It is now generally accepted that the haemostatic system plays an important role in the pathogenesis of atherosclerotic plaques and their acute complications. 1-3 In the acute situation, plaque rupture is followed by vessel occlusion with thrombus and subsequent ischaemic damage. The rate of revascularization is crucial in limiting damage. Clearly, the haemostatic system plays an important role in this setting. Support has gathered for the idea that the coagulation system also has a role in the chronic disease process. Endothelial damage occurs after prolonged exposure to micro-thrombi and clot associated factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and thrombin, which stimulate chemotaxis and proliferation of vascular smooth muscle cells, ultimately promoting the development of atherosclerosis. In addition, fibrin is a component of atherosclerotic plaques. 3 With this in mind, it seems logical to hypothesize that a pro-thrombotic environment and/or a situation where thrombus is not cleared effectively would predispose an individual to the development of atherosclerosis and its clinical sequelae.