Impact of Cilostazol Pharmacokinetics on the Development of Cardiovascular Side Effects in Patients with Cerebral Infarction.

This study investigated the impact of polymorphisms of metabolic enzymes on plasma concentrations of cilostazol and its metabolites, and the influence of the plasma concentrations and polymorphisms on the cardiovascular side effects in 30 patients with cerebral infarction. Plasma concentrations of cilostazol and its active metabolites, and CYP3A5*3 and CYP2C19*2 and *3 genotypes were determined. The median plasma concentration/dose ratio of OPC-13213, an active metabolite by CYP3A5 and CYP2C19, was slightly higher and the median plasma concentration rate of cilostazol to OPC-13015, another active metabolite by CYP3A4, was significantly lower in CYP3A5*1 carriers than in *1 non-carriers (p = 0.082 and p = 0.002, respectively). The CYP2C19 genotype did not affect the pharmacokinetics of cilostazol. A correlation was observed between changes in pulse rate from the baseline and plasma concentrations of cilostazol (R = 0.539, p = 0.002), OPC-13015 (R = 0.396, p = 0.030) and OPC-13213 (R = 0.383, p = 0.037). A multiple regression model, consisting of factors of the plasma concentration of OPC-13015, levels of blood urea nitrogen, and pulse rate at the start of the therapy explained 55.5% of the interindividual variability of the changes in pulse rate. These results suggest that plasma concentrations of cilostazol and its metabolites are affected by CYP3A5 genotypes, and plasma concentration of OPC-13015, blood urea nitrogen, and pulse rate at the start of therapy may be predictive markers of cardiovascular side effects of cilostazol in patients with cerebral infarction.

A novel technique to visualize true lumen in endovascular treatment of the occlusive carotid dissection and the usefulness of external-internal carotid collateral channel.

Background Dissection of the internal carotid artery (ICA) can cause occlusion or severe stenosis and is known to be one of the major causes of ischemic stroke in the young. Endovascular treatment is one of the useful options for carotid dissections, but passing the guidewire through the occlusion (lesion-cross) and confirmation of the true lumen are sometimes difficult. Case presentation A 40-year-old right-handed man complaining of dysarthria and gait disturbance consulted our hospital. Magnetic resonance imaging and angiography revealed right ICA dissection. Because of worsening symptoms with conservative treatment, we performed endovascular treatment. Prior to the lesion-cross, a microcatheter was navigated to the third segment of the internal maxillary artery and a balloon-guiding catheter was navigated to the proximal ICA. Under balloon occlusion of the ICA, superselective angiography via the ipsilateral maxillary artery and slow evacuation from the balloon-guiding catheter were performed. Thereafter, the course of the true lumen was clearly visualized, and we were able to navigate another microcatheter without difficulty. Subsequently, angioplasty and stent placement were successfully accomplished. Conclusion We presented a case of ICA dissection and demonstrated a novel technique for a safe lesion-cross for occlusive ICA dissection.

Riles type 1A common carotid artery occlusion diagnosed by specific external carotid artery Doppler waveform pattern in carotid ultrasonography. Case report.

A 67-year-old man was admitted for evaluation of left homonymous hemianopsia. Carotid ultrasonography showed that the right common carotid artery (CCA) was occluded up to just proximal to the carotid bifurcation, and the patent external carotid artery showed retrograde flow to the patent internal carotid artery via the carotid bifurcation. The Doppler waveform pattern of the external carotid artery showed high end-diastolic flow velocity and low pulsatility index. The diagnosis was Riles type 1A CCA occlusion. Digital subtraction angiography and iodine-123 N-isopropyl-p-iodoamphetamine single photon emission computed tomography were performed to confirm the collateral circulation and adequate intracranial hemodynamic sufficiency. Nonsurgical treatment with antiplatelet therapy was performed for the CCA occlusion. No stroke events have occurred within the 2-year follow-up period.

Surgery after radiosurgery for acoustic neuromas: surgical strategy and histological findings.

OBJECTIVE: To retrospectively review the authors' experience with surgical resections after failed radiosurgery for acoustic neuromas. METHODS: The study group consisted of six patients with acoustic neuromas. The median age was 61 years (range, 18-72 yr). The median marginal radiation dose was 11 Gy (range, 10-12.5 Gy). The median interval between radiosurgery and surgical resection was 28 months (range, 4-74 mo). The operative indications were cerebellar ataxia and symptoms associated with increased intracranial pressure. The median follow-up period was 36 months (range, 11-72 mo) after surgical resection. RESULTS: The tumors were subtotally removed (> or = 80%) in four patients and partially removed (< 80%) in the other two patients. Three patients had intratumoral bleeding. Preexisting facial nerve palsy improved in two patients and deteriorated in one patient, and one patient experienced new facial palsy. No other new neurological deficits emerged after surgery. Histological features were typical of acoustic schwannoma, and some tumors were associated with foamy macrophages, myxoid degeneration, and necrosis attributed to radiation effects. At follow-up, the residual tumor was decreased in five patients and increased in one patient with an expanding intratumoral hematoma. CONCLUSION: Surgical resection after radiosurgery is indicated in the presence of such symptoms as cerebellar ataxia and increased intracranial pressure. It must be carefully considered because of the natural regression of transient tumor swelling over time. Surgical resection should be limited to subtotal removal for functional preservation. In patients with tumor enlargement several years after radiosurgery, the possibility of chronic intratumoral bleeding resulting from delayed radiation injury must be considered.