Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000020384.92499.59
Thalia Shoshana Field, M. Hill
Background— Changes in weather and season have been linked to stroke occurrence. However, the association has been inconsistent across stroke types. Calgary is a city in the Chinook belt and is subject to high variability in weather conditions. Methods— We obtained hourly weather data over a 5-year period from 1996 to 2000; Chinook events were identified according to the accepted definition. We reviewed administrative data to determine stroke occurrence and defined stroke types to maximize specificity of diagnosis. To examine the hypothesis that weather affected the number of strokes occurring in a given day, we compared average daily stroke occurrence on Chinook days and non-Chinook days; we compared mean daily temperature, relative humidity, barometric pressure, and wind speed by the number of strokes occurring on any given day. Results— Annual variation in stroke frequency was observed. No seasonal, monthly, or weekly variation in overall stroke occurrence or occurrence by type was evident. No relationship with changes in weather parameters was observed. Conclusions— We found no association between weather changes and stroke occurrence. A cause-and-effect relationship between weather and stroke occurrence is dubious because of a lack of consistency across studies.
{"title":"Weather, Chinook, and Stroke Occurrence","authors":"Thalia Shoshana Field, M. Hill","doi":"10.1161/01.STR.0000020384.92499.59","DOIUrl":"https://doi.org/10.1161/01.STR.0000020384.92499.59","url":null,"abstract":"Background— Changes in weather and season have been linked to stroke occurrence. However, the association has been inconsistent across stroke types. Calgary is a city in the Chinook belt and is subject to high variability in weather conditions. Methods— We obtained hourly weather data over a 5-year period from 1996 to 2000; Chinook events were identified according to the accepted definition. We reviewed administrative data to determine stroke occurrence and defined stroke types to maximize specificity of diagnosis. To examine the hypothesis that weather affected the number of strokes occurring in a given day, we compared average daily stroke occurrence on Chinook days and non-Chinook days; we compared mean daily temperature, relative humidity, barometric pressure, and wind speed by the number of strokes occurring on any given day. Results— Annual variation in stroke frequency was observed. No seasonal, monthly, or weekly variation in overall stroke occurrence or occurrence by type was evident. No relationship with changes in weather parameters was observed. Conclusions— We found no association between weather changes and stroke occurrence. A cause-and-effect relationship between weather and stroke occurrence is dubious because of a lack of consistency across studies.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"17 1","pages":"1751-1758"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73706893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000019603.29818.9C
R. Kollmar, W. Schäbitz, S. Heiland, D. Georgiadis, P. Schellinger, J. Bardutzky, S. Schwab
Background and Purpose— In contrast to early hypothermia, the effects of delayed hypothermia in focal cerebral ischemia have not been widely addressed. We examined the influence of delayed hypothermia on secondary ischemic injury, MRI lesion size, and neurological outcome after transient focal cerebral ischemia in a rat model. Methods— Rats (n=30) were subjected to transient middle cerebral artery occlusion (MCAO, 120 minutes) by use of the intraluminal filament model. Animals of the treatment group (n=12) were exposed to whole-body hypothermia of 33°C for 5 hours starting 3 hours after MCAO, whereas the control group (n=18) was kept at 37°C throughout the whole experiment. The normothermia- and hypothermia-treated animals were investigated daily by using the Menzies neurological score. Serial MRI was performed 1, 3, and 6 hours after MCAO and on days 1, 2, 3, and 5. After the final MRI scan, the rats were euthanized, and brain slices were stained by 2,3,5-triphenyltetrazolium chloride. Results— Delayed hypothermia resulted in a significant increase of survival rate and a significant improvement of the Menzies score. Moreover, a significant decrease in the extent of hyperintense volumes in T2-weighted scans and a reduction of cerebral edema as calculated from T2-weighted scans throughout the examination period were obvious. The extent of cerebral infarct volume and cerebral brain edema examined by MRI was consistent with 2,3,5-triphenyltetrazolium chloride staining. Conclusions— Our results suggest that even delayed postischemic hypothermia can reduce the extent of infarct volume and brain edema after transient focal cerebral ischemia.
