Tomoji Takigawa

Cilostazol reduces restenosis after carotid artery stenting

BACKGROUND Although carotid artery stenting (CAS) has been proposed as an alternative to carotid endarterectomy in cerebral revascularization, restenosis remains an unsolved issue. Cilostazol is a unique antiplatelet drug that has vasodilatory effects and inhibits smooth muscle cell proliferation. We investigated whether cilostazol reduces restenosis after CAS. METHODS A database of 113 consecutive CAS procedures between April 2002 and December 2007 was assessed retrospectively. All patients received aspirin (100 mg/d) and another antiplatelet drug such as cilostazol (200 mg/d), ticlopidine (200 mg/d), or clopidogrel (75 mg/d) at least 3 days before CAS. Two antiplatelet drugs were continued for 2 to 3 months after CAS and reduced to one thereafter. Patients were evaluated at 3 and 6 months and at 6-month intervals thereafter with duplex ultrasound (DUS) imaging. Angiography was used for confirmation when stenosis was suspected as >50% with DUS imaging. RESULTS We were able to monitor 97 patients for a 12-month period. The overall combined rate of stroke, myocardial infarction, and death was 3.1% at 30 days and 4.1% at 1 year. In-stent recurrent stenosis was documented in 11 patients (11%); in 10 patients (9.7%), this occurred <or=12 months of CAS. In-stent restenosis was significantly reduced in the cilostazol (+) group (0% vs 15.7% [11 of 70], P = .03). Patient characteristics were similar between the cilostazol (+) and cilostazol (-) groups. CONCLUSIONS Although this study was retrospective and nonrandomized, the results suggest that cilostazol administration improves long-term patency after CAS due to its inhibitory effect on smooth muscle cell growth.

Selective arterial embolization with n-butyl cyanoacrylate in the treatment of aneursymal bone cyst of the thoracic vertebra: a case report.

Study Design. A case report of aneurysmal bone cyst of the mobile spine. Objective. To present a pediatric case of aneurysmal bone cyst (ABC) of the mobile spine treated successfully by selective arterial embolization (SAE) with n-butyl cyanoacrylate (NBCA). Summary of Background Data. The endovascular treatment is an important treatment option for the ABC of the mobile spine. However, there are few reported case treated by SAE with NBCA. Methods. A 12-year-old healthy boy was introduced with a complaint of back pain. Computed tomography showed an osteolytic expanding mass in the pedicle, lamina, and spinous process on the level of T10. Magnetic resonance imaging revealed a multicystic mass with fluid-fluid levels that extended into the spinal canal and compressed the spinal cord from the dorsal side. Digital subtraction angiography showed an abnormal blood supply from the posterior spinal branch of the left T9 artery. An abnormal mass was diagnosed as an ABC based on these neuroradiologic examinations. Result. The patient underwent SAE with NBCA (Histoacryl, B. Braun, Melsungen, Germany) diluted with Lipiodol (Laboratorie Guerbet, France) in a rate of 1:4. Computed tomography performed 1 month after treatment revealed partial ossification of the bone cortex. MR imaging showed shrinkage of the cyst and decompression of the spinal cord. Back pain of the patient disappeared and the shrunken cyst was stable without recurrence during the 3-year follow-up period. Conclusion. SAE in a pediatric case with ABC of the mobile spine was effective in improving of clinical symptom and shrinking of the cyst.

Direct measurement of patient's entrance skin dose during neurointerventional procedure to avoid further radiation-induced skin injuries

Although several cases of radiation-induced skin injury (RSI) have been reported in association with neurointerventional procedures such as endovascular embolization for cerebral aneurysm, cerebral arteriovenous malformation, and dural arteriovenous fistula, in most cases the absorbed doses are not measured directly; therefore, we built the first direct measurement system that enables the ideal dosimetry for entrance skin dose (ESD) during neurointerventional procedures to be easily determined. This system was then applied to a 55-year-old man who underwent two transvenous embolizations with a 2-month interval, for a right cavernous sinus dural arteriovenous fistula, to establish the efficacy of precise mapping of ESDs. Throughout the procedures, the patient wore a fitted dosimetry cap that contained 60 radiophotoluminescence glass dosimeter (RPLGD) chips. After the first procedure, temporary epilation occurred in the occipital region. Precise mapping of ESDs revealed that this region was exposed to 4.2Gy. In the first procedure, the X-ray tube was generally positioned straight for an optimal posterior-anterior view; however, in the second procedure we intermittently used the second-best position to prevent further RSI. In this position, the maximum ESD was 1.0Gy in the right posterior-temporal region and the epilation site was exposed to </=0.7Gy. Thus, the patient did not develop any further epilation. We conclude that direct dosimetry using multiple RPLGDs can accurately reveal the maximum ESD and that precise information regarding ESD can prevent further RSIs from subsequent procedures.

