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Kazumi Kimura - One of the best experts on this subject based on the ideXlab platform.
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Post Stroke Dysglycemia and Acute Infarct Volume Growth: A Study Using Continuous Glucose Monitoring.
European neurology, 2016Co-Authors: Takashi Shimoyama, Junichi Uemura, Kazumi Kimura, Naoki Saji, Kensaku ShibazakiAbstract:Background: The aim of the present study was to clarify the effect of glucose profiles after stroke, which was assessed by a continuous glucose monitoring (CGM) device. Methods: Acute ischemic stroke patients within 24 h of onset were prospectively studied. CGM was performed for 72 h after admission. CGM parameters were evaluated as follows: (1) mean glucose level, (2) area under the curve (AUC) for glucose level >140 mg/dl and (3) SD of the glucose level. Infarct Volume was measured at admission and 24 and 72 h after admission using diffusion-weighted imaging. CGM data and Infarct Volume growth were compared at 24 and 72 h. Results: Seventy-eight patients were enrolled in the present study. Spearman's rank correlation coefficients showed that both the mean glucose level (r = 0.433, p 140 mg/dl (r = 0.417, p Conclusion: Post-stroke hyperglycemia was associated with Infarct Volume growth during the acute phase of ischemic stroke.
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Admission hyperglycemia causes Infarct Volume expansion in patients with ICA or MCA occlusion: association of collateral grade on conventional angiography.
European journal of neurology, 2012Co-Authors: Takashi Shimoyama, Yasuyuki Iguchi, Kensaku Shibazaki, Kazumi Kimura, Jyunichi Uemura, Takashi Shiromoto, Masao Watanabe, T. Inoue, Soichiro MochioAbstract:Background and purpose Hyperglycemia (HG) is associated with Infarct Volume expansion in acute ischaemic stroke patients. However, collateral circulation can sustain the ischaemic penumbra and limit the growth of Infarct Volume. The aim of this study was to determine whether the association between HG and Infarct Volume expansion is dependent on collateral circulation. Methods We performed a retrospective analysis of 93 acute ischaemic stroke patients with internal carotid artery or middle cerebral artery occlusion within 24 h of onset were retrospectively studied. HG was diagnosed in patients with an admitting blood glucose value ≥140 mg/dl. Angiographic collateral grade 0–1 was designated as poor collateral circulation and grade 2–4 as good collateral circulation. Infarct Volume was measured at admission and at again within 7 days using diffusion-weighted magnetic resonance images. Results Among 34 patients with poor collateral grade, the change in Infarct Volume was significantly greater in the HG group than in the non-HG group (106.0 ml vs. 22.7 ml, P = 0.002). Among the 59 patients with good collateral circulation, the change in Infarct Volume was greater in the HG group than in the non-HG group (53.3 ml vs. 10.9 ml, P = 0.047). Multiple regression analysis indicated that admission HG (P = 0.004), baseline National Institutes of Health Stroke Scale score (P = 0.018), and poor collateral circulation (P = 0.040) were independently associated with Infarct Volume expansion. Conclusions Infarct Volume expansion was greater in individuals with HG on admission regardless of collateral circulation status.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the Neurological Sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:Abstract Background and purpose The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Methods Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3 h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value ≥ 130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △ Infarct Volume (7 days—baseline) between patients with and without ER. Results 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2 ± 157.1 cm 3 , vs. 85.4 ± 140.7 cm 3 , P = 0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days—baseline) (r = 0.340, P = 0.0014). Regarding ER, ΔInfarct Volume (7 days—baseline) in patients without ER was correlated with admitting blood glucose value(r = 0.372, P = 0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r = 0.225, P = 0.1173). Good outcome (mRS 0–2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P = 0.0418). Conclusion Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the neurological sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value≥130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △Infarct Volume (7 days-baseline) between patients with and without ER. 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2±157.1cm(3), vs. 85.4±140.7 cm(3), P=0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days-baseline) (r=0.340, P=0.0014). Regarding ER, ΔInfarct Volume (7 days-baseline) in patients without ER was correlated with admitting blood glucose value(r=0.372, P=0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r=0.225, P=0.1173). Good outcome (mRS 0-2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P=0.0418). Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume. Copyright © 2011 Elsevier B.V. All rights reserved.