{"title":"Neuroprotective Effect of Delayed Moderate Hypothermia After Focal Cerebral Ischemia: An MRI Study","authors":"R. Kollmar, W. Schäbitz, S. Heiland, D. Georgiadis, P. Schellinger, J. Bardutzky, S. Schwab","doi":"10.1161/01.STR.0000019603.29818.9C","DOIUrl":"https://doi.org/10.1161/01.STR.0000019603.29818.9C","url":null,"abstract":"Background and Purpose— In contrast to early hypothermia, the effects of delayed hypothermia in focal cerebral ischemia have not been widely addressed. We examined the influence of delayed hypothermia on secondary ischemic injury, MRI lesion size, and neurological outcome after transient focal cerebral ischemia in a rat model. Methods— Rats (n=30) were subjected to transient middle cerebral artery occlusion (MCAO, 120 minutes) by use of the intraluminal filament model. Animals of the treatment group (n=12) were exposed to whole-body hypothermia of 33°C for 5 hours starting 3 hours after MCAO, whereas the control group (n=18) was kept at 37°C throughout the whole experiment. The normothermia- and hypothermia-treated animals were investigated daily by using the Menzies neurological score. Serial MRI was performed 1, 3, and 6 hours after MCAO and on days 1, 2, 3, and 5. After the final MRI scan, the rats were euthanized, and brain slices were stained by 2,3,5-triphenyltetrazolium chloride. Results— Delayed hypothermia resulted in a significant increase of survival rate and a significant improvement of the Menzies score. Moreover, a significant decrease in the extent of hyperintense volumes in T2-weighted scans and a reduction of cerebral edema as calculated from T2-weighted scans throughout the examination period were obvious. The extent of cerebral infarct volume and cerebral brain edema examined by MRI was consistent with 2,3,5-triphenyltetrazolium chloride staining. Conclusions— Our results suggest that even delayed postischemic hypothermia can reduce the extent of infarct volume and brain edema after transient focal cerebral ischemia.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"36 1","pages":"1899-1904"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90475284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000019510.32145.A9
M. Okahara, H. Kiyosue, M. Yamashita, Hirohumi Nagatomi, H. Hata, T. Saginoya, Y. Sagara, H. Mori
Background and Purpose— We investigated the sensitivity of 3D–time-of flight (3D-TOF) magnetic resonance angiography (MRA) in the detection of cerebral aneurysms with the use of 3D digital subtraction angiography as the gold standard. We also evaluated the effects of location and number of aneurysms (and experience of the reader) on the sensitivity. Methods— 3D-TOF MRA was performed in 82 patients with 133 cerebral aneurysms. Each patient underwent rotational angiography. Three-dimensional reconstructed images were obtained from data of the rotational angiography (as the gold standard). A blind study with 4 readers of different experiences was performed to evaluate the diagnostic accuracy of 3D-TOF MRA for cerebral aneurysms. Results— One hundred five (79%) of all 133 aneurysms were detected with MRA by a neuroradiologist, 100 (75%) were detected by an experienced neurosurgeon, 84 (63%) were detected by a general radiologist, and 80 (60%) were detected by a resident neuroradiologist. For each reader, the detectability was lower for small aneurysms (<3 mm in maximum diameter) and/or for those located at the internal carotid artery and anterior cerebral artery. False-positive aneurysms were 29 for the neuroradiologist, 19 for the neurosurgeon, 31 for the general radiologist, and 30 for the resident neuroradiologist; most of the aneurysms were at the internal carotid artery. Causes of the false-positive and false-negative results included complex flow in a tortuous artery and susceptibility artifacts. Conclusions— Although MRA is useful in the diagnosis of cerebral aneurysms, sufficient experience and careful attention are necessary for accurate diagnosis of aneurysms located at the internal carotid and anterior cerebral arteries.
{"title":"Diagnostic Accuracy of Magnetic Resonance Angiography for Cerebral Aneurysms in Correlation With 3D-Digital Subtraction Angiographic Images: A Study of 133 Aneurysms","authors":"M. Okahara, H. Kiyosue, M. Yamashita, Hirohumi Nagatomi, H. Hata, T. Saginoya, Y. Sagara, H. Mori","doi":"10.1161/01.STR.0000019510.32145.A9","DOIUrl":"https://doi.org/10.1161/01.STR.0000019510.32145.A9","url":null,"abstract":"Background and Purpose— We investigated the sensitivity of 3D–time-of flight (3D-TOF) magnetic resonance angiography (MRA) in the detection of cerebral aneurysms with the use of 3D digital subtraction angiography as the gold standard. We also evaluated the effects of location and number of aneurysms (and experience of the reader) on the sensitivity. Methods— 3D-TOF MRA was performed in 82 patients with 133 cerebral aneurysms. Each patient underwent rotational angiography. Three-dimensional reconstructed images were obtained from data of the rotational angiography (as the gold standard). A blind study with 4 readers of different experiences was performed to evaluate the diagnostic accuracy of 3D-TOF MRA for cerebral aneurysms. Results— One hundred five (79%) of all 133 aneurysms were detected with MRA by a neuroradiologist, 100 (75%) were detected by an experienced neurosurgeon, 84 (63%) were detected by a general radiologist, and 80 (60%) were detected by a resident neuroradiologist. For each reader, the detectability was lower for small aneurysms (<3 mm in maximum diameter) and/or for those located at the internal carotid artery and anterior cerebral artery. False-positive aneurysms were 29 for the neuroradiologist, 19 for the neurosurgeon, 31 for the general radiologist, and 30 for the resident neuroradiologist; most of the aneurysms were at the internal carotid artery. Causes of the false-positive and false-negative results included complex flow in a tortuous artery and susceptibility artifacts. Conclusions— Although MRA is useful in the diagnosis of cerebral aneurysms, sufficient experience and careful attention are necessary for accurate diagnosis of aneurysms located at the internal carotid and anterior cerebral arteries.