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Biomedical subjects

Kazuo Minematsu

Publications and source records attributed to Kazuo Minematsu.

At least 19 recordsLinked to original sources
PubMed2005

Mortality and cause of death after hospital discharge in 10,981 patients with ischemic stroke and transient ischemic attack.

BACKGROUND: The aim of this study was to examine the 1-year cumulative mortality rate and cause of death, and to identify the predictive factors for death after hospital discharge following ischemic stroke and transient ischemic attack (TIA) using data from the Japan Multicenter Stroke Investigators' Collaboration study. METHODS: We prospectively registered 16,922 consecutive patients with acute ischemic stroke or TIA from May 1999 to April 2000 in 156 Japanese hospitals. We mailed a questionnaire to the 15,322 patients who were alive at hospital discharge. RESULTS: 10,981 patients (6,945 men, 4,036 women, age 70 +/- 11 years, median 71, range 19-100 years) were enrolled in the follow-up study. The mean follow-up period was 271 +/- 110 days (median 272 days; range 1-487 days). The 1-year cumulative mortality was 6.8% (7.0% for 10,234 stroke patients and 3.5% for 747 TIA patients). The causes of death were: cerebrovascular disease, 24.1%; pneumonia, 22.6%; heart disease, 18.1%; cancer, 11.0%, and miscellaneous causes, 24.1%. Multivariate analysis suggested that male gender, age, diabetes mellitus, atrial fibrillation, history of stroke, nonlacunar stroke, functional disability and transfer to another hospital or nursing home on discharge were significant independent predictors of death during the follow-up period. CONCLUSIONS: The major causes of death after hospital discharge were found to be cerebrovascular diseases, pneumonia and heart diseases. Thus, in order to improve survival after hospital discharge, in addition to appropriate management of vascular risk factors following stroke, it appears to be important to take measures to prevent pneumonia and to discharge patients to their own home, if possible.

Age Distribution↗
PubMed2004

Variation in ischemic stroke frequency in Japan by season and by other variables.

BACKGROUND AND PURPOSE: It is unclear whether acute ischemic stroke exhibits a seasonal pattern in Japan. The aim of the present study was to elucidate seasonal differences in acute ischemic stroke. METHODS: Our study enrolled 12,660 patients with ischemic stroke (7943 men, 4717 women; mean age, 70.1 years, S.D. 11.5; median 70; range 18-107). We divided the year into four parts: spring (March-May); summer (June-August); fall (September-November); and winter (December-February). Time of stroke onset was divided into three subgroups: daytime (08:00-16:00), evening (16:00-24:00), and night (24:00-08:00). We examined the association between clinical characteristics, season, and time of stroke onset. RESULTS: Stroke occurred least frequently in spring (22.9%), followed by winter (25.3%), fall (25.8%), and summer (26.0%) (P<0.001). No differences in age, National Institutes of Health Stroke Scale (NIHSS) score, modified Rankin Scale (m-RS) score, history of stroke/transient ischemic attack (TIA), or risk factors for stroke were observed among the four seasons. Stroke in men (63.8% vs. 62.4%; P<0.01), lacunar stroke (LS) (41.2% vs. 39.4%, P<0.01), atherothrombotic stroke (ATS) (34.0% vs. 32.3%; P<0.01), and nighttime stroke (26.5% vs. 24.8%; P<0.05) were observed more frequently in summer compared to other seasons. This contrasts with the findings for stroke in women (39.0% vs. 36.7%; P<0.05), cardioembolic stroke (CES) (23.4% vs. 20.6%; P<0.05), and daytime stroke (47.4% vs. 45.0%; P<0.05), which were more frequent in winter. CONCLUSIONS: Acute ischemic stroke displays seasonal characteristics according to gender, stroke subtype, and time of stroke onset. These results may have important clinical implications in ischemic stroke prevention.

Adolescent↗
PubMed2004

Long-term prognosis, by stroke subtypes, after a first-ever stroke: a hospital-based study over a 20-year period.

