Ryu Fukumitsu

Cerebral infarction due to an embolism after cervical pedicle screw fixation.

Study Design. Case report and clinical discussion. Objective. We report a rare case of delayed onset of cerebral infarction caused by an embolism after cervical pedicle screw (CPS) fixation. Summary of Background Data. CPS has a risk of vertebral artery (VA) injury. CPSs sometimes breach the transverse foramen without rupture of the VA. Most breaches are not considered harmful. Methods. We present a case in a 71-year-old man who underwent an operation for CPS fixation and laminoplasty for cervical spondylomyelopathy. He presented symptoms of hemiparesis 3 days after the operation. The left C4 pedicle screw was proven to breach the transverse foramen. An angiogram showed a thrombus cranial to the screw. Results. The patient underwent anticoagulation therapy without removal of screw. After 2 weeks, the thrombus had disappeared. Subsequently, the pedicle screws were removed. At final follow-up, the patient complained of a grade 4/5 hemiparesis, facial nerve palsy, and hearing loss in his left ear. Conclusion. To our knowledge, this is the first case report of delayed onset of cerebral infarction caused by an embolism after CPS fixation. When a CPS perforates the transverse foramen, even if no apparent VA injury occurs during the operation, the surgeon must take care not to risk cerebral infarction because of an embolism.

The association between expansive arterial remodeling detected by high-resolution MRI in carotid artery stenosis and clinical presentation

OBJECT The purpose of the present study was to investigate the association between carotid artery (CA) expansive remodeling (ER) and symptoms of cerebral ischemia. METHODS One hundred twenty-two consecutive CAs scheduled for CA endarterectomy (CEA) or CA stent placement (CAS) were retrospectively studied. After excluding 22 CAs (2 were contraindicated for MRI, 8 had near-occlusion, 6 had poor image quality, and 6 had restenosis after CEA or CAS), there were 100 CAs (100 patients) included in the final analysis. The study included 50 symptomatic patients (mean age 73.6 ± 8.9 years, 6 women, mean stenosis 68.5% ± 21.3%) and 50 asymptomatic patients (mean age 72.0 ± 5.9 years, 5 women, mean stenosis 79.4% ± 8.85%). Expansive remodeling was defined as enlargement of the internal carotid artery (ICA) with outward plaque growth. The ER ratio was calculated by dividing the maximum distance between the lumen and the outer borders of the plaque perpendicular to the axis of the ICA by the maximal luminal diameter of the distal ICA at a region unaffected by atherosclerosis using long-axis, high-resolution MRI. RESULTS The ER ratio of the atherosclerotic CA was significantly greater than that of normal physiological expansion (carotid bulb; p < 0.01). The ER ratio of symptomatic CA stenosis (median 1.94, interquartile range [IQR] 1.58-2.23) was significantly greater than that of asymptomatic CA stenosis (median 1.52, IQR 1.34-1.81; p = 0.0001). When the cutoff value of the ER ratio was set to 1.88, the sensitivity and specificity to detect symptoms were 0.6 and 0.78, respectively. The ER ratio of symptomatic patients was consistently high regardless of the degree of stenosis. CONCLUSIONS There was a significant correlation between ER ratio and ischemic symptoms. The ER ratio might be a potential indicator of vulnerable plaque, which requires further validation by prospective observational study of asymptomatic patients.

Carotid artery plaque assessment using quantitative expansive remodeling evaluation and MRI plaque signal intensity