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"1 1","pages":"1803-1808"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89670737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000020355.29423.61
Kei Yamada, H. Kubota, O. Kizu, H. Nakamura, Hirotoshi Ito, S. Yuen, O. Tanaka, T. Kubota, M. Makino, M. Van Cauteren, T. Nishimura
Background and Purpose— Diffusion-weighted imaging (DWI) is usually done before administration of intravenous contrast agents. Repetition of DWI is occasionally necessary after administration, but the effects of contrast material on DWI and apparent diffusion coefficient (ADC) values have not yet been fully examined. The present study assesses whether administration of gadolinium-based contrast material significantly affects DWI and ADC values. Methods— We examined DWI data from 39 patients (mean age, 67.9 years; range, 34 to 87 years) who were evaluated with a stroke protocol at our institute. All patients were scanned at the acute or subacute stages of infarct from 3 hours to 5 days after symptom onset. We obtained DWI images using single-shot echo-planar imaging with a b value of 1000 s/mm2. Patients were injected with 0.1 mmol gadopentetate dimeglumine per 1 kg body weight. We examined the signal-to-noise ratio of the normal brain and the infarct and evaluated the contrast-to-noise ratio of each lesion. In addition, we compared the ADC values calculated from the DWI images before and after administration of contrast. The statistical significance of differences between precontrast and postcontrast administration was determined by use of a paired t test. Results— The signal-to-noise and contrast-to-noise ratios of the DW images were not significantly different before and after administration of contrast agent. The ADC values were slightly lower after administration of contrast agent for both normal brain (P =0.0011) and infarcts (P =0.038). The estimated differences in the ADC values were ≈1.3% and 3.5% for normal brain and infarcts, respectively. Conclusions— The lack of a significant difference between the signal-to-noise and contrast-to-noise ratios of DW images before and after administration of contrast agent indicates the feasibility of postcontrast DWI.
{"title":"Effect of Intravenous Gadolinium-DTPA on Diffusion-Weighted Images: Evaluation of Normal Brain and Infarcts","authors":"Kei Yamada, H. Kubota, O. Kizu, H. Nakamura, Hirotoshi Ito, S. Yuen, O. Tanaka, T. Kubota, M. Makino, M. Van Cauteren, T. Nishimura","doi":"10.1161/01.STR.0000020355.29423.61","DOIUrl":"https://doi.org/10.1161/01.STR.0000020355.29423.61","url":null,"abstract":"Background and Purpose— Diffusion-weighted imaging (DWI) is usually done before administration of intravenous contrast agents. Repetition of DWI is occasionally necessary after administration, but the effects of contrast material on DWI and apparent diffusion coefficient (ADC) values have not yet been fully examined. The present study assesses whether administration of gadolinium-based contrast material significantly affects DWI and ADC values. Methods— We examined DWI data from 39 patients (mean age, 67.9 years; range, 34 to 87 years) who were evaluated with a stroke protocol at our institute. All patients were scanned at the acute or subacute stages of infarct from 3 hours to 5 days after symptom onset. We obtained DWI images using single-shot echo-planar imaging with a b value of 1000 s/mm2. Patients were injected with 0.1 mmol gadopentetate dimeglumine per 1 kg body weight. We examined the signal-to-noise ratio of the normal brain and the infarct and evaluated the contrast-to-noise ratio of each lesion. In addition, we compared the ADC values calculated from the DWI images before and after administration of contrast. The statistical significance of differences between precontrast and postcontrast administration was determined by use of a paired t test. Results— The signal-to-noise and contrast-to-noise ratios of the DW images were not significantly different before and after administration of contrast agent. The ADC values were slightly lower after administration of contrast agent for both normal brain (P =0.0011) and infarcts (P =0.038). The estimated differences in the ADC values were ≈1.3% and 3.5% for normal brain and infarcts, respectively. Conclusions— The lack of a significant difference between the signal-to-noise and contrast-to-noise ratios of DW images before and after administration of contrast agent indicates the feasibility of postcontrast DWI.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"42 1","pages":"1799-1802"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88141074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000019600.39315.D0
A. Rabinstein, D. Nichols
