Pub Date : 2002-08-01DOI: 10.1161/01.STR.0000022807.06923.A3
G. D. Jong, F. Kessels, J. Lodder
Background and Purpose— Earlier, we found that lacunar stroke patients with ≥1 asymptomatic lacunar infarcts on CT had leukoaraiosis and hypertension significantly more often than patients without such lesions, and we hypothesized that 2 types of small-vessel disease could be distinguished during life: arteriolosclerosis and microatheromatosis, respectively. Differences in prognosis might sustain this hypothesis of 2 lacunar stroke entities. Therefore, we performed a follow-up in 333 patients with first lacunar stroke, distinguishing those with ≥1 asymptomatic lacunar lesions (LACI+) from those without such lesions (LACI−). Methods— Cross-sectional follow-up was performed after 785±479 days (mean±SD) in 104 LACI+ patients and 865±545 days in 229 LACI− patients. Results— Mortality at the end of follow-up was 33% in LACI+ and 21% in LACI− patients [odds ratio (OR), 1.74; 95% confidence interval (CI), 1.01 to 3.01]. Stroke recurrence rate was 21% in LACI+ and 11% in LACI− (OR, 2.09; 95% CI, 1.08 to 4.06). Forty percent of LACI+ and 26% of LACI− patients had unfavorable outcome at the end of follow-up (OR, 1.95; 95% CI, 1.17 to 3.26). Kaplan-Meier curves showed less favorable survival in LACI+ (log-rank test, P =0.0218) and survival free of stroke (log-rank test, P =0.0121) than in LACI−. When we restricted the analysis to patients with both silent lesions and leukoaraiosis (n=63) compared with those without (n=196), differences were even more pronounced. Conclusions— Prognosis for mortality, recurrent stroke, and overall functional outcome in lacunar stroke patients with ≥1 silent lacunar lesions is more unfavorable than in patients without such lesions. These findings sustain the idea of 2 lacunar stroke entities.
{"title":"Two Types of Lacunar Infarcts: Further Arguments From a Study on Prognosis","authors":"G. D. Jong, F. Kessels, J. Lodder","doi":"10.1161/01.STR.0000022807.06923.A3","DOIUrl":"https://doi.org/10.1161/01.STR.0000022807.06923.A3","url":null,"abstract":"Background and Purpose— Earlier, we found that lacunar stroke patients with ≥1 asymptomatic lacunar infarcts on CT had leukoaraiosis and hypertension significantly more often than patients without such lesions, and we hypothesized that 2 types of small-vessel disease could be distinguished during life: arteriolosclerosis and microatheromatosis, respectively. Differences in prognosis might sustain this hypothesis of 2 lacunar stroke entities. Therefore, we performed a follow-up in 333 patients with first lacunar stroke, distinguishing those with ≥1 asymptomatic lacunar lesions (LACI+) from those without such lesions (LACI−). Methods— Cross-sectional follow-up was performed after 785±479 days (mean±SD) in 104 LACI+ patients and 865±545 days in 229 LACI− patients. Results— Mortality at the end of follow-up was 33% in LACI+ and 21% in LACI− patients [odds ratio (OR), 1.74; 95% confidence interval (CI), 1.01 to 3.01]. Stroke recurrence rate was 21% in LACI+ and 11% in LACI− (OR, 2.09; 95% CI, 1.08 to 4.06). Forty percent of LACI+ and 26% of LACI− patients had unfavorable outcome at the end of follow-up (OR, 1.95; 95% CI, 1.17 to 3.26). Kaplan-Meier curves showed less favorable survival in LACI+ (log-rank test, P =0.0218) and survival free of stroke (log-rank test, P =0.0121) than in LACI−. When we restricted the analysis to patients with both silent lesions and leukoaraiosis (n=63) compared with those without (n=196), differences were even more pronounced. Conclusions— Prognosis for mortality, recurrent stroke, and overall functional outcome in lacunar stroke patients with ≥1 silent lacunar lesions is more unfavorable than in patients without such lesions. These findings sustain the idea of 2 lacunar stroke entities.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"77 1","pages":"2072-2076"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83860427","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 : 2002-08-01DOI: 10.1161/01.STR.0000021900.58396.44
P. Nederkoorn, W. Mali, B. Eikelboom, O. Elgersma, E. Buskens, M. Hunink, L. Kappelle, P. Buijs, A. F. Wüst, A. Lugt, Y. Graaf
Background and Purpose— Carotid endarterectomy has been shown to be beneficial in symptomatic patients with a severe stenosis (70% to 99%) of the internal carotid artery (ICA). Digital subtraction angiography (DSA) is the standard of reference in the diagnosis of carotid artery stenosis but has a relatively high complication rate. In a diagnostic study we investigated the accuracy of noninvasive testing compared with DSA. Methods— In a prospective diagnostic study we performed duplex ultrasound (DUS), magnetic resonance angiography (MRA), and DSA on 350 consecutive symptomatic patients. Stenoses were measured with the observers blinded for clinical information and other test results. Separate and combined test results of DUS and MRA were compared with the reference standard DSA. Only the stenosis measurements of the arteries on the symptomatic side were included in the analyses. Results— DUS analyzed with previously defined criteria resulted in a sensitivity of 87.5% (95% CI, 82.1% to 92.9%) and a specificity of 75.7% (95% CI, 69.3% to 82.2%) in identifying severe ICA stenosis (70% to 99%). Stenosis measurements on MRA yielded a sensitivity of 92.2% (95% CI, 86.2% to 96.2%) and a specificity of 75.7% (95% CI, 68.6% to 82.5%). When we combined MRA and DUS results, agreement between these 2 modalities (84% of patients) gave a sensitivity of 96.3% (95% CI, 90.8% to 99.0%) and a specificity of 80.2% (95% CI, 73.1% to 87.3%) for identifying severe stenosis. Conclusions— MRA showed a slightly better accuracy than DUS in the diagnosis of carotid artery stenosis. To achieve the best accuracy, however, both tests should be performed subsequently.
