Kazunori Toyoda
Kyushu University
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Featured researches published by Kazunori Toyoda.
The Lancet | 2014
Jonathan Emberson; Kennedy R. Lees; Patrick D. Lyden; L Blackwell; Gregory W. Albers; Erich Bluhmki; Thomas G. Brott; Geoff Cohen; Stephen M. Davis; Geoffrey A. Donnan; James C. Grotta; George Howard; Markku Kaste; Masatoshi Koga; Ruediger von Kummer; Maarten G. Lansberg; Richard Lindley; Gordon Murray; Jean Marc Olivot; Mark W. Parsons; Barbara C. Tilley; Danilo Toni; Kazunori Toyoda; Nils Wahlgren; Joanna M. Wardlaw; William Whiteley; Gregory J. del Zoppo; Colin Baigent; Peter Sandercock; Werner Hacke
Summary Background Alteplase is effective for treatment of acute ischaemic stroke but debate continues about its use after longer times since stroke onset, in older patients, and among patients who have had the least or most severe strokes. We assessed the role of these factors in affecting good stroke outcome in patients given alteplase. Methods We did a pre-specified meta-analysis of individual patient data from 6756 patients in nine randomised trials comparing alteplase with placebo or open control. We included all completed randomised phase 3 trials of intravenous alteplase for treatment of acute ischaemic stroke for which data were available. Retrospective checks confirmed that no eligible trials had been omitted. We defined a good stroke outcome as no significant disability at 3–6 months, defined by a modified Rankin Score of 0 or 1. Additional outcomes included symptomatic intracranial haemorrhage (defined by type 2 parenchymal haemorrhage within 7 days and, separately, by the SITS-MOST definition of parenchymal type 2 haemorrhage within 36 h), fatal intracranial haemorrhage within 7 days, and 90-day mortality. Findings Alteplase increased the odds of a good stroke outcome, with earlier treatment associated with bigger proportional benefit. Treatment within 3·0 h resulted in a good outcome for 259 (32·9%) of 787 patients who received alteplase versus 176 (23·1%) of 762 who received control (OR 1·75, 95% CI 1·35–2·27); delay of greater than 3·0 h, up to 4·5 h, resulted in good outcome for 485 (35·3%) of 1375 versus 432 (30·1%) of 1437 (OR 1·26, 95% CI 1·05–1·51); and delay of more than 4·5 h resulted in good outcome for 401 (32·6%) of 1229 versus 357 (30·6%) of 1166 (OR 1·15, 95% CI 0·95–1·40). Proportional treatment benefits were similar irrespective of age or stroke severity. Alteplase significantly increased the odds of symptomatic intracranial haemorrhage (type 2 parenchymal haemorrhage definition 231 [6·8%] of 3391 vs 44 [1·3%] of 3365, OR 5·55, 95% CI 4·01–7·70, p<0·0001; SITS-MOST definition 124 [3·7%] vs 19 [0·6%], OR 6·67, 95% CI 4·11–10·84, p<0·0001) and of fatal intracranial haemorrhage within 7 days (91 [2·7%] vs 13 [0·4%]; OR 7·14, 95% CI 3·98–12·79, p<0·0001). The relative increase in fatal intracranial haemorrhage from alteplase was similar irrespective of treatment delay, age, or stroke severity, but the absolute excess risk attributable to alteplase was bigger among patients who had more severe strokes. There was no excess in other early causes of death and no significant effect on later causes of death. Consequently, mortality at 90 days was 608 (17·9%) in the alteplase group versus 556 (16·5%) in the control group (hazard ratio 1·11, 95% CI 0·99–1·25, p=0·07). Taken together, therefore, despite an average absolute increased risk of early death from intracranial haemorrhage of about 2%, by 3–6 months this risk was offset by an average absolute increase in disability-free survival of about 10% for patients treated within 3·0 h and about 5% for patients treated after 3·0 h, up to 4·5 h. Interpretation Irrespective of age or stroke severity, and despite an increased risk of fatal intracranial haemorrhage during the first few days after treatment, alteplase significantly improves the overall odds of a good stroke outcome when delivered within 4·5 h of stroke onset, with earlier treatment associated with bigger proportional benefits. Funding UK Medical Research Council, British Heart Foundation, University of Glasgow, University of Edinburgh.
