Medical Treatment Failure for Symptomatic Vasospasm After Subarachnoid Hemorrhage Threatens Long-Term Outcome
BACKGROUND AND PURPOSE—Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm. METHODS—We performed a retrospective analysis o...
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Published in | Stroke (1970) Vol. 50; no. 7; pp. 1696 - 1702 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
American Heart Association, Inc
01.07.2019
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Subjects | |
Online Access | Get full text |
ISSN | 0039-2499 1524-4628 1524-4628 |
DOI | 10.1161/STROKEAHA.118.022536 |
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Abstract | BACKGROUND AND PURPOSE—Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm.
METHODS—We performed a retrospective analysis of 1520 subarachnoid hemorrhage patients prospectively enrolled in the Columbia University SAH Outcomes Project between August 1996 and August 2012. One hundred ninety-eight symptomatic vasospasm patients were treated with vasopressors to raise arterial blood pressure, with and without volume expansion. Treatment response, defined as complete or near-complete resolution of the initial neurological deficit, was adjudicated in weekly meetings of the study team based on serial clinical examination after hypertensive treatment. Outcome was evaluated at 1 year with the modified Rankin Scale.
RESULTS—Twenty-one percent of the 198 patients who received hypertensive therapy did not respond to treatment. Treatment failure was associated with an increased risk of death or severe disability at 1 year (modified Rankin Scale score of 4–6; 62% versus 25%; P<0.001). Failure of medical therapy was also associated with an admission troponin I level >0.3 μg/L (64% versus 28%; P=0.001), aneurysm coiling (43% versus 20%; P=0.004), and involvement of >1 symptomatic vascular territory at onset (39% versus 22%; P=0.02). In multivariable analysis, treatment failure was independently associated only with troponin I elevation (adjusted odds ratio, 4.30; 95% CI, 1.69–11.09; P=0.002).
CONCLUSIONS—Failure to respond to induced hypertension for symptomatic vasospasm threatens 1-year outcome. Subarachnoid hemorrhage patients with symptomatic vasospasm who have elevated initial troponin I levels, indicative of neurogenic cardiac injury, are at twice the risk of medical treatment failure. Expedited endovascular therapy should be considered in these patients. |
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AbstractList | BACKGROUND AND PURPOSE—Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm.
METHODS—We performed a retrospective analysis of 1520 subarachnoid hemorrhage patients prospectively enrolled in the Columbia University SAH Outcomes Project between August 1996 and August 2012. One hundred ninety-eight symptomatic vasospasm patients were treated with vasopressors to raise arterial blood pressure, with and without volume expansion. Treatment response, defined as complete or near-complete resolution of the initial neurological deficit, was adjudicated in weekly meetings of the study team based on serial clinical examination after hypertensive treatment. Outcome was evaluated at 1 year with the modified Rankin Scale.
RESULTS—Twenty-one percent of the 198 patients who received hypertensive therapy did not respond to treatment. Treatment failure was associated with an increased risk of death or severe disability at 1 year (modified Rankin Scale score of 4–6; 62% versus 25%; P<0.001). Failure of medical therapy was also associated with an admission troponin I level >0.3 μg/L (64% versus 28%; P=0.001), aneurysm coiling (43% versus 20%; P=0.004), and involvement of >1 symptomatic vascular territory at onset (39% versus 22%; P=0.02). In multivariable analysis, treatment failure was independently associated only with troponin I elevation (adjusted odds ratio, 4.30; 95% CI, 1.69–11.09; P=0.002).
