Rosuvastatin Improves Plaque Morphology in Cerebral Embolism Patients with Normal Low-Density Lipoprotein and Severe Aortic Arch Plaque

The effect of rosuvastatin was investigated on complicated aortic arch plaque (CAP) morphology and lipid profiles in acute cerebral embolism (CE) patients with normal low-density lipoprotein-cholesterol (LDL-c) levels. Transesophageal echocardiography (TEE) studies were performed in 56 consecutive CE patients with LDL-c less than 140 mg/dL who were not taking lipid-lowering agents at baseline. CAP observed by TEE was defined as the presence of greater than 4-mm diameter, ulcerated, or mobile aortic plaque. Patients were divided into those with CAP versus without CAP (group A, n = 24, age 69 ± 8 years) and without CAP (group B, n = 32, age 62 ± 10 years). Of the 24 group A patients, 18 received 5 mg/d of rosuvastatin for 6 months and had follow-up TEE studies. In Group A, the baseline values of high-density lipoprotein-cholesterol (HDL-c) and apolipoprotein A-1 (ApoA-1) were significantly lower than in Group B (44 ± 15 versus 55 ± 15 mg/dL, P = .0059; 103 ± 19 versus 137 ± 25 mg/dL, P = .0006, respectively) and age and serum high-sensitivity C-reactive protein concentration were significantly higher (69 ± 8 vs. 62 ± 10 years, P = .0080; 2.34 ± 3.05 vs. 0.67 ± 1.00 mg/dL, P = .0054, respectively). By multivariate logistic regression analysis, ApoA-1 was shown to be an independent predictor of CAP (odds ratio = .894, 95% confidence intervals .800-.996, P = .0483). In the 18 group A patients receiving rosuvastatin for 6 months, aortic arch plaque diameter and serum LDL-c were significantly decreased (5.8 ± 2.2 to 5.1 ± 2.1 mm, P = .0377; 110 ± 23 to 81 ± 23 mg/dL, P = .0008, respectively), whereas serum HDL-c and ApoA-1 concentrations were significantly increased (42 ± 8 to 52 ± 9 mg/dL, P = .0002; 109 ± 22 to 135 ± 15 mg/dL, P = .0002, respectively). Plaques were morphologically improved in 11 patients, unchanged in 6, and worsened in 1. These data suggest that rosuvastatin improves plaque morphology concomitant with improving lipid profiles in CE patients with normal LDL-c levels.