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Neurological deterioration in small vessel disease may be associated with increase of Infarct Volume
Journal of the Neurological Sciences, 2008Co-Authors: Yuka Terasawa, Yasuyuki Iguchi, Jun-ya Aoki, Noriko Matsumoto, Kensaku Shibazaki, Takeshi Inoue, Kazuto Kobayashi, Kazumi Kimura, Ryuji KajiAbstract:Abstract Background and purpose The mechanism of neurological deterioration in small vessel disease is unclear. We examined the relationship between neurological deterioration and change of Infarct Volume in acute small vessel disease. Methods We studied consecutive patients with acute supratentorial small vessel disease. Patients were classified into two groups (D: group with deterioration, N: group with no deterioration). We performed serial MRI studies, measured Infarct Volumes using NIH Image, and calculated the changes in Infarct Volume (Δ Volume) between initial and follow-up diffusion-weighted imaging (DWI). Results Seventy-two patients (44 males, 68±11 years of age) were enrolled. Fifteen patients exhibited neurological deterioration (group D) and 57 patients did not (group N). Initial Infarct Volume was 0.66 cm 3 in group D and 0.45 cm 3 in group N ( p =0.025). Infarct Volumes on follow-up DWI were 1.41 cm 3 and 0.72 cm 3 , respectively ( p =0.001). The Δ Volume in group D was larger than that in group N (0.76 cm 3 vs 0.27 cm 3 , p =0.001). In order to differentiate D from N group, sensitivity specificity analysis yielded a cut-off value of Δ Volume of 0.5 cm 3 for differentiation of the two groups, which exhibited a sensitivity of 80% and specificity of 84%. Multivariate logistic regression analysis demonstrated that increase in Infarct Volume of over 0.5 cm 3 (odds ratio; 18.0, 95% CI; 1.4 to 270, p =0.027) was independently associated with neurological deterioration in patients with acute small vessel disease. Conclusions Enlargement of Infarct Volume may contribute to neurological deterioration in acute small vessel disease.
William J. Pearce - One of the best experts on this subject based on the ideXlab platform.
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L-NAME reduces Infarct Volume in a filament model of transient middle cerebral artery occlusion in the rat pup.
Pediatric research, 1995Co-Authors: Stephen Ashwal, Daniel J. Cole, Terrill N. Osborne, Suzzanne Osborne, William J. PearceAbstract:The importance of nitric oxide (NO) during focal cerebral ischemia remains controversial as studies have suggested both a neurotoxic and neuroprotective role. In the 7 d old rat pup, NG-nitro-L-arginine, a nitric oxide synthase inhibitor, reduced Infarct Volume in a model of unilateral carotid ligation with 2.5 h exposure to 8% O2. The current study examined whether NO is neurotoxic in a filament model of transient middle cerebral artery occlusion (MCAO) in the 14-18-d-old rat pup. We developed a reproducible filament model of transient MCAO in 14-18-d-old spontaneously hypertensive rats (35 g) by passing a no. 6-0 (0.07-mm) nylon filament via the carotid artery to occlude the middle cerebral artery for 4 h under normoxic conditions. After filament removal and reperfusion for 24 h, we determined Infarct Volume using the mitochondrial stain 2,3,5-triphenyltetrazolium chloride. NO synthesis was inhibited using NG-nitro-L-arginine methyl ester (L-NAME) at a dose of 3 mg/kg, intraperitoneally, 1 h before MCAO. We measured Infarct Volume in control (n = 7) and L-NAME (n = 7) groups. L-NAME reduced Infarct Volume by 55% (p < 0.01). In the control group, Infarct Volume (180 +/- 29 mm3) averaged 49 +/- 7% of the left hemisphere (359 +/- 16 mm3). In the L-NAME-treated group, Infarct Volume (77 +/- 19 mm3) was 22 +/- 5% of the left hemispheric Volume (344 +/- 2 mm3). These findings support earlier studies that used models of neonatal hypoxic-ischemic brain injury and suggest a neurotoxic role of NO. They extend these observations by demonstrating a significant reduction in Infarct Volume in a stroke model in the immature rat pup.
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Low dose L-NAME reduces Infarct Volume in the rat MCAO/reperfusion model.
