Genetics and the Role of Deep Venous Thrombosis DVT

Unlike arteries, veins are thin-walled, low pressure conduits whose function is to return blood from the periphery to the heart. Muscular contractions in the upper and lower extremities propel blood forward and a series of intraluminal valves prevent retrograde flow or reflux. Venous reflux is observed when valvular destruction or dysfunction occurs in association with varicose vein formation. Valvular reflux causes an increase in ambulatory venous pressure and a cascade of pathologic events that manifest themselves clinically as lower extremity edema, pain, itching, skin discoloration, varicose veins, venous ulceration, and, in its severest form, limb loss. These clinical symptoms collectively refer to the disorder known as chronic venous insufficiency (CVI).5 Age, gender, pregnancy, weight, height, race, diet, bowel habits, occupation, posture, previous deep venous thrombosis, and genetics all have been proposed as predisposing factors associated with varicose vein formation. Except for previous deep vein thrombosis and genetics, there is poor evidence that indicates a causative relationship between these predisposing factors and the formation of varicose veins. Refer to Kevin Burnand's textbook, Diseases of the Vein, for further discussion on these predisposing factors.6

There are few reported epidemiologic investigations that suggest a relationship between varicose vein formation and a genetic predisposition.78 It was previously thought that axial destruction of venous valves led to transmission of ambulatory venous hypertension causing reflux and varix formation.6 However, a publication by Labropoulos et al. indicated that the most frequent location for initial varicose vein formation was in the below-knee greater saphenous vein (GSV) and its tributaries, followed by the above-knee GSV, and the saphenofemoral junction.9 This study clearly indicates that vein wall degeneration with subsequent varix formation can occur in any segment of the superficial and deep systems at any time and suggests a genetic component to the disease. In 1969, Gunderson and Hauge reported on the epidemiology of varicose veins observed in the vein

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