The New England Journal of Medicine | 2016
Adnan I. Qureshi; Yuko Y. Palesch; William G. Barsan; Daniel F. Hanley; Chung Y. Hsu; Renee L. Martin; Claudia S. Moy; Robert Silbergleit; Thorsten Steiner; Jose I. Suarez; Kazunori Toyoda; Wang Y; Haruko Yamamoto; Byung Woo Yoon
BACKGROUND Limited data are available to guide the choice of a target for the systolic blood-pressure level when treating acute hypertensive response in patients with intracerebral hemorrhage. METHODS We randomly assigned eligible participants with intracerebral hemorrhage (volume, <60 cm(3)) and a Glasgow Coma Scale (GCS) score of 5 or more (on a scale from 3 to 15, with lower scores indicating worse condition) to a systolic blood-pressure target of 110 to 139 mm Hg (intensive treatment) or a target of 140 to 179 mm Hg (standard treatment) in order to test the superiority of intensive reduction of systolic blood pressure to standard reduction; intravenous nicardipine to lower blood pressure was administered within 4.5 hours after symptom onset. The primary outcome was death or disability (modified Rankin scale score of 4 to 6, on a scale ranging from 0 [no symptoms] to 6 [death]) at 3 months after randomization, as ascertained by an investigator who was unaware of the treatment assignments. RESULTS Among 1000 participants with a mean (±SD) systolic blood pressure of 200.6±27.0 mm Hg at baseline, 500 were assigned to intensive treatment and 500 to standard treatment. The mean age of the patients was 61.9 years, and 56.2% were Asian. Enrollment was stopped because of futility after a prespecified interim analysis. The primary outcome of death or disability was observed in 38.7% of the participants (186 of 481) in the intensive-treatment group and in 37.7% (181 of 480) in the standard-treatment group (relative risk, 1.04; 95% confidence interval, 0.85 to 1.27; analysis was adjusted for age, initial GCS score, and presence or absence of intraventricular hemorrhage). Serious adverse events occurring within 72 hours after randomization that were considered by the site investigator to be related to treatment were reported in 1.6% of the patients in the intensive-treatment group and in 1.2% of those in the standard-treatment group. The rate of renal adverse events within 7 days after randomization was significantly higher in the intensive-treatment group than in the standard-treatment group (9.0% vs. 4.0%, P=0.002). CONCLUSIONS The treatment of participants with intracerebral hemorrhage to achieve a target systolic blood pressure of 110 to 139 mm Hg did not result in a lower rate of death or disability than standard reduction to a target of 140 to 179 mm Hg. (Funded by the National Institute of Neurological Disorders and Stroke and the National Cerebral and Cardiovascular Center; ATACH-2 ClinicalTrials.gov number, NCT01176565 .).
Journal of Neurosurgery | 2007
Kuniaki Ogasawara; Nobuyuki Sakai; Terumasa Kuroiwa; Kohkichi Hosoda; Koji Iihara; Kazunori Toyoda; Chiaki Sakai; Izumi Nagata; Akira Ogawa
OBJECT Intracranial hemorrhage associated with cerebral hyperperfusion syndrome (CHS) following carotid endarterectomy (CEA) or carotid artery stenting (CAS) is a rare but potentially devastating complication. In the present study the authors evaluated 4494 patients with carotid artery stenosis who had undergone CEA or CAS to clarify the clinicopathological features and outcomes of those with CHS and associated intracranial hemorrhage. METHODS Patients with postoperative CHS were retrospectively selected, and clinicopathological features and outcomes were studied. RESULTS Sixty-one patients with CHS (1.4%) were identified, and intracranial hemorrhage developed in 27 of them (0.6%). The onset of CHS peaked on the 6th postoperative day in those who had undergone CEA and within 12 hours in those who had undergone CAS. Results of logistic regression analysis demonstrated that poor postoperative control of blood pressure was significantly associated with the development of intracranial hemorrhage in patients with CHS after CEA (p = 0.0164). Note, however, that none of the tested variables were significantly associated with the development of intracranial hemorrhage in patients with CHS after CAS. Mortality (p = 0.0010) and morbidity (p = 0.0172) rates were significantly higher in patients with intracranial hemorrhage than in those without. CONCLUSIONS Cerebral hyperperfusion syndrome after CEA and CAS occurs with delayed classic and acute presentations, respectively. Although strict control of postoperative blood pressure prevents intracranial hemorrhage in patients with CHS after CEA, there appears to be no relationship between blood pressure control and intracranial hemorrhage in those with CHS after CAS. Finally, the prognosis of CHS in patients with associated intracerebral hemorrhage is poor.