Journal of neurosurgical anesthesiology, 1993Co-Authors: Stephen Ashwal, Daniel J. Cole, Terrill N. Osborne, William J. PearceAbstract:In a variety of recent studies, inhibitors of nitric oxide (NO) synthesis have ameliorated neuronal injury during permanent focal cerebral ischemia, suggesting that NO may contribute to ischemic damage. In other studies, however, these inhibitors increased Infarct Volume during permanent middle cerebral artery occlusion (MCAO). One complication in these studies was that high-dose NO synthase inhibitors increased mean arterial blood pressure (MAP) by 20-30 mm Hg. Thus, it is possible that variations in the effects of NO synthesis inhibitors on Infarct Volume could be related to effects of these inhibitors on MAP and cerebral perfusion during or after ischemia. The present study compared the effects of control (Ringer's lactate solution) versus low-dose NO inhibition (0.1 mg/kg bolus followed by 0.01 mg/kg/min) on cerebral Infarct Volume using L-NAME (NG-nitro-L-arginine methyl ester) administered during a 1-h baseline period, 3-h of MCAO, and 2 h of reperfusion in the spontaneously hypertensive rat. Infarct Volume was determined using the TTC (2,3,5-triphenyltetrazolium chloride) method performed 5 h after onset of occlusion. L-NAME reduced Infarct Volume by 55%. In the control group (n = 7), Infarct Volume measured 116 +/- 4 (SEM) mm3 which was 29 +/- 1% of the left hemispheric Volume (400.5 +/- 0.3 mm3). In the L-NAME group (n = 7), Infarct Volume measured 53 +/- 8 mm3 which was only 13 +/- 2% of the left hemispheric Volume (400.4 +/- 0.5 mm3).(ABSTRACT TRUNCATED AT 250 WORDS)
Daniel J. Cole - One of the best experts on this subject based on the ideXlab platform.
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L-NAME reduces Infarct Volume in a filament model of transient middle cerebral artery occlusion in the rat pup.
Pediatric research, 1995Co-Authors: Stephen Ashwal, Daniel J. Cole, Terrill N. Osborne, Suzzanne Osborne, William J. PearceAbstract:The importance of nitric oxide (NO) during focal cerebral ischemia remains controversial as studies have suggested both a neurotoxic and neuroprotective role. In the 7 d old rat pup, NG-nitro-L-arginine, a nitric oxide synthase inhibitor, reduced Infarct Volume in a model of unilateral carotid ligation with 2.5 h exposure to 8% O2. The current study examined whether NO is neurotoxic in a filament model of transient middle cerebral artery occlusion (MCAO) in the 14-18-d-old rat pup. We developed a reproducible filament model of transient MCAO in 14-18-d-old spontaneously hypertensive rats (35 g) by passing a no. 6-0 (0.07-mm) nylon filament via the carotid artery to occlude the middle cerebral artery for 4 h under normoxic conditions. After filament removal and reperfusion for 24 h, we determined Infarct Volume using the mitochondrial stain 2,3,5-triphenyltetrazolium chloride. NO synthesis was inhibited using NG-nitro-L-arginine methyl ester (L-NAME) at a dose of 3 mg/kg, intraperitoneally, 1 h before MCAO. We measured Infarct Volume in control (n = 7) and L-NAME (n = 7) groups. L-NAME reduced Infarct Volume by 55% (p < 0.01). In the control group, Infarct Volume (180 +/- 29 mm3) averaged 49 +/- 7% of the left hemisphere (359 +/- 16 mm3). In the L-NAME-treated group, Infarct Volume (77 +/- 19 mm3) was 22 +/- 5% of the left hemispheric Volume (344 +/- 2 mm3). These findings support earlier studies that used models of neonatal hypoxic-ischemic brain injury and suggest a neurotoxic role of NO. They extend these observations by demonstrating a significant reduction in Infarct Volume in a stroke model in the immature rat pup.
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Low dose L-NAME reduces Infarct Volume in the rat MCAO/reperfusion model.
