Plaque Characteristics of Asymptomatic Carotid Stenosis and Risk of Stroke

Abstract

Background: The optimal treatment of asymptomatic carotid stenosis (ACS) is controversial. To optimize the risk-benefit ratio of carotid artery revascularization, it is crucial to identify ACS patients who are at increased stroke risk. Recent data suggest that plaque vulnerability depends on its composition. Therefore, we assessed plaque composition in ACS to determine predictors for ipsilateral cerebrovascular events. Methods: 62 patients with 65 ACS ≥50% underwent 3-T MRI of the carotid bifurcation (TOF, special dark-blood weighted noncontrast and contrast-enhanced T₁ and T₂ images) and of the brain. The different plaque components (lipid core, intraplaque hemorrhage, calcification and the status of the fibrous cap) were assessed. Furthermore, the plaque volume and the volume of clinically silent cortical and subcortical infarcts in the territory of the stenosed carotid artery as seen on FLAIR images were determined by using a semi-automated software. Carotid stenosis was considered asymptomatic if there had not been any clinically apparent ischemic events in the corresponding vascular territory within the previous 6 months. During follow-up, information on the occurrence of cerebrovascular events, medical treatment and sonographic changes of the stenosis was collected. Results: At baseline, 24 ACS (37%) were classified as high grade. A lipid-rich necrotic core was the dominant plaque component in 16 ACS (25%). The plaque volume was higher in ACS with a lipid-rich necrotic core as dominant plaque component (p = 0.002) and in patients with prior stroke/TIA (p = 0.010). After a median follow-up of 18.9 months (interquartile range 3.5–30.1) there were 2 ipsilateral strokes and 3 ipsilateral TIAs. The average annual event rate was 7.7%. A lipid-rich necrotic core (HR 7.21; 95% CI 1.12–46.28; p = 0.037), sonographic progression of the stenosis (HR 7.00; 95% CI 1.13–41.34; p = 0.036), history of stroke (HR 11.03; 95% CI 1.23–99.36; p = 0.032), and the volume of clinically asymptomatic ischemic brain lesions (HR 1.14/cm³; 95% CI 1.03–1.25; p = 0.008) predicted cerebrovascular events. Patients on statin therapy at follow-up were at lower risk of events (HR 0.17; 95% CI 0.03–1.00; p = 0.05). Conclusions: In addition to medical history and sonographic findings, a lipid-rich necrotic core within the plaque turned out as a predictor of cerebrovascular events. Therefore, MR imaging of carotid plaques deserves further attention and might be helpful to improve risk stratification of asymptomatic carotid disease. The identified predictors could be combined in a risk model and tested in larger prospective studies.