Abstract

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 is the progression to critical ischaemia, with rest pain and gangrene. The basic underlying pathophysiological processes underlying these major complications of PVD are thrombosis and atherogenesis. However, simply suggesting that these events are solely due to the exposure of the blood to the thrombogenic surface of the ruptured plaque, as is the case in coronary artery disease, may be simplistic. Closer examination suggests that thromboembolism, disease progression and the effect(s) of intervention (or failure of the latter) in PVD can be explained by careful reference to Virchow's triad for thrombogenesis.8 Over 150 years ago, Virchow postulated that three features predispose to thrombus formation: abnormalities in blood flow, blood constituents and the vessel wall.8 Although Virchow was referring to venous thrombosis, these concepts can also be applied to arterial thrombosis. An update of Virchow's triad for thrombogenesis for the new millennium …

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