BACKGROUND AND PURPOSE: The influence of stroke subtype on recurrence, and determinants of recurrence-free survival after a first-ever stroke are not fully understood. We aimed to clarify the long-term prognosis by stroke subtypes and to identify determinants for recurrence and death after a first-ever stroke. METHODS: We enrolled 1,732 consecutive patients (men/women = 1,134/598, mean age of 65 years) with a first-ever acute stroke who were admitted to our Stroke Care Unit during a period of 20 years. Stroke subtypes were classified as atherothrombotic brain infarction, lacunar infarction, cardioembolic infarction, other type of infarction, and brain hemorrhage. The prognosis was assessed by stroke subtypes. RESULTS: During the hospital stay (mean 61 days), 99 patients died: 73 died directly from stroke. A total of 198 patients had recurrent strokes, and 286 died within 3 years after the index stroke. The overall recurrence rate within the first year was 6.5%, which was different among stroke subtypes. Patients with cardioembolic infarction (9.0%) as well as other type of infarction (9.1%) had more recurrent strokes within the initial year compared with the other subtypes. A history of transient ischemic attack (relative risk = 1.38), atrial fibrillation (1.52), ischemic heart disease (1.40), and disability at discharge (2.64) were independent predictors for the recurrence and death within 3 years after the first-ever stroke. CONCLUSIONS: The recurrence rate was different among stroke subtypes within 1 year after the index stroke. Atrial fibrillation, ischemic heart disease, history of transient ischemic attack, and disability at discharge were important determinants for stroke recurrence and death.

Acute Disease↗
PubMed2004

Analysis of 16,922 patients with acute ischemic stroke and transient ischemic attack in Japan. A hospital-based prospective registration study.

OBJECTIVE: The purpose of the present study was to clarify the present status of stroke medicine in Japan using a hospital-based, prospective registration study of 156 hospitals from all over Japan. METHODS: Consecutive patients with acute ischemic stroke and transient ischemic attack (TIA) who presented to hospital within 7 days of onset from May 1999 to April 2000 were enrolled in this study. A common protocol was applied in every participating hospital. RESULTS: A total of 16,922 patients (TIA, 6.4%) with a mean age of 70.6 +/- 11.5 years (median 71 years, range 18-107 years) were enrolled in the study. Lacunar stroke was the most frequent stroke subtype (38.8%), followed by atherothrombotic (33.3%), cardioembolic (21.8%) and other stroke (6.1%). NIH stroke scale score on admission was 8.0 +/- 7.9 (median 5; 25th to 75th percentile, 2-11). 36.8% arrived at hospital within 3 h of symptom onset, and 49.5% within 6 h. The ambulance was used for 70.2% of patients arriving within 3 h after onset, but in only 29.9% of patients visiting the hospital later than 3 h after onset (p < 0.0001). 60.8% displayed good outcome (modified Rankin Scale score of 0-2 at discharge), while 32.3% displayed poor outcome (score 3-5), and mortality rate was 6.9%. CONCLUSIONS: More than half of the acute stroke patients arrived at hospital later than 6 h after onset. Establishment of ideal emergency systems is needed for better management of stroke and for improvement of patient outcome, in particular, in the future after approval of intravenous recombinant tissue plasminogen activator for acute ischemic stroke by the Japanese government.

Adult↗
PubMed2004

Aortic arch atherosclerotic lesions and the recurrence of ischemic stroke.