Stroke | 2008
Kazunori Toyoda; Masahiro Yasaka; Kazunori Iwade; Ken Nagata; Yukihiro Koretsune; Tomohiro Sakamoto; Shinichiro Uchiyama; Jun Gotoh; Takehiko Nagao; Masahiro Yamamoto; Jun Takahashi; Kazuo Minematsu
Background and Purpose— We sought to determine the incidence and severity of bleeding events in patients with stroke and cardiovascular diseases who were taking oral antithrombotic agents in Japan, where the incidence of hemorrhagic stroke is higher than in Western countries. Methods— A prospective, multicenter, observational study was conducted; 4009 patients who were taking oral antithrombotic agents for stroke and cardiovascular diseases were enrolled. The patients were classified into 4 groups according to their antithrombotic treatment: the single antiplatelet agent group (47.2%); the dual antiplatelet agent group (8.7%); the warfarin group (32.4%); and the warfarin plus antiplatelet agent group (11.7%). The primary end point was life-threatening or major bleeding according to the MATCH trial definition. Results— During a median follow-up of 19 months, there were 57 life-threatening and 51 major bleeding events, including 31 intracranial hemorrhages. The annual incidence of the primary end point was 1.21% in the single antiplatelet agent group, 2.00% in the dual antiplatelet agent group, 2.06% in the warfarin group, and 3.56% in the warfarin plus antiplatelet agent group (P<0.001). After adjustment for baseline characteristics, adding an antiplatelet agent to warfarin increased the risk of the primary end point (relative risk=1.76; 95% CI, 1.05 to 2.95), and adding another antiplatelet agent to single antiplatelet agent therapy increased the secondary end point of any bleeding, including minor events (relative risk=1.37; 95% CI, 1.07 to 1.76). Conclusions— The incidence of bleeding events during antithrombotic therapy in Japan was similar to that reported for Western countries, although the trials used different study designs. Dual antithrombotic therapy was independently related to an increased risk of bleeding events.
Neurology | 2005
Kazunori Toyoda; Yasushi Okada; Kazuo Minematsu; Masahiro Kamouchi; Shigeru Fujimoto; Setsuro Ibayashi; Tooru Inoue
Objective: The purpose of this study was to examine the effect of antiplatelet therapy on the initial severity and the acute outcome of intracerebral hemorrhage (ICH). Methods: The authors reviewed records of 251 consecutive patients hospitalized in their cerebrovascular center within 24 hours after onset of ICH. Results: Fifty-seven patients (23%) had development of ICH during oral antiplatelet therapy. The major indication for antiplatelet therapy was the prevention of stroke recurrence (63%). As compared with patients without antiplatelet therapy, those who received antiplatelet therapy more frequently were aged 70 years or older (60% vs 35%; p < 0.001), had previous symptomatic ischemic stroke (54% vs 7%; p < 0.0001), had diabetes mellitus (26% vs 15%; p < 0.05), and had heart disease (32% vs 8%; p < 0.0001). Antiplatelet therapy was predictive of an increase in the hematoma volume by more than 40% on the second hospital day (hematoma enlargement, odds ratio [OR] 7.67, 95% CI 1.62 to 36.4) and the need for emergent surgical evacuation of the hematoma (OR 3.10, 95% CI 1.18 to 8.15). Antiplatelet therapy was an independent predictor for the occurrence of any of hematoma enlargement, emergent death, or evacuation surgery, which suggests that clinical deterioration occurs into the second hospital day (OR 7.45, 95% CI 2.46 to 22.5). Conclusions: Antiplatelet therapy seems to contribute to the acute clinical deterioration of intracerebral hemorrhage.