Introduction— The presence of an aneurysm remnant after incomplete or unsuccessful surgical clipping is associated with persistent risk of regrowth and rupture, and additional treatment is generally recommended. Attempts at surgical re-exploration are technically difficult and carry significant risk. Endovascular therapy can represent a valuable therapeutic alterative in these cases. Methods— We reviewed the information on 21 patients with postsurgical aneurysm remnants treated at our institution with endovascular coil occlusion between 1991 and 2000. Clinical outcome was measured using the modified Rankin scale. Statistical analysis of outcome predictors was performed using the two-tailed Fisher exact test. Results— Sixty-seven percent of the aneurysms were located in the anterior circulation. The median aneurysm size at the time of surgery was 9.9 mm (range 3 to 35 mm). The mean size of the aneurysm remnants before coiling was 6.4 mm (range 3 to 14 mm). Endovascular coiling resulted in total occlusion of the remnants in 81% of the cases. No major complications were associated with the endovascular treatment. Seventy-two percent of patients left the hospital without any functional impairment (modified Rankin scale 0 to 1). No cases of subarachnoid hemorrhage or symptomatic aneurysmal regrowth were noted after endovascular treatment over a mean follow-up of 22 months. Presence of disability or death was associated with an initial (presurgical) presentation with subarachnoid hemorrhage (P =0.04) and an interval between incomplete clipping and endovascular coil embolization ≤1 month (P = 0.0005). Conclusion— Endovascular coil occlusion of postsurgical aneurysm remnants is a safe and efficacious therapeutic alternative in selected cases. Postoperative angiography to identify aneurysm remnants that may be amenable to endovascular treatment should be considered in all patients.
{"title":"Endovascular Coil Embolization of Cerebral Aneurysm Remnants After Incomplete Surgical Obliteration","authors":"A. Rabinstein, D. Nichols","doi":"10.1161/01.STR.0000019600.39315.D0","DOIUrl":"https://doi.org/10.1161/01.STR.0000019600.39315.D0","url":null,"abstract":"Introduction— The presence of an aneurysm remnant after incomplete or unsuccessful surgical clipping is associated with persistent risk of regrowth and rupture, and additional treatment is generally recommended. Attempts at surgical re-exploration are technically difficult and carry significant risk. Endovascular therapy can represent a valuable therapeutic alterative in these cases. Methods— We reviewed the information on 21 patients with postsurgical aneurysm remnants treated at our institution with endovascular coil occlusion between 1991 and 2000. Clinical outcome was measured using the modified Rankin scale. Statistical analysis of outcome predictors was performed using the two-tailed Fisher exact test. Results— Sixty-seven percent of the aneurysms were located in the anterior circulation. The median aneurysm size at the time of surgery was 9.9 mm (range 3 to 35 mm). The mean size of the aneurysm remnants before coiling was 6.4 mm (range 3 to 14 mm). Endovascular coiling resulted in total occlusion of the remnants in 81% of the cases. No major complications were associated with the endovascular treatment. Seventy-two percent of patients left the hospital without any functional impairment (modified Rankin scale 0 to 1). No cases of subarachnoid hemorrhage or symptomatic aneurysmal regrowth were noted after endovascular treatment over a mean follow-up of 22 months. Presence of disability or death was associated with an initial (presurgical) presentation with subarachnoid hemorrhage (P =0.04) and an interval between incomplete clipping and endovascular coil embolization ≤1 month (P = 0.0005). Conclusion— Endovascular coil occlusion of postsurgical aneurysm remnants is a safe and efficacious therapeutic alternative in selected cases. Postoperative angiography to identify aneurysm remnants that may be amenable to endovascular treatment should be considered in all patients.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"24 1","pages":"1809-1815"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85574548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000019422.63054.5F
M. Fisher, M. Moonis
Background and Purpose— The utility of parenteral anticoagulation therapy in acute ischemic stroke has engendered much controversy and discussion. Recent studies of low-molecular-weight heparins in multiple acute stroke subtypes have not demonstrated improved outcome or reduced recurrence risk. Beneficial treatment effects may occur in subgroups such as patients with large artery atherothrombotic stroke, but further studies will be needed to prove this possibility. Summary of Review— The benefits of unfractionated intravenous heparin for reducing early stroke recurrence and improving outcome remain to be established, with the current lack of appropriately powered trials in stroke subgroups at high risk for such early recurrence. To most clinicians, the primary reason to use early intravenous anticoagulation is to prevent early stroke recurrence, not to improve outcome of an established stroke. Unfortunately, effects of reduction of recurrent stroke risk may be counterbalanced by a substantial increased risk of intracerebral hemorrhage with intravenous anticoagulation. Conclusions— Unfractionated intravenous heparin should therefore not be used routinely in acute ischemic stroke, but it may be considered in select stroke groups at high risk for early recurrent ischemic events (ie, patients with atrial fibrillation or acute myocardial infarction and large mural thrombi). However, even in these select populations, new clinical trials will be needed to define the risk-benefit ratio.