BACKGROUND AND PURPOSE: Aortic arch atherosclerotic lesions are often associated with embolic brain infarction. We investigated the relationship between stroke recurrence and the characteristics of aortic arch atherosclerotic lesions. METHODS: Among 487 stroke patients who underwent transesophageal echocardiography, 283 patients with brain embolism diagnosed without significant occlusive lesions (> or =50%) in their cerebral arteries were included in this study. We measured the intima-media thickness (IMT) and evaluated the extension and mobility of the aortic arch atherosclerotic lesions. During a mean follow-up period of 3.4 years, we investigated the relationship between stroke recurrence and the various characteristics of the aortic arch atherosclerotic lesions. RESULTS: An IMT > or =4.0 mm was found in 67 patients (25.3%). In 51 of these patients, the aortic lesions extended to the origin of the branches of the arch. Recurrences of cerebral ischemic events were found in 32 patients (recurrence group) and not in the other 251 (nonrecurrence group). Aortic atheroma > or =4.0 mm (41% versus 22%), aortic atheroma extending to the branches (63% versus 39%), and both (38% versus 16%) were more frequently seen in the recurrence group than in the nonrecurrence group (P<0.05, P<0.1, P<0.01, respectively). After adjustment for age and the presence of hypertension, an aortic atheroma that was > or =4.0 mm as well as extending to the branches was found to be an independent predictor of ischemic stroke recurrence (hazard ratio=2.42, P<0.05). CONCLUSIONS: Stroke recurrence is associated with the severity of the atheroma (IMT > or =4.0 mm) and plaque extension to the branches.

Aged↗
PubMed2004

Vertebral artery occlusion in duplex color-coded ultrasonography.

BACKGROUND AND PURPOSE: To establish the diagnostic criteria for the site of occlusion in the vertebral arteries (VAs) using duplex color-coded ultrasonography. METHODS: In 128 consecutive patients who underwent conventional cerebral angiography, we prospectively measured the diameter, mean flow velocity (MV), peak systolic flow velocity, and end-diastolic flow velocity of both VAs. The diameter-ratio (diameter of contralateral VA divided by that of target VA) and MV-ratio (MV of contralateral VA divided by that of target VA) were determined. Based on the angiographic findings, we classified the VAs into 4 types (5 groups) as follows: (1) the origin of VA occlusion (Origin group: n=9); (2) VA occlusion before branching into the posterior inferior cerebellar artery (PICA) (Before group: n=10); (3A) symptomatic VA occlusion after branching into the PICA (After group: n=12); (3B) asymptomatic or hypoplastic occlusive VA after branching into the PICA (PICA end group: n=15); and (4) no significant occlusive lesions in the VA (Control group: n=194). RESULTS: No flow signals in the VAs apparently indicated the Origin group. Preserved peak systolic flow velocity but end-diastolic flow velocity of zero cm/s indicated the Before group. MV <18 cm/s and MV-ratio > or =1.4 indicated the PICA end group or After group. Furthermore, these groups could be distinguished as follows: a diameter-ratio <1.4 indicated the After group. A diameter-ratio > or =1.4 indicated the PICA end group. Either MV > or =18 cm/s or MV <18 cm/s in combination with MV-ratio <1.4 indicated the Control group. CONCLUSIONS: Duplex color-coded ultrasonography can accurately diagnose the site of VA occlusion.

Angiography, Digital Subtraction↗
PubMed2004

Temporal and topographic profiles of cyclooxygenase-2 expression during 24 h of focal brain ishemia in rats.

Substantial increases in cyclooxygenase-2 (COX-2) mRNA and protein levels were demonstrated in the peri-infarct and focal ischemic areas after 3-24 and 12-24 h, respectively, in rats. In the ischemic core, significant increases in COX-2 mRNA followed 6 h of ischemia, though the peak level was about one-third of that in the peri-infarct area. Increases in COX-2 protein in the ischemic core were not observed during ischemic periods. Diffuse, neuronal COX-2 staining was found in peri-infarct areas as well as in discrete, immunoreactive neurons in the ischemic core. Robust increases in prostaglandin E2 levels in the peri-infarct area were demonstrated following 24 h of ischemia. Prostaglandin production as well as COX-2 expression in ischemic tissues depended on the degree and duration of the reduction in cerebral blood flow.

Analysis of Variance↗
PubMed2004

Early neurological deterioration represents recurrent attack in acute small non-lacunar stroke.

