Anatomy and Pathophysiology of Varicose Veins

Abstract

The venous anatomy of the leg is described with special reference to the superficial venous system. The histologic and histochemical differences between varicose and normal veins are presented. The pathophysiology of varicose veins is related to congential or acquired abnormalities of the deep venous system, venous valves, and/or fascial or vein wall weakness. Increased deep venous pressure may be both proximal and distal in etiology, arising from arteriovenous anastomoses, incompetent communicating veins, or venous obstruction. Primary valvular incompetence arises from venous obstruction (thrombosis), thrombophlebitis, or valvular agenesis. Secondary valvular incompetence occurs from deep venous obstruction or increased venous distensibility (usually secondary to circulating estrogens). Finally, fascial weakness of the vein wall or supporting fascia provided a genetic basis for the pathophysiology of varicose veins. Understanding the anatomy and pathophysiology of varicose veins should lead to a more rational and efficacious treatment.

Biomolecular Mechanisms in Varicose Veins Development

“…Although many studies have been developed recently, the basis of these alterations is still unknown. A great amount of theories have been proposed, such as inhibition of apoptosis, changes in enzyme activity associated with decreased energy metabolism and increased lysosomal activity, and changes in venous tone associated with a loss of vascular reactivity [28][29][30][31][32][33][34][35][36][37][38][39][40]. was detected in fibroblasts, SMCs and endothelial cells, whereas MMP-9 was found in endothelial cells, adventitial microvessels and medial SMCs, which showed stronger immunoreactivity in VVs than in healthy veins [41].…”

“…The most common changes include also irregular thickening of the intima, fibrosis between the intima and adventitia, atrophy and disruption of elastic fibers, thickening of individual collagen fibers, and disorganization of the muscular layers that are heterogeneously distributed throughout the great saphenous vein and its tributaries [28][29][30][31]. Varicose veins are characterized by impaired balance between collagen and elastin with predominance of the former [32].…”

Selective loss of extracellular matrix proteins is linked to biophysical properties of varicose veins assessed by ultrasonography

“…The finding of elastin loss in the whole length of the GSV but type III collagen reduction in only the proximal part of the varicose vein supported this further. Elastin loss in the adventitia and remodelling of 4 For each vein ring undergoing duplex ultrasonography, a the amount of elastin in the adventitia (estimated by the staining score) was correlated with the diameter at rest (r = 0·511; P = 0·005) and b the amount of collagen type III in the intima was correlated with the increase in vein diameter after Valsalva (r = 0·502; P < 0·001) patients were significantly older than those with varicose veins. Biochemical analysis of the elastin and collagen content of varicose veins has shown both proteins to be reduced 10 .…”

“…Varicose veins are by clinical definition dilated and tortuous 3,4,20 . As expected, the luminal diameter of the varicose veins at the SFJ was larger than the control veins, both at rest and during the Valsalva manoeuvre ( Table 2).…”

“…These clinical signs of chronic venous insufficiency occur because of ambulatory venous hypertension resulting from venous reflux, due to either abnormal dilatation of the superficial veins (primary venous insufficiency) or deep vein thrombosis, valvular incompetence and reflux through the perforating veins (secondary venous insufficiency) 4 . Duplex imaging of venous reflux is the standard diagnostic procedure to assign the best surgical approach to varicose veins 5 but so far its value in the pathogenetic classification of the disease is limited.…”