Rosuvastatin prevents aortic arch plaque progression and improves prognosis in ischemic stroke patients.

OBJECTIVES: Complicated aortic arch plaques (CAP) and their progression are important for recurrent ischemic stroke (IS) and its prognosis. We investigated the effects and clinical benefits of rosuvastatin therapy on this pathophysiology. The purpose of this study was to investigate whether rosuvastatin prevention of aortic arch plaque progression improved the prognosis of IS patients. METHODS: Ninety-seven consecutive acute cerebral embolism patients were retrospectively surveyed. All had transesophageal echocardiography (TEE) to assess the presence or absence of CAP, defined as aortic wall thickness ≥4 mm or plaque ulceration. Patients received conventional antithrombotic therapy as clinically indicated. All patients with CAP were recommended to receive 5 mg rosuvastatin/day, administered by their attending physicians; not all physicians followed this recommendation. Six-month follow-up TEEs were performed in patients with CAP who received rosuvastatin. Major adverse cerebrovascular events (MACEs) comprised recurrent IS and death. RESULTS: CAP was detected in 39 patients (40%), and MACEs in 15. Multivariate regression analysis showed that patients with CAP not taking rosuvastatin was an independent risk factor for MACEs (odds ratio = 18.044; 95% confidential interval = 2.089-155.846, p < 0.01). When patients were divided into three groups: those with CAP taking rosuvastatin, those with CAP not taking rosuvastatin, and those without CAP, Kaplan-Meier analysis demonstrated that patients with CAP not taking rosuvastatin had significantly more MACEs than those in the other two groups (long-rank test; χ2 = 6.553, p < 0.05). Six-month TEE follow-ups in the 26 patients with CAP taking rosuvastatin showed significant improvement in CAP diameter with improved lipid profiles; 88% (23/26 patients) showed no morphological CAP progression; 15 of these showed CAP regression. DISCUSSION: Rosuvastatin therapy prevented aortic arch plaque progression in IS patients with CAP, and may also have long-term clinical benefits.

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.

[Spontaneous regression of primary intracranial germinoma: a case report].

Here we report a case in which an intracranial germinoma displayed spontaneous regression. An 11-year-old boy presented with polyuria and headache. Computed tomography (CT) and magnetic resonance imaging (MRI) revealed tumors in the suprasellar and pineal regions, and obstructive hydrocephalus. As repeat MRI demonstrated shrinkage of these tumors, resection was deferred. The patient was discharged and followed up with serial MRI. The tumor continued to regress for three weeks; however, the patient was readmitted due to tumor regrowth. We performed endoscopic biopsy, and histopathologic diagnosis was germinoma. The patient underwent three courses of combined chemotherapy and radiotherapy, and complete response was achieved. Although the precise cause of the transient regression is unknown, racranial germinoma may occasionally unde rgo spontane ous regression.

A rare case of extraventricular neurocytoma.

We report an unusual case of extraventricular (cerebral) neurocytoma with a long, 25-year history, and which appeared to transform to neuroblastoma. In 1978, an 18-year-old woman was treated for right frontal oligodendroglioma. Eighteen years later (in 1996), recurrence of tumor in the fourth ventricle was noted and was treated with gamma-knife radiotherapy. The tumor shrunk transiently, but 7 years later (in 2004), MRI study demonstrated a second recurrence and ventricular dissemination. Partial removal was performed, and histological examination revealed that tumor cells had round or oval nuclei with halos. Frequent mitoses and vascular proliferation were observed. The MIB-1 LI was 80%. Despite postoperative whole-brain radiotherapy to a total dose of 30 Gy, the tumor progressed, and she died at 4 months after the second surgery.