The aim of this study was to identify the frequency and possible pathogenic mechanisms of early neurological deterioration in patients with acute small non-lacunar infarction. We studied 46 patients (35 men, 11 women; age, 70.3+/-10.4 years) with acute small non-lacunar infarction. Small non-lacunar infarction was diagnosed using diffusion-weighted magnetic resonance imaging (DWI) as being <15 mm in diameter and located in the cortex and centrum ovale in the middle cerebral artery territory. The patients were divided into two groups; Group D (n=6) had neurological deterioration within 7 days after symptom onset, while Group N (n=40) did not have any neurological deterioration. In Group D, the interval from symptom onset to clinical deterioration was 3.3+/-1.5 days (range 2-6 days). Blood pressure on admission was higher in Group D than in Group N (p<0.05). In Group D, four of these five patients with follow-up DWI had new acute small ischemic lesions in addition to the initial lesions, indicating recurrent attacks of brain infarction. Neurological deterioration occurred within 7 days after symptom onset in 13% of patients. Neurological deterioration was frequently caused by recurrent infarction detected by DWI.

Acute Disease↗
PubMed2004

Relationships between angiographic findings and National Institutes of Health stroke scale score in cases of hyperacute carotid ischemic stroke.

BACKGROUND AND PURPOSE: Stroke severity in cases of hyperacute carotid ischemic stroke may be related to site of arterial occlusion. We evaluated the relationships between National Institutes of Health Stroke Scale (NIHSS) scores and findings on intra-arterial digital subtraction angiograms (IA-DSA) of patients with ischemic stroke within 6 hr of stroke onset. METHODS: A total of 43 consecutive patients (38 men and five women; mean age, 69.4 +/- 8.7 years) with ischemic stroke in the carotid territory underwent IA-DSA within 6 hr of stroke onset. Baseline NIHSS score was assessed immediately before IA-DSA. Patients were divided into four groups according to site of arterial occlusion: 1) the internal carotid artery (ICA group, n = 10); 2) stem of the middle cerebral artery or stem of the anterior cerebral artery (Stem group, n = 14); 3) branches of middle cerebral artery or anterior cerebral artery (Branch group, n = 11); and 4) no arterial occlusion (Normal group, n = 8). RESULTS: Mean (+/-SD) NIHSS score was 14.7 +/- 7.4. The interval from stroke onset to IA-DSA study was 205 +/- 76 min. NIHSS score was higher in the ICA group (median, 23; range, 6-32) than in the Branch (median, 17; range, 11-25; P =.02) or Normal (median, 15; range, 2-17; P <.001) groups but was not higher than in the Stem group (median, 6; range, 1-11; P =.73). Sensitivity-specificity curve analysis suggested an NIHSS score > or = 10 as indicative of arterial occlusion of the carotid system. A total of 96.9% of patients with NIHSS scores > or = 10 displayed arterial occlusion, and 63.6% of patients with NIHSS scores <10 displayed no arterial occlusion. CONCLUSION: NIHSS score is related to site of arterial occlusion in cases of hyperacute carotid ischemic stroke. An NIHSS score of 10 seems to represent the cut-off for discriminating between patients with arterial occlusion and patients without.

Aged↗
PubMed2003

Characterisation of [123I]iomazenil distribution in a rat model of focal cerebral ischaemia in relation to histopathological findings.

Iodine-123 labelled iomazenil ([(123)I]IMZ) has been reported to be a useful marker of neuronal viability. The brain distribution of [(123)I]IMZ, however, has not been correlated with the pathophysiological response in detail after an ischaemic insult. To characterise [(123)I]IMZ as a marker of neuronal viability, we compared its brain distribution with cyclooxygenase-2 (COX-2) expression, DNA fragmentation and cellular integrity. [(123)I]IMZ and [(125)I]IMP were injected into rats with focal cerebral ischaemia for the purpose of dual-tracer autoradiography. COX-2 and microtubule-associated protein-2 (MAP-2, a marker of cellular integrity) were immunostained. In situ DNA polymerase-I-dependent dUTP incorporation into damaged DNA was used as an indicator of DNA fragmentation. Lesion to normal ratios (LNRs) for [(123)I]IMP and [(125)I]IMZ were calculated. [(123)I]IMZ accumulation was preserved in several regions with impaired [(123)I]IMP accumulation. COX-2 expression was occasionally observed, whereas neither DNA fragmentation nor MAP-2 denaturation was detected in these regions. DNA fragmentation and impaired MAP-2 immunostaining were observed only in the regions with reduced LNRs for both tracers. The LNR for [(123)I]IMZ was significantly lower in regions with impaired MAP-2 immunostaining (0.120+/-0.152, P<0.0001), in regions positive for dUTP incorporation (0.488+/-0.166, P<0.0001) and in regions positive for COX-2 expression (0.626+/-0.186, P<0.001) than in histologically normal regions (0.784+/-0.213). Thus, neuronal DNA is still intact and cellular integrity is maintained in the ischaemic regions with preserved [(123)I]IMZ accumulation. The impairment of [(123)I]IMZ accumulation precedes DNA fragmentation and denaturation of cellular integrity. These results provide the molecular basis of [(123)I]IMZ distribution.

