor 1 (PAI-1) and tissue plasminogen activator (tPA)
Von Willebrand factor (vWf)
Homocysteine

   Vessel wall
 

   The hypercoagulable state in PVD: cause or effect?
 

   Conclusion
 

   Acknowledgments
 

   Notes
 

   References
 

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