{"title":"Preoperative Diagnosis of Carotid Artery Stenosis: Accuracy of Noninvasive Testing","authors":"P. Nederkoorn, W. Mali, B. Eikelboom, O. Elgersma, E. Buskens, M. Hunink, L. Kappelle, P. Buijs, A. F. Wüst, A. Lugt, Y. Graaf","doi":"10.1161/01.STR.0000021900.58396.44","DOIUrl":"https://doi.org/10.1161/01.STR.0000021900.58396.44","url":null,"abstract":"Background and Purpose— Carotid endarterectomy has been shown to be beneficial in symptomatic patients with a severe stenosis (70% to 99%) of the internal carotid artery (ICA). Digital subtraction angiography (DSA) is the standard of reference in the diagnosis of carotid artery stenosis but has a relatively high complication rate. In a diagnostic study we investigated the accuracy of noninvasive testing compared with DSA. Methods— In a prospective diagnostic study we performed duplex ultrasound (DUS), magnetic resonance angiography (MRA), and DSA on 350 consecutive symptomatic patients. Stenoses were measured with the observers blinded for clinical information and other test results. Separate and combined test results of DUS and MRA were compared with the reference standard DSA. Only the stenosis measurements of the arteries on the symptomatic side were included in the analyses. Results— DUS analyzed with previously defined criteria resulted in a sensitivity of 87.5% (95% CI, 82.1% to 92.9%) and a specificity of 75.7% (95% CI, 69.3% to 82.2%) in identifying severe ICA stenosis (70% to 99%). Stenosis measurements on MRA yielded a sensitivity of 92.2% (95% CI, 86.2% to 96.2%) and a specificity of 75.7% (95% CI, 68.6% to 82.5%). When we combined MRA and DUS results, agreement between these 2 modalities (84% of patients) gave a sensitivity of 96.3% (95% CI, 90.8% to 99.0%) and a specificity of 80.2% (95% CI, 73.1% to 87.3%) for identifying severe stenosis. Conclusions— MRA showed a slightly better accuracy than DUS in the diagnosis of carotid artery stenosis. To achieve the best accuracy, however, both tests should be performed subsequently.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"45 1","pages":"2003-2008"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90177028","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 : 2002-08-01DOI: 10.1161/01.STR.0000023890.25066.50
H. Iso, S. Sato, U. Umemura, M. Kudo, K. Koike, A. Kitamura, H. Imano, T. Okamura, Y. Naito, T. Shimamoto
Background and Purpose— The role of serum fatty acids as a risk factor for stroke and stroke subtypes is largely unknown. Methods— A prospective nested case-control study of Japanese 40 to 85 years of age was conducted through the use of frozen serum samples from 7450 participants in cardiovascular risk surveys collected from 1984 to 1989 for 1 community and 1989 to 1992 for the other 2 communities. By the end of 1998, we identified 197 incident strokes whose subtypes were confirmed by imaging studies. Three controls per case were selected by matching for sex, age, community, year of serum storage, and fasting status. Results— Compared with controls, total (n=197), hemorrhagic (n=75), and ischemic (n=122) strokes had similar proportions of n3 polyunsaturated fatty acids, lower proportions of linoleic and arachidonic acids, and higher proportions of saturated and monosaturated acids, determined by gas chromatography. The multivariate odds ratios associated with a 1-SD increase in linoleic acid (5%) after adjustment for hypertension, diabetes, serum total cholesterol, and other cardiovascular risk factors were 0.72 [95% confidence interval (CI), 0.59 to 0.89] for total stroke, 0.66 (95% CI, 0.49 to 0.88) for ischemic stroke, 0.63 (95% CI, 0.46 to 0.88) for lacunar infarction, and 0.81 (95% CI, 0.59 to 1.12) for hemorrhagic stroke. The respective odds ratios for saturated fatty acids (4%) were 1.13 (95% CI, 1.05 to 1.65), 1.35 (95% CI, 1.01 to 1.79), 1.44 (95% CI, 1.03 to 2.01), and 1.21 (95% CI, 0.82 to 1.80). Further adjustment for other fatty acids attenuated these relations, but the relation between linoleic acid and risk of ischemic stroke remained statistically significant. Conclusions— A higher intake of linoleic acid may protect against ischemic stroke, possibly through potential mechanisms of decreased blood pressure, reduced platelet aggregation, and enhanced deformability of erythrocyte cells.
