The physiopathologic characteristics of superficial femoral artery occlusion

Mccombs, P.R.

Surgery Gynecology and Obstetrics 148(5): 775-784

1979


ISSN/ISBN: 0039-6087
PMID: 432795
Document Number: 152514
Occlusive disease of the superficial femoral artery is usually atherosclerotic in nature. The biochemical abnormalities fundamental to the development of this process remain unspecified, but seem to be due to damage to the endothelium and are related to the interactions of low density lipoproteins with arterial tissue. The clinical presentation of patients with superficial femoral artery occlusion is variable, depending on activity, concomitant disease and the degree of collateral formation. Pure superficial femoral artery occlusion carries rather benign implications relative to ultimate limb loss; as a manifestation of diffuse arterial disease it is potentially lethal. The influence of diabetes is probably greatest at the level of the tibial vessels and below, contributing to the relatively poor prognosis of diabetic patients after reconstructive surgical treatment. Collateral channels form in response to pressure and flow gradients across an area of occlusion or stenosis. The profunda femoris artery is the greatest source of collateral vessels to the distal femoropopliteal segment. The incidence of concomitant stenotic lesions at the origin of the profunda femoris artery is high in the presence of superficial femoral artery occlusion. Associated disease in the iliac artery or the profunda femoris artery may combine with superficial femoral artery occlusion to produce advanced leg ischemia. To be hemodynamically significant after exercise, an isolated lesion must narrow the area of the lumen by about 70%. This generally occurs 1st at the level of the adductor canal in the superficial femoral artery. After occlusion occurs, disease progression tends to migrate proximally toward the femoral bifurcation and the profunda femoris artery, leaving the distal vasculature relatively unchanged. Whether the apparent acceleration of progression of the disease in distal vascular beds after arterial reconstruction is significant and whether this implies that pulsatile flow characteristics are potentially an etiologic factor for such lesions are topics for future study.

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