Animals↗
PubMed2003

Transient global amnesia associated with an acute infarction in the retrosplenium of the corpus callosum.

We present a patient with transient global amnesia (TGA) whose diffusion-weighted imaging (DWI) study showed a high-intensity signal in the left retrosplenium of the corpus callosum. In previous studies, lesions in the retrosplenium caused permanent but not transient global amnesia, called retrosplenial amnesia, by involving the thalamocortical portion of the Papez' circuit. This is the first report indicating that TGA can be associated with acute infarction only in the left retrosplenium of the corpus callosum.

Amnesia, Transient Global↗
PubMed2003

Post-ischemic cyclooxygenase-2 expression is regulated by the extent of cerebral blood flow reduction in non-human primates.

We determined whether up to 24 h of ischemia could induce the expression of cyclooxygenase-2 (COX-2) in the brain of nonhuman primates. Randomized animals were subjected to either a 2 h ischemia (group II; n=3) or a 24 h ischemia (group III; n=3). Three animals in group I served as controls. In group III, regional cerebral blood flow (CBF) and the cerebral glucose metabolic rate (CMRglc) were evaluated using positron emission tomography. Upregulation of COX-2 mRNA expression was observed after 2 h of ischemia, but disappeared by 24 h in the ischemic temporal cortex, in which both CMRglc and CBF were markedly reduced. In the ischemic parietal cortex, where CMRglc was preserved, COX-2 expression persisted even 24 h after ischemia. This study is the first to demonstrate neuronal COX-2 induction within potentially viable hypoperfused brain areas in nonhuman primates.

Animals↗
PubMed2003

Extracorporeal double filtration plasmapheresis in acute atherothrombotic brain infarction caused by major artery occlusive lesion.

Extracorporeal double filtration plasmapheresis (EDFP) can quickly lower plasma viscosity and fibrinogen concentration. EDFP has the potential to improve cerebral microcirculation in acute ischemic stroke and ultimately to salvage penumbral tissue. However, no evidence is available to show that EDFP can increase cerebra blood flow (CBF). Therefore, we investigated whether EDFP could increase CBF by quantitative CBF measurements and documented the clinical effects of EDFP in acute ischemic stroke. EDFP was performed ten times in seven patients diagnosed as having acute atherothrombotic brain infarction caused by major artery occlusive lesion. They also fulfilled one of the following entry criteria: 1) diffusion/perfusion mismatch demonstrated by MRI on admission; 2) a hemispheric syndrome, but only a small lesion on diffusion weighted MRI (<25% of MCA territory); or 3) progressing stroke. Exclusion criteria were 1) contraindication of heparin or 2) spontaneous improvement of symptoms. Time from stroke onset to EDFP varied from 5 hr to 7 days. Plasma viscosity was quickly lowered by EDFP without affecting RBC counts, Hb, or Hct in all patients. Positron emission tomography (PET) with 15-O labeled H2O measurements revealed a significant CBF increase from 36.4 +/- 8.3 ml/100 g/min to 40.7 +/- 6.8 ml/100 g/min in the affected hemisphere (P=0.048). Definite CBF improvement was also demonstrated by single photon emission computed tomography (SPECT) in one of two patients who had severe stenosis of the middle cerebral artery. Furthermore, this patient showed remarkable improvement of hemiplegia immediately following EDFP (NIHSS score: 18 to 13). In conclusion, EDFP can increase CBF in ischemic brain tissue in acute atherothrombotic brain infarction. Further clinical studies should focus on the efficacy of EDFP on outcome of patients with this stroke subtype.

