Is There a Genetic Relationship Between Arterial and Venous Thrombosis?

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Thromboembolic disease is the leading cause of morbidity and mortality in the developed world.¹ Arterial thrombosis is the most common underlying cause of acute myocardial infarction, non-hemorrhagic cerebrovascular accidents, and peripheral vascular disease. Pathological manifestations of venous thrombosis largely include deep venous thrombosis (DVT) and/or pulmonary embolus (PE). While arterial thromboembolic events are the foremost cause of death and disability, venous disease also plays an important role. DVT affects approximately two million Americans annually while PE is the most common cause of preventable hospital death accounting for 60,000 deaths in the United States annually.²

Medical textbooks and epidemiological studies characteristically consider arterial and venous thromboembolic disease as distinct entities, each with their own pathophysiological basis, unique risk factors, and distinct therapeutic regimens.^3-6 Arterial clots typically occur in an injured vessel and the most common cause of vascular damage in the arterial system is atherosclerotic vascular disease (ASVD).³ The risk factors for arterial thrombosis are therefore considered the same as those for ASVD. Arterial clots occur in a high flow, high shear environment and these clots, also called white clots, are rich in platelets. Prevention and treatment of arterial thrombosis is often aimed at platelet inhibition. While vascular injury can promote the formation of venous clots, stasis and changes in blood composition (thrombophilia) are the most important risk factors for venous clot development. ³ Venous clots occur in a low flow system. They are rich in fibrin that is enmeshed with red blood cells and are referred to as red clots.

ABBREVATIONS: ASVD = atherosclerotic vascular disease; DVT = deep venous thrombosis; GAIT = Genetic Susceptibility to Thrombosis; PE = pulmonary embolus; VTE = venous thromboembolic event.