{"title":"Linoleic Acid, Other Fatty Acids, and the Risk of Stroke","authors":"H. Iso, S. Sato, U. Umemura, M. Kudo, K. Koike, A. Kitamura, H. Imano, T. Okamura, Y. Naito, T. Shimamoto","doi":"10.1161/01.STR.0000023890.25066.50","DOIUrl":"https://doi.org/10.1161/01.STR.0000023890.25066.50","url":null,"abstract":"Background and Purpose— The role of serum fatty acids as a risk factor for stroke and stroke subtypes is largely unknown. Methods— A prospective nested case-control study of Japanese 40 to 85 years of age was conducted through the use of frozen serum samples from 7450 participants in cardiovascular risk surveys collected from 1984 to 1989 for 1 community and 1989 to 1992 for the other 2 communities. By the end of 1998, we identified 197 incident strokes whose subtypes were confirmed by imaging studies. Three controls per case were selected by matching for sex, age, community, year of serum storage, and fasting status. Results— Compared with controls, total (n=197), hemorrhagic (n=75), and ischemic (n=122) strokes had similar proportions of n3 polyunsaturated fatty acids, lower proportions of linoleic and arachidonic acids, and higher proportions of saturated and monosaturated acids, determined by gas chromatography. The multivariate odds ratios associated with a 1-SD increase in linoleic acid (5%) after adjustment for hypertension, diabetes, serum total cholesterol, and other cardiovascular risk factors were 0.72 [95% confidence interval (CI), 0.59 to 0.89] for total stroke, 0.66 (95% CI, 0.49 to 0.88) for ischemic stroke, 0.63 (95% CI, 0.46 to 0.88) for lacunar infarction, and 0.81 (95% CI, 0.59 to 1.12) for hemorrhagic stroke. The respective odds ratios for saturated fatty acids (4%) were 1.13 (95% CI, 1.05 to 1.65), 1.35 (95% CI, 1.01 to 1.79), 1.44 (95% CI, 1.03 to 2.01), and 1.21 (95% CI, 0.82 to 1.80). Further adjustment for other fatty acids attenuated these relations, but the relation between linoleic acid and risk of ischemic stroke remained statistically significant. Conclusions— A higher intake of linoleic acid may protect against ischemic stroke, possibly through potential mechanisms of decreased blood pressure, reduced platelet aggregation, and enhanced deformability of erythrocyte cells.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"23 1","pages":"2086-2093"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84825003","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 : 2002-08-01DOI: 10.1161/01.STR.0000021001.18101.A5
I. Linfante, R. Llinas, M. Selim, C. Chaves, Sandeep Kumar, R. Parker, L. Caplan, G. Schlaug
Background and Purpose— Early reperfusion is a predictor of good outcome in acute ischemic stroke. We investigated whether middle cerebral artery (MCA) occlusions have a better clinical outcome and proportion of recanalization compared with internal carotid artery (ICA) occlusion after standard treatment with intravenous (IV) tissue plasminogen activator (tPA). Patients— In a retrospective analysis of our prospective stroke database between January 7, 1998, and January 30, 2002, we identified 36 consecutive patients who were treated with IV tPA within 3 hours after symptom onset of a stroke in the distribution of a documented ICA or MCA occlusion. The National Institutes of Health Stroke Scale (NIHSS) score was recorded before tPA, at 24 hours, 3 days, and 3 months after stroke. Three-month outcome was recorded by modified Rankin scale. Magnetic resonance angiography or computed tomographic angiography was obtained before tPA. The presence of recanalization was assessed by transcranial Doppler and/or magnetic resonance angiography within 3 days after stroke onset. Results— Nineteen patients had MCA occlusion, and 17 had ICA-plus-MCA occlusion before tPA. Although there was no difference in age and NIHSS at day 0 between the 2 groups, the MCA group had a lower day 3 NIHSS score compared with the ICA group (P =0.006) in an ANCOVA. In addition, patients who had a MCA occlusion had lower day 1 and 3 NIHSS scores compared with the ICA group (P =0.04 and P =0.03, respectively; Wilcoxon rank sum). Similarly, NIHSS was significantly lower in patients who recanalized on days 1 and 3 (P =0.004 and P =0.003 respectively, Wilcoxon rank sum). When we adjusted for NIHSS score at day 0 in an ANCOVA, the adjusted mean was lower in the group that recanalized compared with the group that did not recanalize (P <0.001). There was a significant difference between the proportion of recanalization in the MCA group (15 of 17 recanalized, 88%) at 3 days after tPA compared with that of the ICA group (5 of 16 recanalized, 31%;P =0.001, Fisher exact test). The 3-month modified Rankin scale was not different between the 2 groups. Conclusions— Despite comparable age and NIHSS scores before IV tPA, MCA occlusions have lower day 1 and 3 NIHSS scores and higher proportion of recanalization compared with ICA occlusions. A combined IV/intra-arterial or mechanical thrombolysis may be needed to achieve early recanalization in ICA occlusions.
