Retrospective angiographic study to determine the effect of atherosclerotic stenoses of upstream arteries on the degree of atherosclerosis in distal vascular territories

Abstract

ObjectiveExperimental coarctation of the aorta prevents the development of downstream atherosclerosis. The aim of this study was to find out whether or not atherosclerotic stenoses protect distal vascular territories from developing atherosclerosis in humans.Design and settingA total of 2125 vascular segments from angiographies of 101 patients were evaluated by calculating the maximum degree of stenosis (NASCET criteria), the degree of calcification, the degree of collaterals and the Friesinger score.ResultsStenosis ≥30–49% was found in 685 vascular segments (32.2%), ≥50–69% in 490 (23.1%), ≥70–89% in 373 (17.6%) and ≥90% in 265 (12.5%). If a stenosis of at least ≥70–89% was present in the common iliac, the external iliac or the common femoral artery, the degrees of stenosis distal to it were lower than those on the contralateral side (19.8±22.3% (CI 11.7 to 28.0) vs 25.2±20.7% (CI 21.2 to 29.1); Friesinger scores 1.1±1.2 (CI 0.6 to 1.5) vs 1.4±1.1 (CI 1.2 to 1.6); degrees of calcification 0.8±1.0 (CI 0.4 to 1.1) vs 1.2±1.1 (CI 1.2 to 1.6); p<0.05 each). This effect depended on the degree of proximal stenosis, but not on collaterals, and was most pronounced distal to stenoses of the common iliac, the superficial femoral and the popliteal artery. In regression models, stenoses of the pelvic arteries were shown to be an independent protective factor for the distal vascular territories.ConclusionsAtherosclerotic stenoses seem to protect distal vascular territories from developing atherosclerosis. The underlying pathophysiological mechanism of this phenomenon remains to be determined. It could be based on pulse pressure reduction.

Arterial tissue stress and the geography of atheroma

“…There are several scenarios that do not fit within the accepted theory; why do some lesions that restrict flow apparently spare and appear to protect downstream vessels? 2 Why is the upper limb spared in comparison with the lower? 3 Why is the peroneal artery in the leg spared when the anterior and posterior tibial vessels are heavily involved? 4 Why is atheroma never seen in the venous system (unless arterialised 5 ) and why is not plaque formed after iatrogenic intimal damage rather than neointimal hyperplasia? 6 The common denominators for atherogenesis are pulse pressure and sites of tissue stress and it is this which we need to understand more in order to make sense of the geography of predisposed atheroma sites as they might pertain to device failure as well as prevention of atherosclerosis.…”