{"title":"Considering the Role of Heparin and Low-Molecular-Weight Heparins in Acute Ischemic Stroke","authors":"M. Fisher, M. Moonis","doi":"10.1161/01.STR.0000019422.63054.5F","DOIUrl":"https://doi.org/10.1161/01.STR.0000019422.63054.5F","url":null,"abstract":"Background and Purpose— The utility of parenteral anticoagulation therapy in acute ischemic stroke has engendered much controversy and discussion. Recent studies of low-molecular-weight heparins in multiple acute stroke subtypes have not demonstrated improved outcome or reduced recurrence risk. Beneficial treatment effects may occur in subgroups such as patients with large artery atherothrombotic stroke, but further studies will be needed to prove this possibility. Summary of Review— The benefits of unfractionated intravenous heparin for reducing early stroke recurrence and improving outcome remain to be established, with the current lack of appropriately powered trials in stroke subgroups at high risk for such early recurrence. To most clinicians, the primary reason to use early intravenous anticoagulation is to prevent early stroke recurrence, not to improve outcome of an established stroke. Unfortunately, effects of reduction of recurrent stroke risk may be counterbalanced by a substantial increased risk of intracerebral hemorrhage with intravenous anticoagulation. Conclusions— Unfractionated intravenous heparin should therefore not be used routinely in acute ischemic stroke, but it may be considered in select stroke groups at high risk for early recurrent ischemic events (ie, patients with atrial fibrillation or acute myocardial infarction and large mural thrombi). However, even in these select populations, new clinical trials will be needed to define the risk-benefit ratio.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"141 1","pages":"1927-1933"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77518012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000019126.43079.7B
Naomi S. Bardach, Shoujun Zhao, Daryl R. Gress, M. Lawton, S. C. Johnston
Background and Purpose— Studies of several complex medical conditions have shown that outcomes are better at hospitals that treat more cases. We tested the hypothesis that patients with subarachnoid hemorrhage treated at high-volume hospitals have better outcomes. Methods— Using a database of all admissions to nonfederal hospitals in California from 1990 to 1999, we obtained discharge abstracts for patients with a primary diagnosis of subarachnoid hemorrhage who were admitted through the emergency department. Hospital volume, defined as the average number of subarachnoid hemorrhage cases admitted each year, was divided into quartiles. Rates of mortality, adverse outcomes (death or discharge to long-term care), length of stay, and hospital charges were computed by univariate analysis and by multivariable general estimating equations, with adjustment for demographic and admission characteristics. Results— A total of 12 804 patients were admitted for subarachnoid hemorrhage through the emergency departments of 390 hospitals. Hospital volumes varied from 0 to 8 cases per year in the first quartile to 19 to 70 cases per year in the fourth quartile. The mortality rate in the lowest volume quartile (49%) was larger than that in the highest volume quartile (32%, P <0.001). In multivariable analysis, the difference persisted (odds ratio comparing highest with lowest volume quartiles 0.57, 95% CI 0.48 to 0.67;P <0.001). At higher volume hospitals, lengths of stay were longer, and hospital charges were greater in univariate and multivariable models (all P <0.001). Only 4.8% of those admitted to hospitals in the lowest volume quartile were transferred to hospitals in the highest quartile. Conclusions— In this study of discharge abstracts in California, hospitals that treated more cases of subarachnoid hemorrhage had substantially lower rates of in-hospital mortality. Few patients with subarachnoid hemorrhage are being transferred to high-volume centers.