{"title":"Clinical and Vascular Outcome in Internal Carotid Artery Versus Middle Cerebral Artery Occlusions After Intravenous Tissue Plasminogen Activator","authors":"I. Linfante, R. Llinas, M. Selim, C. Chaves, Sandeep Kumar, R. Parker, L. Caplan, G. Schlaug","doi":"10.1161/01.STR.0000021001.18101.A5","DOIUrl":"https://doi.org/10.1161/01.STR.0000021001.18101.A5","url":null,"abstract":"Background and Purpose— Early reperfusion is a predictor of good outcome in acute ischemic stroke. We investigated whether middle cerebral artery (MCA) occlusions have a better clinical outcome and proportion of recanalization compared with internal carotid artery (ICA) occlusion after standard treatment with intravenous (IV) tissue plasminogen activator (tPA). Patients— In a retrospective analysis of our prospective stroke database between January 7, 1998, and January 30, 2002, we identified 36 consecutive patients who were treated with IV tPA within 3 hours after symptom onset of a stroke in the distribution of a documented ICA or MCA occlusion. The National Institutes of Health Stroke Scale (NIHSS) score was recorded before tPA, at 24 hours, 3 days, and 3 months after stroke. Three-month outcome was recorded by modified Rankin scale. Magnetic resonance angiography or computed tomographic angiography was obtained before tPA. The presence of recanalization was assessed by transcranial Doppler and/or magnetic resonance angiography within 3 days after stroke onset. Results— Nineteen patients had MCA occlusion, and 17 had ICA-plus-MCA occlusion before tPA. Although there was no difference in age and NIHSS at day 0 between the 2 groups, the MCA group had a lower day 3 NIHSS score compared with the ICA group (P =0.006) in an ANCOVA. In addition, patients who had a MCA occlusion had lower day 1 and 3 NIHSS scores compared with the ICA group (P =0.04 and P =0.03, respectively; Wilcoxon rank sum). Similarly, NIHSS was significantly lower in patients who recanalized on days 1 and 3 (P =0.004 and P =0.003 respectively, Wilcoxon rank sum). When we adjusted for NIHSS score at day 0 in an ANCOVA, the adjusted mean was lower in the group that recanalized compared with the group that did not recanalize (P <0.001). There was a significant difference between the proportion of recanalization in the MCA group (15 of 17 recanalized, 88%) at 3 days after tPA compared with that of the ICA group (5 of 16 recanalized, 31%;P =0.001, Fisher exact test). The 3-month modified Rankin scale was not different between the 2 groups. Conclusions— Despite comparable age and NIHSS scores before IV tPA, MCA occlusions have lower day 1 and 3 NIHSS scores and higher proportion of recanalization compared with ICA occlusions. A combined IV/intra-arterial or mechanical thrombolysis may be needed to achieve early recanalization in ICA occlusions.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"52 1","pages":"2066-2071"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84958937","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 : 2002-08-01DOI: 10.1161/01.STR.0000025518.34157.51
D. Gladstone, S. Black, A. Hakim
Background— Neuroprotective drugs for acute stroke have appeared to work in animals, only to fail when tested in humans. With the failure of so many clinical trials, the future of neuroprotective drug development is in jeopardy. Current hypotheses and methodologies must continue to be reevaluated, and new strategies need to be explored. Summary of Review— In part 1, we review key challenges and complexities in translational stroke research by focusing on the “disconnect” in the way that neuroprotective agents have traditionally been assessed in clinical trials compared with animal models. In preclinical studies, determination of neuroprotection has relied heavily on assessment of infarct volume measurements (instead of functional outcomes), short-term (instead of long-term) end points, transient (instead of permanent) ischemia models, short (instead of extended) time windows for drug administration, and protection of cerebral gray matter (instead of both gray and white matter). Clinical trials have often been limited by inappropriately long time windows, insufficient statistical power, insensitive outcome measures, inclusion of protocol violators, failure to target specific stroke subtypes, and failure to target the ischemic penumbra. In part 2, we explore new concepts in ischemic pathophysiology that should encourage us also to think beyond the hyperacute phase of ischemia and consider the design of trials that use multiagent therapy and exploit the capacity of the brain for neuroplasticity and repair. Conclusions— By recognizing the strengths and limitations of animal models of stroke and the shortcomings of previous clinical trials, we hope to move translational research forward for the development of new therapies for the acute and subacute stages after stroke.
