An experimental and angiographic explanation of why ulcerated carotid bulbs embolize.

The flow dynamics and pressure relationships in an ulcerated atherosclerotic carotid bulb obtained at post-mortem were studied and correlated with angiographic findings in a similar live patient. Using the lost wax technique, we created replicas of an ulcerated atherosclerotic carotid bulb from a fresh cadaver, and placed those replicas in a circuit of pulsating non-Newtonian fluid. Flow profiles were adjusted to replicate human physiologic flows, and flow rates of 400, 600, and 800 milliliters per minute were evaluated. In the replicas, the slipstreams were opacified with isobaric dyes, and images were recorded both on 35 mm film and on SuperVHS high speed video. Data were collected from needles placed radially in the common carotid artery, in the region of the maximal atherosclerotic narrowing, and in the internal carotid artery. Though pressure relationships could not be obtained in the live human for ethical reasons, angiography in a similar stenosis was evaluated for slipstream dynamics. The post-mortem replica had a 55% diameter stenosis (88% area stenosis) of the carotid bulb with a shallow 3 mm ulcer. Flow in the common carotid artery showed undisturbed slipstreams, but as these slipstreams entered the narrow bulb, they crowded together, accelerating dramatically, with a jet continuing distally beyond the maximal narrowing for at least 2 vessel diameters, where flow again became normal. As fluid entered the narrowed bulb, radial pressures decreased and within the ulcer a vortex circulation was found. Similar findings were observed on the angiographic images of the live patient. This combination of events, the slowly swirling fluid in the ulcer, which would allow platelet aggregates to form, and the intermittent low pressure of the Bernoulli effect which could pull the aggregates into the adjacent rapidly flowing blood may help explain how ulcerated carotid plaques lead to embolic stroke.