CONCLUSIONS—Failure to respond to induced hypertension for symptomatic vasospasm threatens 1-year outcome. Subarachnoid hemorrhage patients with symptomatic vasospasm who have elevated initial troponin I levels, indicative of neurogenic cardiac injury, are at twice the risk of medical treatment failure. Expedited endovascular therapy should be considered in these patients. Background and Purpose- Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm. Methods- We performed a retrospective analysis of 1520 subarachnoid hemorrhage patients prospectively enrolled in the Columbia University SAH Outcomes Project between August 1996 and August 2012. One hundred ninety-eight symptomatic vasospasm patients were treated with vasopressors to raise arterial blood pressure, with and without volume expansion. Treatment response, defined as complete or near-complete resolution of the initial neurological deficit, was adjudicated in weekly meetings of the study team based on serial clinical examination after hypertensive treatment. Outcome was evaluated at 1 year with the modified Rankin Scale. Results- Twenty-one percent of the 198 patients who received hypertensive therapy did not respond to treatment. Treatment failure was associated with an increased risk of death or severe disability at 1 year (modified Rankin Scale score of 4-6; 62% versus 25%; P<0.001). Failure of medical therapy was also associated with an admission troponin I level >0.3 μg/L (64% versus 28%; P=0.001), aneurysm coiling (43% versus 20%; P=0.004), and involvement of >1 symptomatic vascular territory at onset (39% versus 22%; P=0.02). In multivariable analysis, treatment failure was independently associated only with troponin I elevation (adjusted odds ratio, 4.30; 95% CI, 1.69-11.09; P=0.002). Conclusions- Failure to respond to induced hypertension for symptomatic vasospasm threatens 1-year outcome. Subarachnoid hemorrhage patients with symptomatic vasospasm who have elevated initial troponin I levels, indicative of neurogenic cardiac injury, are at twice the risk of medical treatment failure. Expedited endovascular therapy should be considered in these patients. Background and Purpose- Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm. Methods- We performed a retrospective analysis of 1520 subarachnoid hemorrhage patients prospectively enrolled in the Columbia University SAH Outcomes Project between August 1996 and August 2012. One hundred ninety-eight symptomatic vasospasm patients were treated with vasopressors to raise arterial blood pressure, with and without volume expansion. Treatment response, defined as complete or near-complete resolution of the initial neurological deficit, was adjudicated in weekly meetings of the study team based on serial clinical examination after hypertensive treatment. Outcome was evaluated at 1 year with the modified Rankin Scale. Results- Twenty-one percent of the 198 patients who received hypertensive therapy did not respond to treatment. Treatment failure was associated with an increased risk of death or severe disability at 1 year (modified Rankin Scale score of 4-6; 62% versus 25%; P<0.001). Failure of medical therapy was also associated with an admission troponin I level >0.3 μg/L (64% versus 28%; P=0.001), aneurysm coiling (43% versus 20%; P=0.004), and involvement of >1 symptomatic vascular territory at onset (39% versus 22%; P=0.02). In multivariable analysis, treatment failure was independently associated only with troponin I elevation (adjusted odds ratio, 4.30; 95% CI, 1.69-11.09; P=0.002). Conclusions- Failure to respond to induced hypertension for symptomatic vasospasm threatens 1-year outcome. Subarachnoid hemorrhage patients with symptomatic vasospasm who have elevated initial troponin I levels, indicative of neurogenic cardiac injury, are at twice the risk of medical treatment failure. Expedited endovascular therapy should be considered in these patients.Background and Purpose- Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and the long-term impact of treatment failure with hypertensive therapy for symptomatic vasospasm. Methods- We performed a retrospective analysis of 1520 subarachnoid hemorrhage patients prospectively enrolled in the Columbia University SAH Outcomes Project between August 1996 and August 2012. One hundred ninety-eight symptomatic vasospasm patients were treated with vasopressors to raise arterial blood pressure, with and without volume expansion. Treatment response, defined as complete or near-complete resolution of the initial neurological deficit, was adjudicated in weekly meetings of the study team based on serial clinical examination after hypertensive