{"title":"Toward Wisdom From Failure: Lessons From Neuroprotective Stroke Trials and New Therapeutic Directions","authors":"D. Gladstone, S. Black, A. Hakim","doi":"10.1161/01.STR.0000025518.34157.51","DOIUrl":"https://doi.org/10.1161/01.STR.0000025518.34157.51","url":null,"abstract":"Background— Neuroprotective drugs for acute stroke have appeared to work in animals, only to fail when tested in humans. With the failure of so many clinical trials, the future of neuroprotective drug development is in jeopardy. Current hypotheses and methodologies must continue to be reevaluated, and new strategies need to be explored. Summary of Review— In part 1, we review key challenges and complexities in translational stroke research by focusing on the “disconnect” in the way that neuroprotective agents have traditionally been assessed in clinical trials compared with animal models. In preclinical studies, determination of neuroprotection has relied heavily on assessment of infarct volume measurements (instead of functional outcomes), short-term (instead of long-term) end points, transient (instead of permanent) ischemia models, short (instead of extended) time windows for drug administration, and protection of cerebral gray matter (instead of both gray and white matter). Clinical trials have often been limited by inappropriately long time windows, insufficient statistical power, insensitive outcome measures, inclusion of protocol violators, failure to target specific stroke subtypes, and failure to target the ischemic penumbra. In part 2, we explore new concepts in ischemic pathophysiology that should encourage us also to think beyond the hyperacute phase of ischemia and consider the design of trials that use multiagent therapy and exploit the capacity of the brain for neuroplasticity and repair. Conclusions— By recognizing the strengths and limitations of animal models of stroke and the shortcomings of previous clinical trials, we hope to move translational research forward for the development of new therapies for the acute and subacute stages after stroke.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"29 1","pages":"2123-2136"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82661552","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 : 2002-08-01DOI: 10.1161/01.STR.0000022810.76115.C0
A. Ristić, J. Marinković, Nataa T. Dragaevic, D. Stanisavljević, V. Kostic
Background and Purpose— The aim of this study was to prospectively evaluate the long-term prognosis of hemiballismus due to first-ever ischemic strokes. Methods— A cohort of 27 patients with hemiballismus due to first-ever ischemic strokes was followed for a mean period of 30 months (range, 5 days to 150 months). Results— During the follow-up period there were 11 deaths (44%). The survival rate was 85% (95% CI, 71% to 99%) at 6 months, 81% (95% CI, 65% to 97%) at 15 months, 51% (95% CI, 24% to 78%) at 36 months, and only 32% (95% CI, 4% to 60%) at 150 months. The survival rate free from recurrent stroke was 96% (95% CI, 87% to 100%) at 6 months, 91% (95% CI, 79% to 100%) at 12 months, 80% (95% CI, 61% to 99%) at 24 months, and 27% (95% CI, 0% to 71%) at 150 months. Conclusions— The long-term prognosis of patients with vascular hemiballismus is similar to that of other stroke patients, ie, it follows the etiologic pattern of hemiballismus.
{"title":"Long-Term Prognosis of Vascular Hemiballismus","authors":"A. Ristić, J. Marinković, Nataa T. Dragaevic, D. Stanisavljević, V. Kostic","doi":"10.1161/01.STR.0000022810.76115.C0","DOIUrl":"https://doi.org/10.1161/01.STR.0000022810.76115.C0","url":null,"abstract":"Background and Purpose— The aim of this study was to prospectively evaluate the long-term prognosis of hemiballismus due to first-ever ischemic strokes. Methods— A cohort of 27 patients with hemiballismus due to first-ever ischemic strokes was followed for a mean period of 30 months (range, 5 days to 150 months). Results— During the follow-up period there were 11 deaths (44%). The survival rate was 85% (95% CI, 71% to 99%) at 6 months, 81% (95% CI, 65% to 97%) at 15 months, 51% (95% CI, 24% to 78%) at 36 months, and only 32% (95% CI, 4% to 60%) at 150 months. The survival rate free from recurrent stroke was 96% (95% CI, 87% to 100%) at 6 months, 91% (95% CI, 79% to 100%) at 12 months, 80% (95% CI, 61% to 99%) at 24 months, and 27% (95% CI, 0% to 71%) at 150 months. Conclusions— The long-term prognosis of patients with vascular hemiballismus is similar to that of other stroke patients, ie, it follows the etiologic pattern of hemiballismus.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"1099 1","pages":"2109-2111"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76734804","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 : 2002-08-01DOI: 10.1161/01.STR.0000021410.83049.32
K. Sugioka, T. Hozumi, R. Sciacca, Y. Miyake, Inna Titova, G. Gaspard, R. Sacco, S. Homma, M. D. Di Tullio