{"title":"Association Between Subarachnoid Hemorrhage Outcomes and Number of Cases Treated at California Hospitals","authors":"Naomi S. Bardach, Shoujun Zhao, Daryl R. Gress, M. Lawton, S. C. Johnston","doi":"10.1161/01.STR.0000019126.43079.7B","DOIUrl":"https://doi.org/10.1161/01.STR.0000019126.43079.7B","url":null,"abstract":"Background and Purpose— Studies of several complex medical conditions have shown that outcomes are better at hospitals that treat more cases. We tested the hypothesis that patients with subarachnoid hemorrhage treated at high-volume hospitals have better outcomes. Methods— Using a database of all admissions to nonfederal hospitals in California from 1990 to 1999, we obtained discharge abstracts for patients with a primary diagnosis of subarachnoid hemorrhage who were admitted through the emergency department. Hospital volume, defined as the average number of subarachnoid hemorrhage cases admitted each year, was divided into quartiles. Rates of mortality, adverse outcomes (death or discharge to long-term care), length of stay, and hospital charges were computed by univariate analysis and by multivariable general estimating equations, with adjustment for demographic and admission characteristics. Results— A total of 12 804 patients were admitted for subarachnoid hemorrhage through the emergency departments of 390 hospitals. Hospital volumes varied from 0 to 8 cases per year in the first quartile to 19 to 70 cases per year in the fourth quartile. The mortality rate in the lowest volume quartile (49%) was larger than that in the highest volume quartile (32%, P <0.001). In multivariable analysis, the difference persisted (odds ratio comparing highest with lowest volume quartiles 0.57, 95% CI 0.48 to 0.67;P <0.001). At higher volume hospitals, lengths of stay were longer, and hospital charges were greater in univariate and multivariable models (all P <0.001). Only 4.8% of those admitted to hospitals in the lowest volume quartile were transferred to hospitals in the highest quartile. Conclusions— In this study of discharge abstracts in California, hospitals that treated more cases of subarachnoid hemorrhage had substantially lower rates of in-hospital mortality. Few patients with subarachnoid hemorrhage are being transferred to high-volume centers.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"41 1","pages":"1851-1856"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74713647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000020121.41527.5D
Xiaoying Wang, Tatsuro Mori, T. Sumii, E. Lo
Background and Purpose— Apoptotic-like pathways may contribute to brain cell death after intracerebral hemorrhage. In this study, we used a simplified in vitro model of hemoglobin neurotoxicity to map the caspase cascades involved and to document the role of oxidative stress. Methods— Primary neuronal cultures were obtained from rat cerebral cortex and exposed to hemoglobin to induce cell death. Cytotoxicity was assessed via measurements of mitochondrial viability (MTT assay) and lactate dehydrogenase (LDH assay). Activation of caspase-3, -8, and -9 was measured by Western blot and enzyme activity assays. Various caspase inhibitors (zVADfmk, zDEVDfmk, zIETDfmk, and zLEHDfmk) were tested for neuroprotective efficacy. The role of oxidative stress was assessed with the use of U83836E as a potent scavenger of free radicals. Results— Exposure of primary cortical neurons to hemoglobin induced a dose- and time-dependent cytotoxicity. Western blots showed upregulation of cleaved caspase-3. Enzyme assays showed an increase in caspase-9–like and caspase-3–like activity. However, caspase inhibition did not result in neuroprotection. In contrast, the free radical scavenger U83836E significantly reduced hemoglobin-induced neuronal death. Combination treatment with both U83836E and the broad spectrum caspase inhibitor zVADfmk did not yield additional protection. Conclusions— Upstream and downstream caspases were upregulated after hemoglobin-induced neurotoxicity in vitro, but only an antioxidant approach with a potent free radical scavenger significantly improved neuronal survival. These data suggest that in addition to the activation of caspase cascades, parallel pathways of oxidative stress may predominate in this model of hemoglobin neurotoxicity.
{"title":"Hemoglobin-Induced Cytotoxicity in Rat Cerebral Cortical Neurons: Caspase Activation and Oxidative Stress","authors":"Xiaoying Wang, Tatsuro Mori, T. Sumii, E. Lo","doi":"10.1161/01.STR.0000020121.41527.5D","DOIUrl":"https://doi.org/10.1161/01.STR.0000020121.41527.5D","url":null,"abstract":"Background and Purpose— Apoptotic-like pathways may contribute to brain cell death after intracerebral hemorrhage. In this study, we used a simplified in vitro model of hemoglobin neurotoxicity to map the caspase cascades involved and to document the role of oxidative stress. Methods— Primary neuronal cultures were obtained from rat cerebral cortex and exposed to hemoglobin to induce cell death. Cytotoxicity was assessed via measurements of mitochondrial viability (MTT assay) and lactate dehydrogenase (LDH assay). Activation of caspase-3, -8, and -9 was measured by Western blot and enzyme activity assays. Various caspase inhibitors (zVADfmk, zDEVDfmk, zIETDfmk, and zLEHDfmk) were tested for neuroprotective efficacy. The role of oxidative stress was assessed with the use of U83836E as a potent scavenger of free radicals. Results— Exposure of primary cortical neurons to hemoglobin induced a dose- and time-dependent cytotoxicity. Western blots showed upregulation of cleaved caspase-3. Enzyme assays showed an increase in caspase-9–like and caspase-3–like activity. However, caspase inhibition did not result in neuroprotection. In contrast, the free radical scavenger U83836E significantly reduced hemoglobin-induced neuronal death. Combination treatment with both U83836E and the broad spectrum caspase inhibitor zVADfmk did not yield additional protection. Conclusions— Upstream and downstream caspases were upregulated after hemoglobin-induced neurotoxicity in vitro, but only an antioxidant approach with a potent free radical scavenger significantly improved neuronal survival. These data suggest that in addition to the activation of caspase cascades, parallel pathways of oxidative stress may predominate in this model of hemoglobin neurotoxicity.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"195 1","pages":"1882-1888"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75540966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000020091.07144.C7
