Anatomic and Hemodynamic Correlations in Carotid Artery Stenosis

Abstract

Pressures were measured in the carotid arteries of 61 patients proximal and distal to atherosclerotic plaques which were carefully studied by angiography and anatomical dissection. (1) An atherosclerotic plaque causing a constriction of less than 47% luminal diameter leaving a lumen greater than 3.0 mm in diameter never caused pressure drops of greater than 10 mm Hg. Stenoses of greater than 63% luminal diameter leaving lumens less than 1.0 mm in diameter always caused pressure drops. (2) Atherosclerotic plaques producing defects which narrowed the lumen fell into a distinct pattern: (a) Type 1 lesions—This basic lesion filled the bulb of the internal carotid artery near its origin, causing a 1 to 2 cm smooth elliptical encroachment on the lumen. (b) Type 2 lesions—Short localized areas of thickening in addition to the basic lesion caused bar-like defects of the lumen at the origin of the internal carotid artery or near the distal end of the lesion. (c) Type 3 lesions—Multiple bar-like defects were sometimes seen. (d) Type 4 lesions—The areas of increased thickening of the lesion were sometimes quite narrow, producing diaphragm-like defects on the lumen. Although theoretically these various types of stenoses should produce different hemodynamic changes, insufficient numbers of observations were made to corroborate these presumptions. (3) Angiograms in general mimicked the gross appearance of the plaques and predicted the actual degree of stenosis produced but did not identify many diaphragm defects, ulcerations, or small thrombi.

Collateral Circulation in Symptomatic Intracranial Atherosclerosis

“…Above 50% luminal stenosis, some individuals demonstrate hemodynamic impairment in antegrade flow with corresponding collateral recruitment. Hemodynamic impairment in intracranial atherosclerosis measured by TIMI and TICI grade occurs at the same threshold predicted both mathematically and at the level that pressure drops become ubiquitous in extracranial plaque (Deweese et al, 1970). This relationship was evident in our results that demonstrated decreasing TIMI and TICI grade with increasing stenosis.…”

Major Variation in Carotid Bifurcation Anatomy: A Possible Risk Factor for Plaque Development?

“…Severe atheromatous disease can lead to secondary changes in vessel anatomy. For example, blood pressure and blood flow decrease beyond a stenosis of Ն80%, [23][24][25] and the ICA narrows distal to a stenosis of Ն70%. 14,26 In contrast, changes in blood flow or pressure do not occur distal to lesions of Ͻ50%, and there is no poststenotic narrowing.…”

“…14,[23][24][25] However, by excluding angiograms with Ն30% stenosis, we minimized such secondary effects. Moreover, our analysis of disease-free, contralateral bifurcations produced very similar results (Table 1).…”

The Extracranial–Intracranial Bypass Trial: implications for future investigations

“…Arterial stenosis or occlusion can cause a reduction in the pressure of distal arterial vessels, but the degree of stenosis or the presence of arterial occlusion does not accurately predict the hemodynamic status of the distal circulation. 33 Although stenoses of the extracranial carotid artery resulting in reductions in luminal diameter Ն 50-70% are known to reduce the distal pressure in some cases, 10 collateral circulation can maintain normal cerebral perfusion pressure and normal flow in many of these patients. Up to 60% of patients with complete occlusion of the carotid artery may have no evidence of hemodynamic compromise in the distal circulation.…”