Thromb Haemost 2006; 96: 111–2 Arterial and venous thromboembolic diseases have historically been viewed as separate pathophysiological entities until recently, partly as a result of the obvious anatomical differences and divisions of the arterial and venous systems, as well as their separate, distinct clinical presentations. However, it has become increasingly clear that this dichotomy of vascular disease is over simplistic and probably hinders rather than promotes our understanding of the underlying pathogenesis of the condition. Indeed, some generalisations are often readily made by the uninitiated.Agreed, venous thromboembolic disease is predominantly fibrin-rich clot (‘red clot’), related to stasis or venous wall damage in deep veins, and embolising to the pulmonary vasculature; thus, ‘venous clots’respond well to anticoagulation therapy. In contrast, arterial thrombus within the coronary or peripheral artery is considered predominantly platelet-rich clot (‘white clot’) and in this ‘high flow’ arterial system, antiplatelet therapies are beneficial, for example, in the setting of acute coronary syndromes (ACS). As always, these generalisations can be overtly misleading. In atrial fibrillation (AF), which is a common and important cause of intracardiac thrombus – resulting in stroke and systemic (arterial) thromboembolism – stasis within the left atrial appendage and a preponderance of coagulation abnormalities results in fibrin-rich thrombus (‘red clot’) formation (1). Hence, the superiority of anticoagulation as thromboprophylaxis inAF and in keeping with the observation that the benefit of antiplatelet therapy in AF is not much beyond what would be expected from the effect of co-existant vascular disease. Similarly, anticoagulation can sometimes be complementary or an alternative to antiplatelet therapy in ACS (2). As another example, subjects who sustain a retinal vein thrombosis commonly have associated cardiovascular risk factors and the causes of mortality on follow-up are usually arterial vascular events, such as myocardial infarction and stroke (3). Perhaps an appreciation of the underlying prothrombotic mechanisms may improve our understanding of the common pathophysiological features with both venous and arterial thromboembolism. With arterial disease, the processes of endothelial damage/dysfunction, inflammation and thrombogenesis (with coagulation/platelet abnormalities) are well-recognised, resulting in the dynamic, progressive disease of atherothrombotic disease (4). Indeed, thrombogenesis and atherogenesis are closely related. Compared to arterial thrombosis, the pathogenesis of venous thromboembolism (VTE) is probably less well understood, where the classic risk factors (such as malignancy, pregnancy, oestrogen use, immobilization) are absent. As atherosclerosis is known to involve platelet and coagulation activation, as well as fibrin turnover, it is not unreasonable to suggest that a plausible pathophysiological link exists between VTE and atherosclerosis. This notion is given further credence as both conditions have many risk factors in common, including older age, obesity, diabetes mellitus, hyperlipidaemia and hypertension (5). In this issue of Thrombosis and Haemostasis, Bova et al. (see pages 132-6) explore the potential association between idiopathicVTE and adverse arterial events.Their choice of idiopathic VTE is significant, as it represents 25%-50% of all VTEs (7). Their case-control study is well-designed, with the patient and control groups being evenly-matched for number and gender, as well as known arteriovenous disease risk factors, whilst followup was prospective and lasted an average of 40 months. Bova et al. (6) conclude that there is a higher risk of adverse cardiovascular outcomes in idiopathic VTE patients (HR:2.84; 95% CI:1.11–7.27; p=0.03), compared to the control population. Of note, all VTE patients were treated with anticoagulation for approximately 13.9 months, thereby further reducing the risk of cardiovascular adverse events, such as ischaemic stroke and myocardial infarction. Their findings are in keeping with their previous report (8), where the risk of atherosclerosis (as defined by carotid ultrasonography) was higher in spontaneous (idiopathic) VTE when compared to secondary VTE patients (OR: 2.3; 95%CI:1.4–3.7) or controls (OR: 1.8; 95%CI: 1.1–2.9). However, the obvious limitations of a cross-sectional analysis apply, and such a study design reveals associations rather than causality. Also, statistical © 2006 Schattauer GmbH, Stuttgart