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Comparison of Symptomatic and Asymptomatic Atherosclerotic Carotid Plaque Features with in Vivo MR Imaging¹

¹ From the Departments of Radiology (T.S., M.S.F., C.Y.) and Surgery (T.S.H.), University of Washington, 815 Mercer St, Box 358050, Seattle, WA 98109; Department of Radiology, People's Liberation Army General Hospital, Beijing, China (J.C., L.M., Y.Q.C.); Mountain-Whisper-Light Statistical Consulting, Seattle, Wash (N.L.P.); and Veterans Affairs Puget Sound Health Care System, Seattle, Wash (T.S.H.). Received March 7, 2005; revision requested May 2; revision received July 18; accepted August 11; final version accepted October 3. Supported by NIH grants R01HL56874, P01HL072262, and R01HL073401. Address correspondence to T.S. (e-mail: Tobias.Saam{at}med.uni-muenchen.de).

Purpose: To retrospectively determine if in vivo magnetic resonance (MR) imaging can simultaneously depict differences between symptomatic and asymptomatic carotid atherosclerotic plaque.

Materials and Methods: Institutional review board approval and informed consent were obtained for this HIPAA-compliant study. Twenty-three patients (21 men, two women; mean age, 66.1 years ± 11.0 [standard deviation]) with unilateral symptomatic carotid disease underwent 1.5-T time-of-flight MR angiography and 1.5-T T1-, intermediate-, and T2-weighted MR imaging. Both carotid arteries were reviewed. One observer recorded quantitative and morphologic information, which included measurement of the area of the lumen, artery wall, and main plaque components; fibrous cap status (thick, thin, or ruptured); American Heart Association (AHA) lesion type (types I–VIII); and location (juxtaluminal vs intraplaque) and type of hemorrhage. Plaques associated with neurologic symptoms and asymptomatic plaques were compared with Wilcoxon signed rank and McNemar tests.

Results: Compared with asymptomatic plaques, symptomatic plaques had a higher incidence of fibrous cap rupture (P = .007), juxtaluminal hemorrhage or thrombus (P = .039), type I hemorrhage (P = .021), and complicated AHA type VI lesions (P = .004) and a lower incidence of uncomplicated AHA type IV and V lesions (P = .005). Symptomatic plaques also had larger hemorrhage (P = .003) and loose matrix (P = .014) areas and a smaller lumen area (P = .008). No significant differences between symptomatic and asymptomatic plaques were found for quantitative measurements of the lipid-rich necrotic core, calcification, and the vessel wall or for the occurrence of intraplaque hemorrhage or type II hemorrhage.

Conclusion: This study revealed significant differences between symptomatic and asymptomatic plaques in the same patient.

© RSNA, 2006

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