Human and animal studies have revealed a stabilization of atherosclerotic plaques by statins. However, the stabilization of human carotid plaques has not been thoroughly described pathologically. This analysis explored the relationship between statin therapy and plaque stability in carotid endarterectomy (CEA) specimens. We analyzed specimens harvested between May 2015 and February 2017, from 79 consecutive patients presenting with > 70% carotid artery stenoses, of whom 66 were untreated (group 1) and 13 treated (group 2) with a statin. Immunohistochemistry was performed, using an endothelial specific antibody to CD31, CD34 and platelet derived growth factor receptor-β. The prevalence of plaque ruptures (P = 0.009), lumen thrombi (P = 0.009), inflammatory cells (P = 0.008), intraplaque hemorrhages (P = 0.030) and intraplaque microvessels (P < 0.001) was significantly lower in group 2 than in group 1. Among 66 patients presenting with strokes and infarct sizes > 1.0 cm3 on magnetic resonance imaging, the mean infarct volume was significantly smaller (P = 0.031) in group 2 (4.2 ± 2.5 cm3) than in group 1 (8.2 ± 7.1 cm3). The difference in mean concentration of low-density lipoprotein cholesterol between group 1 (121 ± 32 mg/dl) and group 2 (105 ± 37 mg/dl) was non-significant (P = 0.118). This analysis of plaques harvested from patients undergoing CEA suggests that statin therapy mitigates the plaque instability, which, in patients presenting with strokes, might decrease infarct volume.Electronic supplementary materialThe online version of this article (10.1007/s00380-018-1193-6) contains supplementary material, which is available to authorized users.

Background: Unstable atherosclerotic carotid plaques cause cerebral thromboemboli and ischemic events. However, this instability has not been pathologically quantified, so we sought to quantify it in patients undergoing carotid endarterectomy (CEA). Methods and Results:Carotid plaques were collected during CEA from 67 symptomatic and 15 asymptomatic patients between May 2015 and August 2016. The specimens were stained with hematoxylin-eosin and elastica-Masson. Immunohistochemistry was performed using an endothelial-specific antibody to CD31, CD34 and PDGFRβ. The histopathological characteristics of the plaques were studied. By multiple-variable logistic regression analysis, plaque instability correlated with the presence of plaque rupture [odds ratio (OR), 9.75; P=0.013], minimum fibrous cap thickness (OR per 10 μm 0.70; P=0.025), presence of microcalcifications in the fibrous cap (OR 7.82; P=0.022) and intraplaque microvessels (OR 1.91; P=0.043). Receiver-operating characteristics analyses showed that these factors combined into a single score diagnosed symptomatic carotid plaques in patients with carotid artery stenosis with a high level of accuracy (area under the curve 0.92; 95% confidence interval 0.85-0.99 vs. asymptomatic).Conclusions: This analysis of carotid plaque instability strongly suggested that the diagnostic scoring of carotid plaque instability improves the understanding and treatment of carotid artery disease in patients undergoing CEA.

Intracranial hemorrhages can occur after carotid revascularization due to cerebral hyperperfusion syndrome (CHS). Subarachnoid hemorrhages associated with CHS after carotid artery stenting (CAS) have been reported in many cases; however, they are rare after carotid endarterectomy (CEA). We report a case of subarachnoid hemorrhage (SAH) associated with CHS after CEA performed in the acute phase of a cerebral infarction. A 50-year-old man was admitted to our hospital with transient right hemiparesis and dysarthria. Magnetic resonance imaging (MRI) demonstrated a cerebral infarction in the left cerebral hemisphere. Digital subtraction angiography revealed a severe stenosis in the right cervical internal carotid artery. Medical treatment was started; however, cerebral infarction progressed. CEA was performed on the 7th day after admission. On the first postoperative day, MRI demonstrated SAH in the sulcus of the frontal and parietal lobes. Xenon CT revealed an increased cerebral blood flow (CBF) in the left cerebral hemisphere. We diagnosed CHS after CEA. We continued sedation using Propofol and maintained the systolic blood pressure below 120 mmHg using nicardipine. Sedation was stopped on postoperative day 3. The patient was discharged with slight dysarthria on postoperative day 17. SAH due to CHS is rare but can occur early after CEA. Careful patient management is required after CEA in consideration of SAH due to CHS.

No abstract

Background Scintillating scotoma caused by optic nerve compression by aneurysm is rare. We report a case of scintillating scotoma following optic nerve compression caused by an unruptured anterior communicating artery aneurysm. Case presentation A 64-year-old woman visited our department with a scintillating scotoma. Magnetic resonance imaging demonstrated no new lesions, although her previously diagnosed anterior communicating artery aneurysm had increased in size. Thus, we performed neck clipping. The operative view showed that the aneurysm compressed the right optic nerve. Her symptoms disappeared after the operation. These findings suggest that scintillating scotoma may be caused by compression of the optic nerve by the anterior communicating artery aneurysm. Conclusion Although scintillating scotoma is a common condition, aneurysms should be considered as a potential cause.