V. Kothari, R. Stevens, A. Adler, I. Stratton, S. Manley, H. Neil, R. Holman
Background and Purpose— People with type 2 diabetes are at elevated risk of stroke compared with those without diabetes. Relative risks have been examined in earlier work, but there is no readily available method for predicting the absolute risk of stroke in a diabetic individual. We developed mathematical models to estimate the risk of a first stroke using data from 4549 newly diagnosed type 2 diabetic patients enrolled in the UK Prospective Diabetes Study. Methods— During 30 700 person-years of follow-up, 188 first strokes (52 fatal) occurred. Model fitting was carried out by maximum likelihood estimation using the Newton-Raphson method. Diagnostic plots were used to compare survival probabilities calculated by the model with those calculated using nonparametric methods. Results— Variables included in the final model were duration of diabetes, age, sex, smoking, systolic blood pressure, total cholesterol to high-density lipoprotein cholesterol ratio and presence of atrial fibrillation. Not included in the model were body mass index, hemoglobin A1c, ethnicity, and ex-smoking status. The use of the model is illustrated with a hypothetical study power calculation. Conclusions— This model forecasts the absolute risk of a first stroke in people with type 2 diabetes using variables readily available in routine clinical practice.
{"title":"UKPDS 60: Risk of Stroke in Type 2 Diabetes Estimated by the UK Prospective Diabetes Study Risk Engine","authors":"V. Kothari, R. Stevens, A. Adler, I. Stratton, S. Manley, H. Neil, R. Holman","doi":"10.1161/01.STR.0000020091.07144.C7","DOIUrl":"https://doi.org/10.1161/01.STR.0000020091.07144.C7","url":null,"abstract":"Background and Purpose— People with type 2 diabetes are at elevated risk of stroke compared with those without diabetes. Relative risks have been examined in earlier work, but there is no readily available method for predicting the absolute risk of stroke in a diabetic individual. We developed mathematical models to estimate the risk of a first stroke using data from 4549 newly diagnosed type 2 diabetic patients enrolled in the UK Prospective Diabetes Study. Methods— During 30 700 person-years of follow-up, 188 first strokes (52 fatal) occurred. Model fitting was carried out by maximum likelihood estimation using the Newton-Raphson method. Diagnostic plots were used to compare survival probabilities calculated by the model with those calculated using nonparametric methods. Results— Variables included in the final model were duration of diabetes, age, sex, smoking, systolic blood pressure, total cholesterol to high-density lipoprotein cholesterol ratio and presence of atrial fibrillation. Not included in the model were body mass index, hemoglobin A1c, ethnicity, and ex-smoking status. The use of the model is illustrated with a hypothetical study power calculation. Conclusions— This model forecasts the absolute risk of a first stroke in people with type 2 diabetes using variables readily available in routine clinical practice.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"5 1","pages":"1776-1781"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81280948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2002-07-01DOI: 10.1161/01.STR.0000020092.41820.58
K. Kapinya, Diana Löwl, C. Fütterer, M. Maurer, K. Waschke, N. Isaev, U. Dirnagl
Background and Purpose— We tested whether volatile anesthetics induce neuroprotection that is maintained for a prolonged time. Methods— Rats were pretreated for 3 hours with 1 minimal anesthetic concentration of isoflurane or halothane in normal air (anesthetic preconditioning [AP]). The animals were subjected to permanent middle cerebral artery occlusion (MCAO) at 0, 12, 24, or 48 hours after AP. Halothane-pretreated animals were subjected to MCAO 24 hours after AP. Histological evaluation of infarct volumes was performed 4 days after MCAO. Cerebral glucose utilization was measured 24 hours after AP with isoflurane. Primary cortical neuronal cultures were exposed to 1.4% isoflurane for 3 hours. Oxygen-glucose deprivation (OGD) was performed 24 hours after AP. Injury was assessed 24 hours later by measuring the release of lactate dehydrogenase into the medium 24 hours after OGD. Results— Isoflurane anesthesia at 0, 12, and 24 hours before MCAO or halothane anesthesia 24 hours before MCAO significantly reduced infarct volumes (125±42 mm3, P =0.024; 118±51 mm3, P =0.008; 120±49 mm3, P =0.009; and 121±48 mm3, P =0.018, respectively) compared with control volumes (180±51 mm3). Three hours of isoflurane anesthesia in rats did not have any effect on local or mean cerebral glucose utilization measured 24 hours later. Western blot analysis from cortical extracts of AP-treated animals revealed an increase of the inducible NO synthase (iNOS) protein beginning 6 hours after AP. The iNOS inhibitor aminoguanidine (200 mg/kg IP) eliminated the infarct-sparing effect of AP. In cultured cortical neurons, isoflurane exposure 24 hours before OGD decreased the OGD-induced release of lactate dehydrogenase by 49% (P =0.002). Conclusions— Pretreatment with volatile anesthetics induces prolonged neuroprotection in vitro and in vivo, a process in which iNOS seems to be critically involved.
