Coagulation and the vessel wall in thrombosis and atherosclerosis

The blood coagulation system is a key survival mechanism that has developed to protect man against lethal bleeding. A second function of blood coagulation is its close interaction with immunity. The immune-mediated coagulation responses may broadly be regarded as an element of response to injury. Pathological coagulation responses, including thromboembolism and disseminated intravascular coagulation (DIC), could therefore be regarded as excessive immune responses to a vessel wall injury. Virchow's triad, which comprises changes in the components of the blood, the state of the vessel wall, and the blood flow, was originally proposed for venous thrombosis. However, lately it appears that the same principles can be applied to arterial thrombosis and even DIC. It has even been postulated that all forms of thrombosis may be part of a continuous spectrum of the same disease. Over the past few years, an accumulation of evidence has shown that the etiopathogenetic mechanisms behind venous and arterial thrombosis are quite similar. The traditional elements of Virchow's triad are found to apply to both arterial and venous thrombosis. Yet, nowadays more emphasis is placed on the vessel wall and vascular bed specificity and the interaction with inflammation and hypercoagulability. This narrative review will discuss recent advances in research on the possible interactions between coagulation, the vascular endothelium, and atherosclerosis as well as the consequences of such interactions for venous and arterial thrombosis.