treatment. Outcome was evaluated at 1 year with the modified Rankin Scale. Results- Twenty-one percent of the 198 patients who received hypertensive therapy did not respond to treatment. Treatment failure was associated with an increased risk of death or severe disability at 1 year (modified Rankin Scale score of 4-6; 62% versus 25%; P<0.001). Failure of medical therapy was also associated with an admission troponin I level >0.3 μg/L (64% versus 28%; P=0.001), aneurysm coiling (43% versus 20%; P=0.004), and involvement of >1 symptomatic vascular territory at onset (39% versus 22%; P=0.02). In multivariable analysis, treatment failure was independently associated only with troponin I elevation (adjusted odds ratio, 4.30; 95% CI, 1.69-11.09; P=0.002). Conclusions- Failure to respond to induced hypertension for symptomatic vasospasm threatens 1-year outcome. Subarachnoid hemorrhage patients with symptomatic vasospasm who have elevated initial troponin I levels, indicative of neurogenic cardiac injury, are at twice the risk of medical treatment failure. Expedited endovascular therapy should be considered in these patients. |
Author | Velazquez, Angela Agarwal, Sachin Connolly, E. Sander Schmidt, J. Michael Claassen, Jan Witsch, Jens Falo, Cristina Mayer, Stephan A. Suwatcharangkoon, Sureerat De Marchis, Gian Marco Meyers, Emma |
AuthorAffiliation | From the Division of Neurology, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand (S.S.) Neurological Intensive Care Unit, Departments of Neurology (S.S., G.M.D.M., J.W., E.M., A.V., C.F., J.M.S., S.A., J.C.), Columbia University Medical Center, New York, NY Neurosurgery (E.S.C.), Columbia University Medical Center, New York, NY Department of Neurology, Henry Ford Hospital, Detroit, MI (S.A.M.) |
AuthorAffiliation_xml | – name: From the Division of Neurology, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand (S.S.) Neurological Intensive Care Unit, Departments of Neurology (S.S., G.M.D.M., J.W., E.M., A.V., C.F., J.M.S., S.A., J.C.), Columbia University Medical Center, New York, NY Neurosurgery (E.S.C.), Columbia University Medical Center, New York, NY Department of Neurology, Henry Ford Hospital, Detroit, MI (S.A.M.) |
Author_xml | – sequence: 1 givenname: Sureerat surname: Suwatcharangkoon fullname: Suwatcharangkoon, Sureerat organization: From the Division of Neurology, Department of Medicine, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand (S.S.) Neurological Intensive Care Unit, Departments of Neurology (S.S., G.M.D.M., J.W., E.M., A.V., C.F., J.M.S., S.A., J.C.), Columbia University Medical Center, New York, NY Neurosurgery (E.S.C.), Columbia University Medical Center, New York, NY Department of Neurology, Henry Ford Hospital, Detroit, MI (S.A.M.) – sequence: 2 givenname: Gian surname: De Marchis middlename: Marco fullname: De Marchis, Gian Marco – sequence: 3 givenname: Jens surname: Witsch fullname: Witsch, Jens – sequence: 4 givenname: Emma surname: Meyers fullname: Meyers, Emma – sequence: 5 givenname: Angela surname: Velazquez fullname: Velazquez, Angela – sequence: 6 givenname: Cristina surname: Falo fullname: Falo, Cristina – sequence: 7 givenname: J. surname: Schmidt middlename: Michael fullname: Schmidt, J. Michael – sequence: 8 givenname: Sachin surname: Agarwal fullname: Agarwal, Sachin – sequence: 9 givenname: E. surname: Connolly middlename: Sander fullname: Connolly, E. Sander – sequence: 10 givenname: Jan surname: Claassen fullname: Claassen, Jan – sequence: 11 givenname: Stephan surname: Mayer middlename: A. fullname: Mayer, Stephan A. |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31164068$$D View this record in MEDLINE/PubMed |
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Snippet | BACKGROUND AND PURPOSE—Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and... Background and Purpose- Symptomatic vasospasm is a common cause of morbidity and mortality after subarachnoid hemorrhage. We sought to identify predictors and... |
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SubjectTerms | Adult Aged Blood Pressure - drug effects Female Follow-Up Studies Humans Male Middle Aged Retrospective Studies Subarachnoid Hemorrhage - complications Subarachnoid Hemorrhage - drug therapy Subarachnoid Hemorrhage - physiopathology Treatment Failure Vasoconstrictor Agents - administration & dosage Vasoconstrictor Agents - adverse effects Vasospasm, Intracranial - drug therapy Vasospasm, Intracranial - etiology Vasospasm, Intracranial - physiopathology |
Title | Medical Treatment Failure for Symptomatic Vasospasm After Subarachnoid Hemorrhage Threatens Long-Term Outcome |
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