High-Intensity Signals in Carotid Plaques on T1-Weighted Magnetic Resonance Imaging Predict Coronary Events in Patients With Coronary Artery Disease

Objectives The purpose of this study was to determine whether high-intensity carotid plaques visualized by a noncontrast T1-weighted imaging technique, magnetization-prepared rapid acquisition with gradient echo (MPRAGE), predict future coronary events in patients with clinically stable coronary artery disease (CAD). Background Coronary plaque vulnerability to rupture can be assessed by examining for the presence of atherosclerosis and measuring intima media thickness (IMT) in surrogate vessels such as the carotid arteries. We previously showed that MPRAGE successfully identifies vulnerable carotid plaques as high-intensity signals. It remains unclear, however, if the presence of carotid high-intensity plaques (HIP) is associated with an increased risk of coronary events. Methods We examined the signal intensity of carotid plaques in 217 patients with clinically stable CAD using MPRAGE with magnetic resonance imaging and measured IMT with ultrasonography. A carotid HIP was defined as a signal >200% that of the adjacent muscle. All patients were divided into 2 groups according to the presence or absence of HIP, namely, the HIP group (n = 116) and the non-HIP group (n = 101), and were followed up for as long as 72 months. Results The presence of HIP was significantly associated with cardiac events compared to the non-HIP group (log-rank p < 0.0001). Furthermore, multivariate Cox regression analysis identified the presence of HIP as the strongest independent predictor of cardiac events (hazard ratio: 3.15; 95% confidence interval: 1.93 to 5.58, p < 0.0001) compared with IMT (hazard ratio: 1.62, 95% confidence interval: 0.97 to 2.44, p = 0.055) and other coronary risk factors. Conclusions Characterization of carotid plaques using magnetic resonance imaging with MPRAGE provides more clinically relevant information for the risk assessment of CAD patients than IMT. (J Am Coll Cardiol 2011;58:416-22) (C) 2011 by the American College of Cardiology Foundation