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Thrombophilia: a genetic predisposition to thrombosis.

Thrombophilia or hypercoagulability is a state of increased risk of forming obstructive arterial or venous clots (1). Normally there is a homeostatic balance between hemostasis, i.e. clotting at the site of injury and maintenance of blood in the fluid state within the vascular compartment. Thrombophilia tilts this delicate balance. The pathogenesis of thrombotic disorders is heavily dependent upon the local and rheologic factors. These are exemplified in conditions of stagnation (usually in the venous system) but also occur in rapid flow in the arterial system particularly with vascular disease or following contact with artificial surface (e.g. prosthetic heart valves). In the latter, platelets tend to adhere to damaged or defective vascular surfaces and are often the inciting stimulus to thrombosis. In the slowflow situation, the elements of Virchow's triad prevail. These of course are stasis, hypercoagulability, and vascular damage. Hypercoagulability and vascular damage are obviously also important events in arterial thromboembolism. Whilst this article will concentrate on genetic thrombophilia predominantly in venous thromboembolism, the recent appreciation of genetic abnormalities predisposing arterial thrombosis independent of the usual risk factors will also be mentioned. This specifically refers to conditions other than hypertension, hypercholesterolemia, obesity, smoking, and other well-known risk factors.