Journal of neurosurgical anesthesiology, 1993Co-Authors: Stephen Ashwal, Daniel J. Cole, Terrill N. Osborne, William J. PearceAbstract:In a variety of recent studies, inhibitors of nitric oxide (NO) synthesis have ameliorated neuronal injury during permanent focal cerebral ischemia, suggesting that NO may contribute to ischemic damage. In other studies, however, these inhibitors increased Infarct Volume during permanent middle cerebral artery occlusion (MCAO). One complication in these studies was that high-dose NO synthase inhibitors increased mean arterial blood pressure (MAP) by 20-30 mm Hg. Thus, it is possible that variations in the effects of NO synthesis inhibitors on Infarct Volume could be related to effects of these inhibitors on MAP and cerebral perfusion during or after ischemia. The present study compared the effects of control (Ringer's lactate solution) versus low-dose NO inhibition (0.1 mg/kg bolus followed by 0.01 mg/kg/min) on cerebral Infarct Volume using L-NAME (NG-nitro-L-arginine methyl ester) administered during a 1-h baseline period, 3-h of MCAO, and 2 h of reperfusion in the spontaneously hypertensive rat. Infarct Volume was determined using the TTC (2,3,5-triphenyltetrazolium chloride) method performed 5 h after onset of occlusion. L-NAME reduced Infarct Volume by 55%. In the control group (n = 7), Infarct Volume measured 116 +/- 4 (SEM) mm3 which was 29 +/- 1% of the left hemispheric Volume (400.5 +/- 0.3 mm3). In the L-NAME group (n = 7), Infarct Volume measured 53 +/- 8 mm3 which was only 13 +/- 2% of the left hemispheric Volume (400.4 +/- 0.5 mm3).(ABSTRACT TRUNCATED AT 250 WORDS)
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Temporary focal cerebral ischemia in spontaneously hypertensive rats: the effect of ibuprofen on Infarct Volume.
The Journal of pharmacology and experimental therapeutics, 1993Co-Authors: Daniel J. Cole, P M Patel, Lowell Reynolds, John C. Drummond, Suzzanne MarcantonioAbstract:Arachidonic acid metabolism results in the generation of oxygen radicals and production of prostanoids which are proposed to adversely influence cerebral ischemia. Inhibition of cyclooxygenase, an enzymatic step in arachidonic acid metabolism, has effected an improvement in histologic outcome after cerebral ischemia. However, there has been no attempt to determine whether this effect occurs during vascular occlusion or during reperfusion. We assessed the effect of cyclooxygenase inhibition on Infarct Volume in the setting of either temporary or permanent middle cerebral artery occlusion (MCAo). Rats were allotted to one of the following groups: Groups I and II, 180 min of MCAo and 120 min of reperfusion; and Groups III and IV, 180 min of permanent MCAo. In Groups I and III, vehicle only was given, whereas in Groups II and IV, ibuprofen was given throughout the study period (MCAo with or without reperfusion). After the ischemic period the brains were analyzed for Infarct Volume (mm3, mean +/- S.D.) by 2,3,5-triphenyltetrazolium chloride stain. For animals in which reperfusion was allowed, ibuprofen reduced Infarct Volume (Group I, 122 +/- 15 mm3 vs. Group II, 63 +/- 7 mm3). However, in animals with permanent MCAo, ibuprofen worsened Infarct Volume (Group III, 79 +/- 8 mm3 vs. Group IV, 110 +/- 13 mm3). These data suggest that the beneficial effect of cyclooxygenase inhibition occurs during reperfusion.
Kensaku Shibazaki - One of the best experts on this subject based on the ideXlab platform.
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Post Stroke Dysglycemia and Acute Infarct Volume Growth: A Study Using Continuous Glucose Monitoring.
European neurology, 2016Co-Authors: Takashi Shimoyama, Junichi Uemura, Kazumi Kimura, Naoki Saji, Kensaku ShibazakiAbstract:Background: The aim of the present study was to clarify the effect of glucose profiles after stroke, which was assessed by a continuous glucose monitoring (CGM) device. Methods: Acute ischemic stroke patients within 24 h of onset were prospectively studied. CGM was performed for 72 h after admission. CGM parameters were evaluated as follows: (1) mean glucose level, (2) area under the curve (AUC) for glucose level >140 mg/dl and (3) SD of the glucose level. Infarct Volume was measured at admission and 24 and 72 h after admission using diffusion-weighted imaging. CGM data and Infarct Volume growth were compared at 24 and 72 h. Results: Seventy-eight patients were enrolled in the present study. Spearman's rank correlation coefficients showed that both the mean glucose level (r = 0.433, p 140 mg/dl (r = 0.417, p Conclusion: Post-stroke hyperglycemia was associated with Infarct Volume growth during the acute phase of ischemic stroke.
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Admission hyperglycemia causes Infarct Volume expansion in patients with ICA or MCA occlusion: association of collateral grade on conventional angiography.
