Evolution of Atherosclerotic Carotid Plaque Morphology: Do Ulcerated Plaques Heal? A Serial Multidetector CT Angiography Study

<i>Background:</i> Atherosclerotic carotid plaque rupture may lead to thromboembolization, causing transient ischemic attack or ischemic stroke. Carotid plaque ulceration on angiography is associated with plaque rupture. Although healing of ruptured plaques has been described in coronary arteries, little is known about the natural development of plaque ulcerations in carotid arteries. We therefore explored the evolution of carotid plaque surface morphology with serial multidetector CT angiography (MDCTA). <i>Methods:</i> From a registry of patients with transient ischemic attack or minor ischemic stroke, we selected 83 patients who had undergone serial MDCTA of the carotid arteries. Arteries subjected to revascularization procedures between the two scans were excluded (n = 11). Plaque surface morphology was classified as smooth, irregular or ulcerated on both baseline and follow-up MDCTA. Progression (i.e. development of irregularities or ulceration) and regression (i.e. disappearance of irregularities or ulceration) in morphology were evaluated. <i>Results:</i> The mean time interval between the MDCTA scans was 21 ± 13 months. At baseline, 28 (18%) arteries were normal, 124 (80%) contained atherosclerotic plaque and 3 (2%) were occluded. Plaque surface morphology was smooth in 86 arteries (55%), irregular in 23 (15%) and ulcerated in 15 (10%). At follow-up, surface morphology was unchanged in 88% of arteries, had progressed in 8% and regressed in 4%. Most importantly, plaque morphology remained unchanged in most ulcerated plaques (10/15; 67%). One ulcerated plaque had progressed, whereas 4 had regressed. New ulcerations had developed in 2 nonulcerated plaques. <i>Conclusion:</i> MDCTA allows evaluation of temporal changes in atherosclerotic carotid plaque morphology. Plaque surface morphology remained unchanged in most arteries. Carotid ulcerations persist for a long time, and may remain a potential source of thromboembolism.