背景和目的:我们测试了挥发性麻醉药是否能诱导神经保护并维持较长时间。方法:大鼠在正常空气中用最低浓度的异氟醚或氟烷预处理3小时(麻醉预处理[AP])。动物在AP后0,12,24或48小时进行永久性大脑中动脉闭塞(MCAO)。在AP后24小时进行卤化物预处理的动物MCAO。MCAO后4天进行梗死体积的组织学评估。用异氟醚治疗后24小时测定脑葡萄糖利用率。原代皮质神经元培养物暴露于1.4%异氟烷中3小时。AP 24小时后进行氧葡萄糖剥夺(OGD)， 24小时后通过测量乳酸脱氢酶在OGD后24小时释放到培养基中来评估损伤。结果- MCAO前0、12、24小时异氟醚麻醉或MCAO前24小时氟烷麻醉可显著降低梗死面积(125±42 mm3, P =0.024;118±51 mm3, P =0.008;120±49 mm3, P =0.009;与对照组(180±51 mm3)比较，分别为121±48 mm3, P =0.018。大鼠异氟醚麻醉3小时对24小时后测量的局部或平均脑葡萄糖利用率没有任何影响。AP处理动物皮质提取物的Western blot分析显示，AP处理后6小时开始诱导NO合成酶(iNOS)蛋白增加。iNOS抑制剂氨基胍(200 mg/kg IP)消除了AP的梗死保护作用。在培养的皮质神经元中，OGD前24小时暴露异氟醚可使OGD诱导的乳酸脱氢酶释放减少49% (P =0.002)。结论:挥发性麻醉药预处理在体外和体内均可延长神经保护时间，iNOS似乎在这一过程中起关键作用。
{"title":"Tolerance Against Ischemic Neuronal Injury Can Be Induced by Volatile Anesthetics and Is Inducible NO Synthase Dependent","authors":"K. Kapinya, Diana Löwl, C. Fütterer, M. Maurer, K. Waschke, N. Isaev, U. Dirnagl","doi":"10.1161/01.STR.0000020092.41820.58","DOIUrl":"https://doi.org/10.1161/01.STR.0000020092.41820.58","url":null,"abstract":"Background and Purpose— We tested whether volatile anesthetics induce neuroprotection that is maintained for a prolonged time. Methods— Rats were pretreated for 3 hours with 1 minimal anesthetic concentration of isoflurane or halothane in normal air (anesthetic preconditioning [AP]). The animals were subjected to permanent middle cerebral artery occlusion (MCAO) at 0, 12, 24, or 48 hours after AP. Halothane-pretreated animals were subjected to MCAO 24 hours after AP. Histological evaluation of infarct volumes was performed 4 days after MCAO. Cerebral glucose utilization was measured 24 hours after AP with isoflurane. Primary cortical neuronal cultures were exposed to 1.4% isoflurane for 3 hours. Oxygen-glucose deprivation (OGD) was performed 24 hours after AP. Injury was assessed 24 hours later by measuring the release of lactate dehydrogenase into the medium 24 hours after OGD. Results— Isoflurane anesthesia at 0, 12, and 24 hours before MCAO or halothane anesthesia 24 hours before MCAO significantly reduced infarct volumes (125±42 mm3, P =0.024; 118±51 mm3, P =0.008; 120±49 mm3, P =0.009; and 121±48 mm3, P =0.018, respectively) compared with control volumes (180±51 mm3). Three hours of isoflurane anesthesia in rats did not have any effect on local or mean cerebral glucose utilization measured 24 hours later. Western blot analysis from cortical extracts of AP-treated animals revealed an increase of the inducible NO synthase (iNOS) protein beginning 6 hours after AP. The iNOS inhibitor aminoguanidine (200 mg/kg IP) eliminated the infarct-sparing effect of AP. In cultured cortical neurons, isoflurane exposure 24 hours before OGD decreased the OGD-induced release of lactate dehydrogenase by 49% (P =0.002). Conclusions— Pretreatment with volatile anesthetics induces prolonged neuroprotection in vitro and in vivo, a process in which iNOS seems to be critically involved.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"39 1","pages":"1889-1898"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81600382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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