American Journal of Neuroradiology, Vol 19, Issue 4 761-766, Copyright © 1998 by American Society of Neuroradiology
ARTICLES |
Why do ulcerated atherosclerotic carotid artery plaques embolize? A flow dynamics study
SG Imbesi and CW Kerber
Department of Radiology, University of California, Davis Medical Center, Sacramento, USA.
PURPOSE: We describe and analyze flow dynamics and pressure relationships in an ulcerated atherosclerotic human carotid bulb. METHODS: Replicas of an ulcerated atherosclerotic human carotid bulb were created using the lost wax technique. The resulting replicas were placed in a circuit of pulsating non-Newtonian fluid and flows were adjusted to replicate human physiological flow profiles. Common carotid artery total flow volumes of 400, 600, and 800 mL/min were studied. Slipstreams were opacified with isobaric dyes. Images were recorded on 35 mm film and on super VHS video. A pressure recording device was calibrated; data were received from needles placed radially and longitudinally in the common carotid artery, narrowed bulb/ulcer, and internal carotid artery. Multiple pressure recordings were obtained in the replicas. RESULTS: Measurements of the replica showed a 59% diameter stenosis and an 88% area stenosis of the carotid bulb with a shallow 3.3-mm ulcer. Analysis of flow in the common carotid artery showed undisturbed slipstreams, but as these streams entered the narrowed carotid bulb they crowded together and accelerated significantly. This accelerated jet continued for at least two vessel diameters into the more normal portions of the internal carotid artery, where flow remained disturbed peripherally and often assumed a helical pattern but was nonturbulent. As fluid entered the narrowed bulb, radial pressures decreased. Most important, at peak systole, lower radial pressure with a vortex circulation was found at the ulceration. CONCLUSION: This combination of events (ie, slowly swirling fluid within the ulcer, allowing platelet aggregates to form, and the intermittent Bernoulli effect, pulling the aggregates into the rapidly flowing blood) may help explain how ulcerated carotid plaques lead to embolic stroke.
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