Abstract

Thrombophilia is considered as a condition predisposing to the development of thrombosis. Arterial thrombosis usually occurs after the erosion or rupture of an atherosclerotic plaque and, through platelet-mediated thrombi, can cause ischaemic injuries especially in tissues with a terminal vascular bed. Indeed, cardiac ischaemia and stroke are the most severe clinical manifestations of atherothrombosis. Ischaemia can arise slowly from the progression of atherosclerotic disease (stable angina, claudication) or acutely in the case of vascular (atherosclerotic plaque rupture) or intracardiac (atrial fibrillation, mechanical valve prostheses) thromboembolisation. Venous thromboembolism (VTE) is the most common vascular disease after acute myocardial infarction and stroke. It is represented by two main clinical events: deep venous thrombosis (DVT) and pulmonary embolism (PE), which often constitute an unique clinical picture in which PE follows DVT. Although VTE is a common disease, the underlying pathogenic mechanisms are only partially known, particularly in comparison to those of atherothrombosis. During the past decades, progress has been made in the identification and characterisation of the cellular and molecular mechanisms that interdependently influence Virchow’s triad. It is now accepted that the combination of stasis and hypercoagulability, much more than endothelial damage, is crucial for the occurrence of VTE; venous thrombi are mainly constituted by fibrin and red blood cells, and less by platelets. In contrast, platelets are essential for primary haemostasis, repair of damaged endothelium and play a pivotal role in the development of atherosclerosis. Inflammation, lipids and the immune system, through a complex interplay, are also important determinants of arterial and, albeit to a lesser extent, of venous thrombosis. Pathophysiological and epidemiological findings have enabled the definition of the main risk factors for atherothrombosis and VTE, listed in Tables I and ​andII.II. This review summarises the recent epidemiological data on the main risk factors for venous and arterial thrombosis, and considers the mechanisms by which they mediate the disease. Table I Classical risk factors for cardiovascular disease35.

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