Annals of Neurology | 2008
Sohei Yoshimura; Kazunori Toyoda; Tomoyuki Ohara; Hikaru Nagasawa; Noriko Ohtani; Takahiro Kuwashiro; Hiroaki Naritomi; Kazuo Minematsu
Takotsubo cardiomyopathy, which is characterized by transient left ventricular apical ballooning, is a known complication of subarachnoid hemorrhage. The aim of this study was to identify the clinical characteristics of acute ischemic stroke patients who experienced development of takotsubo cardiomyopathy.
Journal of the Neurological Sciences | 2004
Kazunori Toyoda; Kenichiro Fujii; Masahiro Kamouchi; Hiroshi Nakane; Shoji Arihiro; Yasushi Okada; Setsuro Ibayashi; Mitsuo Iida
BACKGROUND Edaravone has potent free radical quenching and antioxidant actions. The agent has been recently in commercial use for acute ischemic stroke patients. In this study, we investigated the therapeutic effect of edaravone on severe carotid-territorial stroke. METHODS Stroke patients with internal carotid artery occlusion and baseline NIH Stroke Scale Score > or =15 were treated for 14 days with drip intravenous infusion of edaravone (n=30) and were compared with a historical control cohort of similar patients (n=31). Glycerol was also administered to all patients in both groups. RESULTS Infarct volume (P<0.02) and midline shift (P<0.02) on CT performed on day 2 of the patients treated with edaravone were smaller than those without edaravone. For patients with edaravone, infarct volume (P<0.0001) and midline shift (P<0.0001) on days 5-7 were greater than those on day 2. Hemorrhagic transformation of infarcts on day 2 was less severe in patients with than without edaravone (P<0.03). Within 14 days after the onset of stroke, 6 patients with edaravone (20%) and 14 without edaravone (45%) died directly of stroke (P<0.03). Among all patients, only two treated with edaravone were independent without any assistance 8 weeks after the onset. CONCLUSIONS Edaravone was associated with delayed evolution of infarcts and edema in patients with severe carotid-territorial stroke and decreased mortality during the acute stage. The agent, however, failed to prevent evolution of infarcts and edema on later days, and did not significantly improve functional outcome among the surviving patients.
Neurology | 2008
Shoichiro Sato; Kazunori Toyoda; Toshiyuki Uehara; Naomi Toratani; Chiaki Yokota; H. Moriwaki; Hiroaki Naritomi; Kazuo Minematsu
Objective: The NIH Stroke Scale (NIHSS) may not appropriately assess the spectrum of posterior circulation (PC)–related neurologic deficits. We determined the cutoff baseline NIHSS score that predicts independent daily life activity during the chronic stage in anterior circulation (AC) vs PC ischemic strokes. Methods: A total of 310 consecutive patients hospitalized within 3 days after the onset of an ischemic stroke were prospectively enrolled in the study. Patients on thrombolytic therapy were excluded. In all patients, infarcts and vascular lesions were identified primarily using magnetic resonance techniques. A favorable outcome was defined as a modified Rankin Scale score of ≤2 at 3 months poststroke. Results: In 101 patients with PC stroke, the total baseline NIHSS score was lower (p < 0.001), and the subscores of ataxia (p < 0.001) and visual fields (p = 0.043) were higher than in 209 patients with AC stroke. Multivariate-adjusted OR for the favorable outcome in patients with PC vs AC stroke was 2.339 (95% CI 1.331–4.109, p = 0.003). A low baseline NIHSS score was independently predictive of a favorable outcome in both patients with PC (OR 1.547, 95% CI 1.232–1.941) and AC (1.279, 1.188–1.376) stroke. The optimal cutoff scores of the baseline NIHSS for the favorable outcome were ≤5 for patients with PC stroke (sensitivity, 84%; specificity, 81%) and ≤8 for patients with AC stroke (sensitivity, 80%; specificity, 82%). Conclusions: The cutoff score of the baseline NIH Stroke Scale (NIHSS) for a favorable chronic outcome was relatively low in patients with PC stroke compared to patients with AC stroke. The NIHSS appears to have limitations with respect to its use when comparing the neurologic severity of PC and AC stroke.