Background and Purpose— Large atherosclerotic plaques in the aortic arch detected by transesophageal echocardiography (TEE) are associated with increased risk of ischemic stroke in the elderly. The atherosclerotic process also affects aortic distensibility, which can also be assessed by TEE. The purpose of this study was to evaluate the possible association of aortic stiffness by TEE with ischemic stroke in elderly patients. Methods— We performed TEE in 40 consecutive elderly patients aged ≥55 years with acute ischemic stroke and in 42 consecutive control subjects aged ≥55 years. Aortic stiffness index &bgr;, which has been used in the literature to express the stiffness of the aortic wall, was calculated as follows: &bgr;=ln (systolic blood pressure/diastolic blood pressure)/([Dmax−Dmin]/Dmin), where ln is natural logarithm, Dmax is maximum aortic lumen diameter, and Dmin is minimum aortic lumen diameter by TEE. The association of index &bgr; with ischemic stroke was evaluated by logistic regression analysis after adjustment for potential confounders, including thickness of aortic arch plaques. Results— Index &bgr; was significantly greater in stroke patients than in controls (9.7±5.0 versus 5.3±3.5;P <0.0001). When aortic plaque thickness and other stroke risk factors were entered in multivariate analysis, index &bgr; was found to be independently associated with ischemic stroke (odds ratio, 1.28 per unit increase; 95% CI, 1.10 to 1.52). Conclusions— Aortic stiffness by TEE is associated with ischemic stroke, independent of thickness of aortic arch plaques and other stroke risk factors. This suggests that aortic stiffness by TEE may add prognostic information when assessing the risk of ischemic stroke in the elderly.
{"title":"Impact of Aortic Stiffness on Ischemic Stroke in Elderly Patients","authors":"K. Sugioka, T. Hozumi, R. Sciacca, Y. Miyake, Inna Titova, G. Gaspard, R. Sacco, S. Homma, M. D. Di Tullio","doi":"10.1161/01.STR.0000021410.83049.32","DOIUrl":"https://doi.org/10.1161/01.STR.0000021410.83049.32","url":null,"abstract":"Background and Purpose— Large atherosclerotic plaques in the aortic arch detected by transesophageal echocardiography (TEE) are associated with increased risk of ischemic stroke in the elderly. The atherosclerotic process also affects aortic distensibility, which can also be assessed by TEE. The purpose of this study was to evaluate the possible association of aortic stiffness by TEE with ischemic stroke in elderly patients. Methods— We performed TEE in 40 consecutive elderly patients aged ≥55 years with acute ischemic stroke and in 42 consecutive control subjects aged ≥55 years. Aortic stiffness index &bgr;, which has been used in the literature to express the stiffness of the aortic wall, was calculated as follows: &bgr;=ln (systolic blood pressure/diastolic blood pressure)/([Dmax−Dmin]/Dmin), where ln is natural logarithm, Dmax is maximum aortic lumen diameter, and Dmin is minimum aortic lumen diameter by TEE. The association of index &bgr; with ischemic stroke was evaluated by logistic regression analysis after adjustment for potential confounders, including thickness of aortic arch plaques. Results— Index &bgr; was significantly greater in stroke patients than in controls (9.7±5.0 versus 5.3±3.5;P <0.0001). When aortic plaque thickness and other stroke risk factors were entered in multivariate analysis, index &bgr; was found to be independently associated with ischemic stroke (odds ratio, 1.28 per unit increase; 95% CI, 1.10 to 1.52). Conclusions— Aortic stiffness by TEE is associated with ischemic stroke, independent of thickness of aortic arch plaques and other stroke risk factors. This suggests that aortic stiffness by TEE may add prognostic information when assessing the risk of ischemic stroke in the elderly.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"36 1","pages":"2077-2081"},"PeriodicalIF":0.0,"publicationDate":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88446691","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.0000020124.61998.BC
M. Koistinaho, M. Kettunen, D. Holtzman, R. Kauppinen, L. Higgins, J. Koistinaho
Background and Purpose— Epidemiological findings and experimental data on transgenic mice show that Alzheimer’s disease–related changes render the brain more susceptible to ischemic damage. We studied whether the previously observed vulnerability in mice overexpressing the 751–amino-acid isoform of human amyloid precursor protein (APP751) is regulated by human apolipoprotein E (apoE) alleles, which determine the relative risk for Alzheimer’s disease and the susceptibility to various forms of acute brain damage. Methods— Aged apoE knock out (KO) mice, mice overexpressing APP751 in the apoE KO background and mice expressing either human apoE3 or apoE4 and APP751 in the apoE KO background were exposed to permanent occlusion of the middle cerebral artery (MCA). Infarct volumes were quantified from T2-weighted magnetic resonance images 24 hours after the MCA occlusion. Local cortical blood flow was monitored by laser Doppler flowmetry. Ischemia-induced microgliosis was detected by immunohistochemistry. Results— Overexpression of human APP751 significantly increased the infarct volumes in apoE KO mice. Furthermore, this APP751-induced ischemic vulnerability was attenuated by the coexpression of either human apoE isoform. MCA occlusion resulted in a similar relative reduction in cortical blood flow in all mouse groups. Vascular anatomy showed no variation in the MCA territory between the groups. Instead, the expression of human apoE isoforms reduced the ischemia-induced microgliosis. Conclusions— Expression of either the human apoE3 or apoE4 isoform protects against the increased ischemic vulnerability observed in aged mice overexpressing human APP751, probably by modulating the inflammatory response induced by MCA occlusion.