Percutaneous transluminal angioplasty for atherosclerotic stenoses of intracranial vessels.

To study the efficacy and long-term outcome of percutaneous transluminal angioplasty (PTA) with/without stent placement for intracranial atherosclerotic stenoses, we reviewed our treated cases retrospectively. Between May 1992 and October 2003, PTA with/without stents was performed in 64 intracranial and skull base vessels in 62 patients, including 24 middle cerebral arteries, 16 internal carotid arteries, 13 vertebral arteries, and 11 basilar arteries. PTA was technically successful in 55 vessels (86%). However, four vessels (6%) failed to achieve satisfactory dilatation. We encountered five periprocedural strokes as symptomatic complications, for a mortality rate of 4.7% and a morbidity rate of 3.1%. All the patients with stent placements survived angioplasty without any complication. In the clinical follow-up available for one week to 11.5 years (mean, 4.7 years), there were three strokes related to the treated vessels. The annual stroke rate in the affected territory was estimated at 1.2% per year. According to these results, PTA for intracranial atherosclerotic stenoses seems to be a beneficial therapy for immediate anatomical results and long-term stroke prevention. Stent-assisted PTA could help patients achieve successful dilatation and avoid complications.

Cilostazol suppression of arterial intimal hyperplasia is associated with decreased expression of sialyl Lewis X homing receptors on mononuclear cells and E-selectin in endothelial cells

BACKGROUND An inflammatory reaction in vascular tissue is a potential factor linking restenosis after angioplasty. Although cilostazol, a selective phosphodiesterase type 3 inhibitor that is a unique antiplatelet drug and vasodilator, has been reported to be anti-inflammatory, its effect on the inflammatory action of mononuclear cells homing to endothelial cells is not clearly understood. In this study, whether cilostazol inhibits neointimal formation and improves inflammatory actions by inhibiting sialyl Lewis X (SLX) expression on mononuclear cells and E-selectin expression on endothelial cells was evaluated. METHODS The effect of cilostazol (1, 3, 10, 30 μM) on expression of E-selectin in human umbilical vein endothelial cells and SLX in rat mononuclear cells stimulated with lipopolysaccharide by immunofluorescence and real-time polymerase chain reaction (n = 3) was studied. Additionally, a double-balloon injury model was used on rat carotid arteries to evaluate vascular intimal hyperplasia. 0.1% cilostazol was administered 3 days before the first balloon injury, and the second balloon injury was performed 7 days after the first injury. Cilostazol administration was continued until rats were sacrificed 14 days after the second angioplasty. The expression of SLX on mononuclear cells and E-selectin on endothelial cells by immunofluorescence (n = 10) and real-time polymerase chain reaction (n = 5) were studied. RESULTS Cilostazol effectively inhibited the expression of SLX on mononuclear cells and E-selectin on endothelial cells. Cilostazol inhibited the migration of mononuclear cells in neointimal regions and neointimal hyperplasia after balloon injury. The numbers of macrophages and T-lymphocytes and the hyperplasia area in neointimal regions decreased from 71.06 ± 20.04, 1121 ± 244.4 cells per section, 206,400 ± 96,150 mm(2) to 29.65 ± 16.73, 374.2 ± 124.5 cells per section, and 101,900 ± 16,150 mm(2) due to the administration of cilostazol. CONCLUSIONS These results demonstrate that the protective effect of cilostazol against neointimal hyperplasia may be mediated by its anti-inflammatory actions of mononuclear cells homing to endothelial cells by decreasing SLX and E-selectin expression. CLINICAL RELEVANCE It is reported that cilostazol inhibits neointimal hyperplasia by decreasing the expression of some cell-adhesion molecules. We evaluated the effects of cilostazol for the expression of sialyl Lewis X (SLX) on mononuclear cells and E-selectin on endothelial cells, which interaction is the first step of inflammation action. Cilostazol was thought to show the anti-inflammatory actions by decreasing SLX and E-selectin expression in addition to decreasing the expression of some cell-adhesion molecules.

Bioactive Coils Cause Headache and Fever After Endovascular Treatment of Intracranial Aneurysms

Background.— Based on our encounters with patients who have been treated for unruptured intracranial aneurysms by endovascular coil embolization using bioactive coils, we observed that such patients often present with headaches and fever.