OBJECTIVE Plaque characteristics and morphology are important indicators of plaque vulnerability. MRI-detected intraplaque hemorrhage has a great effect on plaque vulnerability. Expansive remodeling, which has been considered compensatory enlargement of the arterial wall in the progression of atherosclerosis, is one of the criteria of vulnerable plaque in the coronary circulation. The purpose of this study was risk stratification of carotid artery plaque through the evaluation of quantitative expansive remodeling and MRI plaque signal intensity. METHODS Both preoperative carotid artery T1-weighted axial and long-axis MR images of 70 patients who underwent carotid endarterectomy (CEA) or carotid artery stenting (CAS) were studied. The expansive remodeling ratio (ERR) was calculated from the ratio of the linear diameter of the artery at the thickest segment of the plaque to the diameter of the artery on the long-axis image. Relative plaque signal intensity (rSI) was also calculated from the axial image, and the patients were grouped as follows: Group A = rSI ≥ 1.40 and ERR ≥ 1.66; Group B = rSI< 1.40 and ERR ≥ 1.66; Group C = rSI ≥ 1.40 and ERR < 1.66; and Group D = rSI < 1.40 and ERR < 1.66. Ischemic events within 6 months were retrospectively evaluated in each group. RESULTS Of the 70 patients, 17 (74%) in Group A, 6 (43%) in Group B, 7 (44%) in Group C, and 6 (35%) in Group D had ischemic events. Ischemic events were significantly more common in Group A than in Group D (p = 0.01). CONCLUSIONS In the present series of patients with carotid artery stenosis scheduled for CEA or CAS, patients with plaque with a high degree of expansion of the vessel and T1 high signal intensity were at higher risk of ischemic events. The combined assessment of plaque characterization with MRI and morphological evaluation using ERR might be useful in risk stratification for carotid lesions, which should be validated by a prospective, randomized study of asymptomatic patients.

Expression of Vasohibin-1 in Human Carotid Atherosclerotic Plaque

AIM In patients with carotid plaque, intraplaque hemorrhage arising from ruptured neovascular vessels within the neointima is an important cause of stroke. The expression of Vasohibin-1 (VASH1), a negative feedback regulator of angiogenesis, occurs in the microvessel endothelial cells of various solid tumors and the arterial wall. However, the roles of VASH1 in the pathogenesis of atherosclerotic diseases remain unclear. The present study aimed to clarify the relevance of the VASH1 expression and plaque instability in human carotid plaques. METHODS We used quantitative real-time PCR and immunostaining to examine 12 atheromatous plaque specimens obtained via carotid endarterectomy. The distal areas of specimens lacking macroscopic atherosclerotic lesions served as controls. RESULTS Compared with that observed in the controls, the VASH1 gene expression increased significantly in the atheromatous plaque (p=0.018). Moreover, the VASH1 mRNA levels correlated positively with those of VEGFA, CD31 and VCAM1 (r=0.788, p=0.004; r=0.99, p ＜ 0.001; r=0.94, p ＜ 0.001, respectively). Finally, the immunohistochemical analyses revealed the VASH1 expression in the neointimal microvessel endothelial cells of carotid plaque. CONCLUSIONS The VASH1 expression levels in atheroma reflect both enhanced neovascularization and the inflammatory burden. Therefore, the VASH1 level may be a novel biomarker for evaluating plaque instability in patients with carotid arteriosclerosis and predicting ischemic stroke.

Endoglin (CD105) is a more appropriate marker than CD31 for detecting microvessels in carotid artery plaques.

Background: Microvascular proliferation is a major risk factor for plaque vulnerability in patients with carotid stenosis. There are several vascular endothelial markers such as CD31 and CD105, but it is unclear which marker is most sensitive for microvessels. This study sought to examine the correlations between CD31 and CD105 expression in microvessels on carotid plaques and clinical manifestations. Methods: We studied 13 lesions in 12 patients. The patients underwent carotid endarterectomy and samples were stained for CD31 and CD105. The numbers of microvessels positive for these markers within a field of view were counted. Results: The average numbers of microvessels were 5.8 ± 5.4 for CD31 and 9.2 ± 9.3 for CD105 (P = 0.04). More microvessels were positive for CD105 than there were for CD31 in patients with diabetes mellitus (P = 0.04). Conclusion: In patients with carotid artery stenosis, CD105 is more appropriate than CD31 for detecting microvessels in carotid plaques. In patients with diabetes mellitus, CD105 is significantly more highly expressed in microvessels than CD31.