{"title":"Expression of Human Apolipoprotein E Downregulates Amyloid Precursor Protein-Induced Ischemic Susceptibility","authors":"M. Koistinaho, M. Kettunen, D. Holtzman, R. Kauppinen, L. Higgins, J. Koistinaho","doi":"10.1161/01.STR.0000020124.61998.BC","DOIUrl":"https://doi.org/10.1161/01.STR.0000020124.61998.BC","url":null,"abstract":"Background and Purpose— Epidemiological findings and experimental data on transgenic mice show that Alzheimer’s disease–related changes render the brain more susceptible to ischemic damage. We studied whether the previously observed vulnerability in mice overexpressing the 751–amino-acid isoform of human amyloid precursor protein (APP751) is regulated by human apolipoprotein E (apoE) alleles, which determine the relative risk for Alzheimer’s disease and the susceptibility to various forms of acute brain damage. Methods— Aged apoE knock out (KO) mice, mice overexpressing APP751 in the apoE KO background and mice expressing either human apoE3 or apoE4 and APP751 in the apoE KO background were exposed to permanent occlusion of the middle cerebral artery (MCA). Infarct volumes were quantified from T2-weighted magnetic resonance images 24 hours after the MCA occlusion. Local cortical blood flow was monitored by laser Doppler flowmetry. Ischemia-induced microgliosis was detected by immunohistochemistry. Results— Overexpression of human APP751 significantly increased the infarct volumes in apoE KO mice. Furthermore, this APP751-induced ischemic vulnerability was attenuated by the coexpression of either human apoE isoform. MCA occlusion resulted in a similar relative reduction in cortical blood flow in all mouse groups. Vascular anatomy showed no variation in the MCA territory between the groups. Instead, the expression of human apoE isoforms reduced the ischemia-induced microgliosis. Conclusions— Expression of either the human apoE3 or apoE4 isoform protects against the increased ischemic vulnerability observed in aged mice overexpressing human APP751, probably by modulating the inflammatory response induced by MCA occlusion.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"41 1","pages":"1905-1910"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82511333","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.0000019291.99038.4C
S. Ho, C. Metreweli, C. H. Yu
Background and Purpose— The development of intracranial collateral circulation is associated with a lower risk of stroke. A noninvasive technique that can reliably detect the presence of intracranial collaterals would be a valuable factor in the assessment of risk in patients with occlusive cerebrovascular disease. Methods— Color velocity imaging quantification was used to measure the blood flow volume of the common carotid and vertebral arteries in 40 patients with carotid occlusive disease. The blood flow volumes in these arteries were correlated with angiographic evidence of collaterals to establish the best cutoffs for detecting intracranial collateral circulation. Results— A blood flow volume of either ≥370 mL/min in the common carotid artery or ≥120 mL/min in the vertebral artery was indicative of the presence of intracranial collaterals. The sensitivity and specificity for the common carotid artery were 92.3% [95% confidence interval (CI), 62.1 to 99.6] and 92.1% (95% CI, 77.5 to 97.9), respectively. The sensitivity and specificity for the vertebral artery were 75.0% (95% CI, 35.6 to 95.5) and 87.5% (95% CI, 66.5 to 96.7), respectively. Conclusions— Color velocity imaging quantification offers a noninvasive, accurate method for detecting the presence of intracranial collateral circulation and quantifying its magnitude. This technique would be a useful adjunct in screening or continuous monitoring of patients with severe carotid occlusive disease.