European journal of neurology, 2012Co-Authors: Takashi Shimoyama, Yasuyuki Iguchi, Kensaku Shibazaki, Kazumi Kimura, Jyunichi Uemura, Takashi Shiromoto, Masao Watanabe, T. Inoue, Soichiro MochioAbstract:Background and purpose Hyperglycemia (HG) is associated with Infarct Volume expansion in acute ischaemic stroke patients. However, collateral circulation can sustain the ischaemic penumbra and limit the growth of Infarct Volume. The aim of this study was to determine whether the association between HG and Infarct Volume expansion is dependent on collateral circulation. Methods We performed a retrospective analysis of 93 acute ischaemic stroke patients with internal carotid artery or middle cerebral artery occlusion within 24 h of onset were retrospectively studied. HG was diagnosed in patients with an admitting blood glucose value ≥140 mg/dl. Angiographic collateral grade 0–1 was designated as poor collateral circulation and grade 2–4 as good collateral circulation. Infarct Volume was measured at admission and at again within 7 days using diffusion-weighted magnetic resonance images. Results Among 34 patients with poor collateral grade, the change in Infarct Volume was significantly greater in the HG group than in the non-HG group (106.0 ml vs. 22.7 ml, P = 0.002). Among the 59 patients with good collateral circulation, the change in Infarct Volume was greater in the HG group than in the non-HG group (53.3 ml vs. 10.9 ml, P = 0.047). Multiple regression analysis indicated that admission HG (P = 0.004), baseline National Institutes of Health Stroke Scale score (P = 0.018), and poor collateral circulation (P = 0.040) were independently associated with Infarct Volume expansion. Conclusions Infarct Volume expansion was greater in individuals with HG on admission regardless of collateral circulation status.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the Neurological Sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:Abstract Background and purpose The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Methods Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3 h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value ≥ 130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △ Infarct Volume (7 days—baseline) between patients with and without ER. Results 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2 ± 157.1 cm 3 , vs. 85.4 ± 140.7 cm 3 , P = 0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days—baseline) (r = 0.340, P = 0.0014). Regarding ER, ΔInfarct Volume (7 days—baseline) in patients without ER was correlated with admitting blood glucose value(r = 0.372, P = 0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r = 0.225, P = 0.1173). Good outcome (mRS 0–2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P = 0.0418). Conclusion Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the neurological sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value≥130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △Infarct Volume (7 days-baseline) between patients with and without ER. 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2±157.1cm(3), vs. 85.4±140.7 cm(3), P=0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days-baseline) (r=0.340, P=0.0014). Regarding ER, ΔInfarct Volume (7 days-baseline) in patients without ER was correlated with admitting blood glucose value(r=0.372, P=0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r=0.225, P=0.1173). Good outcome (mRS 0-2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P=0.0418). Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume. Copyright © 2011 Elsevier B.V. All rights reserved.
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Neurological deterioration in small vessel disease may be associated with increase of Infarct Volume
Journal of the Neurological Sciences, 2008Co-Authors: Yuka Terasawa, Yasuyuki Iguchi, Jun-ya Aoki, Noriko Matsumoto, Kensaku Shibazaki, Takeshi Inoue, Kazuto Kobayashi, Kazumi Kimura, Ryuji KajiAbstract:Abstract Background and purpose The mechanism of neurological deterioration in small vessel disease is unclear. We examined the relationship between neurological deterioration and change of Infarct Volume in acute small vessel disease. Methods We studied consecutive patients with acute supratentorial small vessel disease. Patients were classified into two groups (D: group with deterioration, N: group with no deterioration). We performed serial MRI studies, measured Infarct Volumes using NIH Image, and calculated the changes in Infarct Volume (Δ Volume) between initial and follow-up diffusion-weighted imaging (DWI). Results Seventy-two patients (44 males, 68±11 years of age) were enrolled. Fifteen patients exhibited neurological deterioration (group D) and 57 patients did not (group N). Initial Infarct Volume was 0.66 cm 3 in group D and 0.45 cm 3 in group N ( p =0.025). Infarct Volumes on follow-up DWI were 1.41 cm 3 and 0.72 cm 3 , respectively ( p =0.001). The Δ Volume in group D was larger than that in group N (0.76 cm 3 vs 0.27 cm 3 , p =0.001). In order to differentiate D from N group, sensitivity specificity analysis yielded a cut-off value of Δ Volume of 0.5 cm 3 for differentiation of the two groups, which exhibited a sensitivity of 80% and specificity of 84%. Multivariate logistic regression analysis demonstrated that increase in Infarct Volume of over 0.5 cm 3 (odds ratio; 18.0, 95% CI; 1.4 to 270, p =0.027) was independently associated with neurological deterioration in patients with acute small vessel disease. Conclusions Enlargement of Infarct Volume may contribute to neurological deterioration in acute small vessel disease.