Stroke | 2009
Kazunori Toyoda; Masatoshi Koga; Masaki Naganuma; Yoshiaki Shiokawa; Jyoji Nakagawara; Eisuke Furui; Kazumi Kimura; Hiroshi Yamagami; Yasushi Okada; Yasuhiro Hasegawa; Kazuomi Kario; Satoshi Okuda; Kazutoshi Nishiyama; Kazuo Minematsu
Background and Purpose— A retrospective, multicenter, observational study was conducted to document clinical outcomes and to identify outcome predictors in patients treated with low-dose intravenous recombinant tissue plasminogen activator (0.6 mg/kg alteplase), which was approved in Japan in 2005, within 3 hours of stroke onset. Methods— Consecutive patients with stroke treated with recombinant tissue plasminogen activator in 10 Japanese stroke centers were included. Results— A total of 600 patients (377 men, 72±12 years old) were studied. Median National Institutes of Health Stroke Scale scores decreased from 13 before recombinant tissue plasminogen activator to 8 at 24 hours later. Symptomatic intracerebral hemorrhage within 36 hours with a ≥1-point increase from the baseline National Institutes of Health Stroke Scale score developed in 23 patients (3.8%; 95% CI, 2.6% to 5.7%). At 3 months, 43 patients had died (7.2%; 5.4% to 9.5%), and 199 patients (33.2%; 29.5% to 37.0%) had a modified Rankin Scale score ≤1. Analysis of 399 patients with a premorbid modified Rankin Scale score ≤1 who met the criteria of the European license (≤80 years old, an initial National Institutes of Health Stroke Scale score ≤24, etc) showed that 40.6% (35.9% to 45.5%) had a 3-month modified Rankin Scale score ≤1. After multivariate adjustment, younger age, lower initial National Institutes of Health Stroke Scale score, absence of internal carotid artery occlusion, higher Alberta Stroke Program Early CT Score on CT, and absence of intravenous antihypertensives just before recombinant tissue plasminogen activator were independently related to a 3-month modified Rankin Scale score ≤1. Congestive heart failure and hyperglycemia were independently related to mortality. Conclusions— Three-month outcomes of patients receiving low-dose intravenous recombinant tissue plasminogen activator therapy in the present study were similar to those from postmarketing surveys using 0.9 mg/kg alteplase.
Lancet Neurology | 2014
Kazunori Toyoda; Toshiharu Ninomiya
Chronic kidney disease, defined as a reduced glomerular filtration rate or increased urinary albumin excretion, is recognised as a rapidly growing global health burden, and increasing evidence suggests that it contributes to the risk and severity of cerebrovascular diseases. In particular, chronic kidney disease is an established risk factor for stroke and is also strongly associated with subclinical cerebrovascular abnormalities and cognitive impairment, partly because it shares several traditional and non-traditional risk factors, and sometimes uraemia-related and dialysis-related factors, with cerebrovascular diseases. The effect of chronic kidney disease on incident stroke differs among regions and races and is greater in Asian than in non-Asian people. Chronic kidney disease seems to be predictive of severe neurological deficits and poor vital and functional outcomes after both ischaemic and haemorrhagic strokes, which is partly due to the limitations of pharmacotherapies, including limited use and effects of novel oral anticoagulants, other antithrombotic treatments, and reperfusion treatment for hyperacute ischaemic stroke. In view of the strong two-way association between stroke and kidney disease, the pathophysiological interactions between the brain and kidney should be the subject of intensive study.