Aged↗
PubMed2003

Cyclooxygenase-2 expression associated with spreading depression in a primate model.

The authors previously provided evidence that spreading depression (SD) can be evoked in primates. Cyclooxygenase-2 (COX-2) expression has been found to increase in the rodent cortex undergoing SD, and the authors sought to determine whether this association exists in primate brain. In the present study, neuronal COX-2 expression was induced during SD in the primate cortex. The mean expression ratio of COX-2 messenger RNA in animals with SD was significantly higher than that measured in controls (1.69 vs. 0.5; P = 0.02). Induction of COX-2 in these animals was also detected by human microarray analysis. Results show that, as in rodents, neuronal COX-2 is induced in the primate cortex in response to SD.

Animals↗
PubMed2003

Clinical and radiographic features of lobar cerebral hemorrhage: hypertensive versus non-hypertensive cases.

OBJECTIVES: The underlying cause of lobar intracerebral hemorrhage (ICH) is often difficult to determine, since these vascular abnormalities are not necessarily visualized in radiographic studies. We sought to determine the clinical features of hypertensive and nonhypertensive lobar ICH, and further predict the presence or absence of vascular abnormalities in terms of clinical features and radiographic abnormalities. PATIENTS AND METHODS: Eighty-one patients with lobar ICH were retrospectively assigned to either hypertensive or non-hypertensive groups based on their blood pressure levels during the chronic phase or a history of antihypertensive medication. The clinical and radiographic features of these two groups were compared. RESULTS: Forty-nine patients (60%) were hypertensive, and the other thirty-two (40%) were non-hypertensive. In the non-hypertensive group, amyloid angiopathy (n = 6), aneurysms (n = 5), arteriovenous malformation (n = 4), use of anticoagulants (n = 2), liver cirrhosis (n = 2) and thrombasthenia (n = 1) were found as underlying causes. There were no significant differences between these two groups in the frequencies of stroke risk factors except for hypertension, clinical features and initial neurological findings. On the contrary, subarachnoid extension of the hematoma on CT was significantly more frequent in the non-hypertensive lobar ICH group than in the hypertensive group (p < 0.001). The patients with subarachnoid extension were more likely to have vascular abnormality than those without subarachnoid extension (p < 0.01). CONCLUSION: Subarachnoid extension of the hematoma on CT strongly indicates a non-hypertensive cause, and more specifically, it suggests lobar ICH caused by vascular abnormalities.

Aged↗
PubMed2003

Predisposing factors for enlargement of intracerebral hemorrhage in patients treated with warfarin.

To elucidate predisposing factors for enlargement of intracerebral hematoma (ICH) during warfarin therapy, we reviewed 47 patients on warfarin who developed acute ICH and determined relationships among ICH enlargement, INR reversal and clinical data. Among 36 patients treated to counteract the effects of warfarin within 24 h of onset, ICH increased in 10 patients (enlarged group), but remained unchanged in the remaining 26 (unchanged group), while ICH remained unchanged in another 11 patients in whom the effect of warfarin was reversed after 24 h. The international normalized ratio (INR) was counteracted immediately in 11 patients treated with prothrombin complex concentrate (PCC) but gradually in the other 36 treated by reducing the dose of warfarin, or by administering vitamin K or fresh frozen plasma. Multivariate analysis with a logistic regression model showed an INR value <2.0 at admission or for 24 h after immediate INR correction with PCC prevented ICH enlargement (OR 0.069, 95%CI 0.006-0.789, p = 0.031). An INR value of >2.0 within 24 h of ICH seems an important predisposing factor for ICH enlargement.

Adolescent↗