Junichi Uemura - One of the best experts on this subject based on the ideXlab platform.
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Post Stroke Dysglycemia and Acute Infarct Volume Growth: A Study Using Continuous Glucose Monitoring.
European neurology, 2016Co-Authors: Takashi Shimoyama, Junichi Uemura, Kazumi Kimura, Naoki Saji, Kensaku ShibazakiAbstract:Background: The aim of the present study was to clarify the effect of glucose profiles after stroke, which was assessed by a continuous glucose monitoring (CGM) device. Methods: Acute ischemic stroke patients within 24 h of onset were prospectively studied. CGM was performed for 72 h after admission. CGM parameters were evaluated as follows: (1) mean glucose level, (2) area under the curve (AUC) for glucose level >140 mg/dl and (3) SD of the glucose level. Infarct Volume was measured at admission and 24 and 72 h after admission using diffusion-weighted imaging. CGM data and Infarct Volume growth were compared at 24 and 72 h. Results: Seventy-eight patients were enrolled in the present study. Spearman's rank correlation coefficients showed that both the mean glucose level (r = 0.433, p 140 mg/dl (r = 0.417, p Conclusion: Post-stroke hyperglycemia was associated with Infarct Volume growth during the acute phase of ischemic stroke.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the neurological sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value≥130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △Infarct Volume (7 days-baseline) between patients with and without ER. 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2±157.1cm(3), vs. 85.4±140.7 cm(3), P=0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days-baseline) (r=0.340, P=0.0014). Regarding ER, ΔInfarct Volume (7 days-baseline) in patients without ER was correlated with admitting blood glucose value(r=0.372, P=0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r=0.225, P=0.1173). Good outcome (mRS 0-2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P=0.0418). Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume. Copyright © 2011 Elsevier B.V. All rights reserved.
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Admission hyperglycemia and serial Infarct Volume after t-PA therapy in patients with and without early recanalization.
Journal of the Neurological Sciences, 2011Co-Authors: Kazumi Kimura, Yasuyuki Iguchi, Jun-ya Aoki, Kensaku Shibazaki, Yuki Sakamoto, Kenichiro Sakai, Junichi UemuraAbstract:Abstract Background and purpose The present study examined the effects of admission hyperglycemia and early recanalization (ER) after t-PA administration on Infarct Volume and patient outcome. Methods Acute ischemic stroke patients with major artery occlusion treated with t-PA within 3 h of onset were studied prospectively. Hyperglycemia was identified as admitting blood glucose value ≥ 130 mg/dl. We compared serial Infarct Volume and patient outcome between normoglycemic and hyperglycemic groups, and assessed correlation between admitting blood glucose value and △ Infarct Volume (7 days—baseline) between patients with and without ER. Results 97 patients (ICA occlusion in 30, M1 in 44, and M2 in 23 patients) were enrolled in the present study; 52 had hyperglycemia, and 40 had ER. The initial Infarct Volume did not differ between the normoglycemic and hyperglycemic groups. However, Infarct Volume at 7 days was larger in the hyperglycemic group than in the normoglycemic group (156.2 ± 157.1 cm 3 , vs. 85.4 ± 140.7 cm 3 , P = 0.0061) and the baseline admitting blood glucose value was correlated with ΔInfarct Volume (7 days—baseline) (r = 0.340, P = 0.0014). Regarding ER, ΔInfarct Volume (7 days—baseline) in patients without ER was correlated with admitting blood glucose value(r = 0.372, P = 0.0078). However, in patients with ER, ΔInfarct Volume was not associated with admitting blood glucose value (r = 0.225, P = 0.1173). Good outcome (mRS 0–2) at 3 months was more frequent in normoglycemic patients than hyperglycemic patients (43.2% vs. 22.2%, P = 0.0418). Conclusion Admission hyperglycemia was associated with Infarct Volume expansion and patient outcome in t-PA patients. However, if ER occurs, hyperglycemia should not adversely affect Infarct Volume.