RESUMEN
Objective: The most important function required for the stroke center is prompt treatment for acute stroke. We report the initial results of stroke care under the new medical care system of stroke center in a new hospital that merges three hospitals with different management bases to verify the effect of stroke center on mechanical thrombectomy. Methods: We investigated changes in the number of inpatients and surgical treatments compared with the past 3 years (Stages I, II, and III) with stage IV one year after the new hospital was opened, and examined the effect of establishing a stroke center on mechanical thrombectomy for acute main cerebral artery occlusion. Results: From stage I to stage IV, the number of hospitalized patients increased from 396, 485, 482 to 630, respectively, and the proportion of patients with cerebrovascular disease increased from 57.6%, 55.7%, 60.4% to 68.3%, respectively. Total surgical treatment increased from 137, 195, 224 to 297, respectively, especially endovascular therapy increased markedly from 22, 36, 68 to 118, respectively. The main treatment contents of endovascular treatment in stage IV were ruptured cerebral aneurysm embolization 22 cases, unruptured cerebral aneurysm embolization 13 cases, carotid artery stenting 23 cases, other intracranial or extracranial artery angioplasty/stenting 9 cases, and mechanical thrombectomy 34 cases. In particular, mechanical thrombectomy was significantly increased to 34 in stage IV, compared to 4 in stage I, 4 in stage II, and 17 in stage III (degree of contribution [DC] 25.0%, contribution ratio [CR] 34.0%). Conclusion: With the establishment of the stroke center, the number of cases of acute cerebral infarction within the adaptation time who received mechanical thrombectomy remarkably increased. It is considered that the effect and validity of function aggregation by establishing stroke center are shown.
RESUMEN
A case in which metallic embolism was suspected after carotid artery stenting (CAS) is described. A 79-year-old woman was referred to our hospital because of a severe stenosis of the left cervical internal carotid artery (ICA). Carotid ultrasound revealed that the plaque was fibrous and was accompanied with partial calcification. The carotid stenosis was treated by CAS. The magnetic resonance imaging (MRI) taken in the following day of the CAS demonstrated that a new abnormal spot at the left frontal lobe. The spot appeared as a signal void on T1, T2, diffusion, susceptibility-weighted image (SWI), and fluid attenuated inversion recovery (FLAIR) image, and was surrounded by a high-signal halo on T2 and diffusion-weighted images (DWIs). The spot also demonstrated "blooming" appearance on SWIs. Despite the lesion she was asymptomatic all through the postoperative course, and she left our hospital on postoperative day 6. Follow-up MRI obtained 27 months after the CAS demonstrated that the lesion remained at the left frontal lobe without any signal changes. The patient remained asymptomatic at the last follow-up. Considering the location of the new abnormal spot (in the vascular territory of the catheterized vessel), these imaging characteristics and asymptomatic clinical course, the spot likely suggested metallic embolism. This is the first case in which the metallic embolism was suspected after CAS.
RESUMEN
Cilostazol is a selective inhibitor of phosphodiesterase type III that downregulates tenascin-C (TNC), a matricellular protein, which may cause delayed cerebral infarction after aneurysmal subarachnoid hemorrhage (SAH). The authors increased the dosage and evaluated the dose-dependent effects of cilostazol on delayed cerebral infarction and outcomes in SAH patients. This was a retrospective cohort study in a single center. One hundred fifty-six consecutive SAH patients including 67 patients of admission World Federation of Neurological Surgeons grades IV-V who underwent aneurysmal obliteration within 48 h post-SAH from 2007 to 2017 were analyzed. Cilostazol (0 to 300 mg/day) was administered from 1-day post-clipping or post-coiling to day 14 or later. Cilostazol treatment dose-dependently decreased delayed cerebral infarction and tended to improve outcomes, although cilostazol did not affect other outcome measures including angiographic vasospasm. On multivariate analyses, 300 mg/day (100 mg three times) cilostazol independently decreased delayed cerebral infarction and improved 3-month outcomes, but other regimens including 200 mg/day (100 mg twice) cilostazol were not independent prognostic factors. Propensity score-matched analyses showed that the 300 mg/day cilostazol cohort had lower plasma TNC levels and a lower incidence of delayed cerebral infarction associated with better outcomes compared with the non-cilostazol cohort. The 300 mg/day cilostazol may improve post-SAH outcomes by reducing plasma TNC levels and delayed cerebral infarction, but not vasospasm. Further studies are warranted to investigate if 300 mg/day cilostazol is more beneficial to post-SAH outcomes than a usual dose of 200 mg/day cilostazol that was demonstrated to be effective in randomized controlled trials.