Double-balloon Remodeling for Coil Embolization of a Primitive Trigeminal Artery Variant Aneurysm: A Case Report

Here we describe the case of a patient with a wide-necked unruptured aneurysm arising at origin of a persistent primitive trigeminal artery (PTA) variant from the right internal carotid artery (ICA), supplying the territory of the right superior cerebellar artery and the anterior inferior cerebellar artery. To preserve the ICA and the PTA variant, coil embolization of the aneurysm was performed using a double-balloon remodeling technique (HyperForm™ and Hyper-Glide™ Occlusion Balloon Systems; ev3 Endovascular Inc., Irvine, CA, USA). The association of a PTA variant with an aneurysm is very rare. To our knowledge, this is the first description of the use of coil embolization using double-balloon remodeling to treat a PTA variant aneurysm. This technique permits complete embolization and reduces the risk of cerebral and cerebellar ischemia.

Spinal Cord Infarction in the Region of the Posterior Spinal Artery After Embolization for Vertebral Artery Dissection

BACKGROUND Endovascular surgery for vertebral artery dissections (VADs) carries the risk of spinal cord infarction (SCI). Although SCI in the region of the anterior spinal artery (ASA) has been reported, SCI in the region of the posterior spinal artery (PSA) is rare. OBJECTIVE To investigate PSA infarction after endovascular surgery for VAD. METHODS Infarction in the region of the PSA after endovascular surgery for VADs carried out in consecutive 21 cases was investigated. The variables of aneurysmal location, status, intra-aneurysmal thrombosis, antithrombotic therapy, and endovascular procedure were investigated in relation to the occurrence of spinal cord or brain stem infarction. RESULTS Thirteen cases were unruptured aneurysms, and 8, ruptured aneurysms. The endovascular surgical method was internal trapping in 10 cases, stent-assisted coil embolization in 8 cases, and proximal occlusion (PO) in 3 cases. Periprocedural symptomatic infarction was detected in 4 of the 21 cases (19%): 3 SCIs and 1 lower medulla infarction, after 1 stent-assisted coil embolization and 3 PO. All 3 symptomatic SCIs were PSA infarction. On univariate analysis, the variables of posterior inferior cerebellar artery-involved-type, PO, and intraprocedural proximal flow arrest were significantly correlated with occurrence of PSA infarction. CONCLUSION PSA infarction after endovascular surgery for VAD seems not to be a rare potential complication. Insufficiency of collateral blood flow and artery-to-artery embolism due to intraprocedural flow stagnation of the VA seem to be the possible mechanisms of PSA infarction in addition to previously reported mechanisms such as direct obliteration by the embolic materials and extended thrombosis of the VA stump.

Treatment Strategy Based on Plaque Vulnerability and the Treatment Risk Evaluation for Internal Carotid Artery Stenosis

Carotid endarterectomy (CEA) and carotid artery stenting (CAS) are not appropriate treatment procedure for internal carotid artery stenosis (ICAS) in some patients. The importance of plaque vulnerability and the treatment risk evaluation has been reported. We analyzed whether treatment selection contributes to the outcome. We retrospectively examined 121 patients who underwent CEA or CAS. Treatment was selected based on plaque vulnerability and the treatment risk evaluation. We selected CAS for patients with stable plaques and CEA for patients with unstable plaques, and considered the other treatment for high-risk patients. The patients were classified as the stable plaque (Stable: n = 42), the unstable plaque and CEA low risk (Unstable/Low: n = 30), and the CEA high-risk (Unstable/High: n = 49). Frequency of perioperative stroke, myocardial infarction, death, and systemic complications was examined. CEA and CAS were performed in 35 and 86 patients, respectively. One patient (2.9%) had a stroke in CEA and five patients (5.8%) in CAS (P = 0.50). Systemic complications were observed in two patients (5.7%) in CEA and six (7.1%) in CAS (P = 0.80). There were no differences in stroke (Stable; 2.4%, Unstable/Low; 3.2%, and Unstable/High; 8.2%) and systemic complications (Stable; 9.5%, Unstable/Low; 3.3%, and Unstable/High; 6.1%) among three groups (P = 0.44 and P = 0.59, respectively). The treatment selection based on plaque vulnerability and the treatment risk evaluation could provide good treatment outcome for high-risk patients. It is ideal to select an appropriate treatment for ICAS by one neurovascular team.