{"title":"Color Velocity Imaging Quantification in the Detection of Intracranial Collateral Flow","authors":"S. Ho, C. Metreweli, C. H. Yu","doi":"10.1161/01.STR.0000019291.99038.4C","DOIUrl":"https://doi.org/10.1161/01.STR.0000019291.99038.4C","url":null,"abstract":"Background and Purpose— The development of intracranial collateral circulation is associated with a lower risk of stroke. A noninvasive technique that can reliably detect the presence of intracranial collaterals would be a valuable factor in the assessment of risk in patients with occlusive cerebrovascular disease. Methods— Color velocity imaging quantification was used to measure the blood flow volume of the common carotid and vertebral arteries in 40 patients with carotid occlusive disease. The blood flow volumes in these arteries were correlated with angiographic evidence of collaterals to establish the best cutoffs for detecting intracranial collateral circulation. Results— A blood flow volume of either ≥370 mL/min in the common carotid artery or ≥120 mL/min in the vertebral artery was indicative of the presence of intracranial collaterals. The sensitivity and specificity for the common carotid artery were 92.3% [95% confidence interval (CI), 62.1 to 99.6] and 92.1% (95% CI, 77.5 to 97.9), respectively. The sensitivity and specificity for the vertebral artery were 75.0% (95% CI, 35.6 to 95.5) and 87.5% (95% CI, 66.5 to 96.7), respectively. Conclusions— Color velocity imaging quantification offers a noninvasive, accurate method for detecting the presence of intracranial collateral circulation and quantifying its magnitude. This technique would be a useful adjunct in screening or continuous monitoring of patients with severe carotid occlusive disease.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"4 1","pages":"1795-1798"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79533718","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.0000020123.80940.B2
A. Hartmann, J. Pile-Spellman, C. Stapf, R. Sciacca, A. Faulstich, J. Mohr, H. Schumacher, H. Mast
Background and Purpose— Independently assessed data on frequency, severity, and determinants of neurological deficits after endovascular treatment of brain arteriovenous malformations (AVMs) are scarce. Methods— From the prospective Columbia AVM Study Project, 233 consecutive patients with brain AVM receiving ≥1 endovascular treatments were analyzed. Neurological impairment was assessed by a neurologist using the Rankin Scale before and after completed endovascular therapy. Multivariate logistic regression models were used to identify demographic, clinical, and morphological predictors of treatment-related neurological deficits. The analysis included the components used in the Spetzler-Martin risk score for AVM surgery (AVM size, venous drainage pattern, and eloquence of AVM location). Results— The 233 patients were treated with 545 endovascular procedures. Mean follow-up time was 9.6 months (SD, 18.1 months). Two hundred patients (86%) experienced no change in neurological status after treatment, and 33 patients (14%) showed treatment-related neurological deficits. Of the latter, 5 (2%) had persistent disabling deficits (Rankin score >2), and 2 (1%) died. Increasing patient age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01 to 1.08], number of embolizations (OR, 1.41; 95% CI, 1.16 to 1.70), and absence of a pretreatment neurological deficit (OR, 4.55; 95% CI, 1.03 to 20.0) were associated with new neurological deficits. None of the morphological AVM characteristics tested predicted treatment complications. Conclusions— From independent neurological assessment and prospective data collection, our findings suggest a low rate of disabling treatment complications in this center for endovascular brain AVM treatment. Risk predictors for endovascular treatment differ from those for AVM surgery.
{"title":"Risk of Endovascular Treatment of Brain Arteriovenous Malformations","authors":"A. Hartmann, J. Pile-Spellman, C. Stapf, R. Sciacca, A. Faulstich, J. Mohr, H. Schumacher, H. Mast","doi":"10.1161/01.STR.0000020123.80940.B2","DOIUrl":"https://doi.org/10.1161/01.STR.0000020123.80940.B2","url":null,"abstract":"Background and Purpose— Independently assessed data on frequency, severity, and determinants of neurological deficits after endovascular treatment of brain arteriovenous malformations (AVMs) are scarce. Methods— From the prospective Columbia AVM Study Project, 233 consecutive patients with brain AVM receiving ≥1 endovascular treatments were analyzed. Neurological impairment was assessed by a neurologist using the Rankin Scale before and after completed endovascular therapy. Multivariate logistic regression models were used to identify demographic, clinical, and morphological predictors of treatment-related neurological deficits. The analysis included the components used in the Spetzler-Martin risk score for AVM surgery (AVM size, venous drainage pattern, and eloquence of AVM location). Results— The 233 patients were treated with 545 endovascular procedures. Mean follow-up time was 9.6 months (SD, 18.1 months). Two hundred patients (86%) experienced no change in neurological status after treatment, and 33 patients (14%) showed treatment-related neurological deficits. Of the latter, 5 (2%) had persistent disabling deficits (Rankin score >2), and 2 (1%) died. Increasing patient age [odds ratio (OR), 1.04; 95% confidence interval (CI), 1.01 to 1.08], number of embolizations (OR, 1.41; 95% CI, 1.16 to 1.70), and absence of a pretreatment neurological deficit (OR, 4.55; 95% CI, 1.03 to 20.0) were associated with new neurological deficits. None of the morphological AVM characteristics tested predicted treatment complications. Conclusions— From independent neurological assessment and prospective data collection, our findings suggest a low rate of disabling treatment complications in this center for endovascular brain AVM treatment. Risk predictors for endovascular treatment differ from those for AVM surgery.","PeriodicalId":22274,"journal":{"name":"Stroke: Journal of the American Heart Association","volume":"23 1","pages":"1816-1820"},"PeriodicalIF":0.0,"publicationDate":"2002-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90555051","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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