ANGIOGRAPHIC AND HEMODYNAMIC EFFECT OF HIGH CONCENTRATION OF INTRA-ARTERIAL NICARDIPINE IN CEREBRAL VASOSPASM

Neurosurgery ◽  
2008 ◽  
Vol 63 (6) ◽  
pp. 1080-1087 ◽  
Author(s):  
Italo Linfante ◽  
Raquel Delgado-Mederos ◽  
Vincenzo Andreone ◽  
Matthew Gounis ◽  
Laura Hendricks ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vessel Diameter ◽  
High Concentration ◽  
Symptomatic Vasospasm ◽  
High Concentrations

Abstract OBJECTIVE Nicardipine has been used to treat cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage. Intra-arterial (IA) infusion of high concentrations of nicardipine decreases procedure time, but it may affect hemodynamic parameters. In addition, a quantitative measurement of improvement of vessel diameter on the angiograms has not been performed. METHODS We conducted a single-center, retrospective database analysis of consecutive patients with symptomatic vasospasm after aneurysmal subarachnoid hemorrhage who failed medical management and received IA nicardipine between September 2005 and June 2006. Nicardipine (1 mg/mL/min) was infused intra-arterially by microcatheter. Blood pressure, heart rate, and intracranial pressure were recorded during the infusion. The effect of IA nicardipine on the vessel's diameter was measured on angiography by two blinded investigators. RESULTS Forty-six treatment sessions were performed in 22 consecutive patients (13 women; age, 56.4 ±13 years). Fourteen patients received IA nicardipine alone, and 8 patients had additional angioplasty. The average nicardipine dose was 12 ± 10 mg (range, 2–25 mg). The mean decrease of systolic, diastolic, and mean blood pressure was 17.4 ± 18.3 mm Hg, 7.7 ± 10.4 mm Hg, and 10.9 ± 11.6 mm Hg, respectively. There was no change in intracranial pressure. Measurement of 49 vessels in the 14 patients treated with nicardipine alone showed a significant increase in arterial diameters (range, 1–74%; P < 0.0001). At the time of discharge, 11 patients (50%) were functionally independent (modified Rankin Scale score, 0–2). CONCLUSION High concentrations of IA nicardipine infusion have a reversible effect on blood pressure and heart rate. IA nicardipine results also in a significant improvement in vessel diameter in patients with vasospasm after aneurysmal subarachnoid hemorrhage.

scholarly journals Increased levels of lipid peroxides as predictive of symptomatic vasospasm and poor outcome after aneurysmal subarachnoid hemorrhage

2002 ◽  
Vol 97 (6) ◽  
pp. 1302-1305 ◽  
Author(s):  
Takao Kamezaki ◽  
Kiyoyuki Yanaka ◽  
Sohji Nagase ◽  
Keishi Fujita ◽  
Noriyuki Kato ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Lipid Peroxides ◽  
Medical Complication ◽  
Content Type ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Delayed Cerebral Vasospasm ◽  
Fine Print

Object. Cerebral vasospasm remains a devastating medical complication of aneurysmal subarachnoid hemorrhage (SAH). Reactive oxygen species and subsequent lipid peroxidation are reported to participate in the causes of cerebral vasospasm. This clinical study was performed to investigate the relationships between levels of lipid peroxides in cerebrospinal fluid (CSF) and both delayed cerebral vasospasm and clinical outcome after SAH. Methods. Levels of phosphatidylcholine hydroperoxide (PCOOH) and cholesteryl ester hydroperoxide (CEOOH) in the CSF were measured in 20 patients with aneurysmal SAH. The patients' CSF was collected within 48 hours of hemorrhage onset and on Day 6 or 7 post-SAH. On Day 7, angiography was performed to verify the degree and extent of the vasospasm. The relationship between the patients' clinical profiles and the levels of lipid peroxides in the CSF were investigated. Both PCOOH and CEOOH were detectable in CSF, and their levels decreased within 7 days after onset of SAH. The levels of CEOOH within 48 hours after onset of hemorrhage were significantly higher in patients in whom symptomatic vasospasm later developed than in patients in whom symptomatic vasospasm did not develop (p = 0.002). Levels of PCOOH measured within 48 hours after onset of hemorrhage were significantly higher in patients with poor outcomes than in patients with good outcomes (p = 0.043). Conclusions. Increased levels of lipid peroxides measured in the CSF during the acute stage of SAH were predictive of both symptomatic vasospasm and poor outcome. Measurements of lipid peroxides in the CSF may be useful prognostically for patient outcomes as well as for predicting symptomatic vasospasm.

THERAPEUTIC HYPOTHERMIA IN PATIENTS WITH ANEURYSMAL SUBARACHNOID HEMORRHAGE, REFRACTORY INTRACRANIAL HYPERTENSION, OR CEREBRAL VASOSPASM

Neurosurgery ◽  
2009 ◽  
Vol 64 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Martin A. Seule ◽  
Carl Muroi ◽  
Susanne Mink ◽  
Yasuhiro Yonekawa ◽  
Emanuela Keller
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Side Effects ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Vasospasm ◽  
Conventional Treatment ◽  
Mild Hypothermia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Poor Grade ◽  
Fisher Grade

Abstract OBJECTIVE To evaluate the feasibility and safety of mild hypothermia treatment in patients with aneurysmal subarachnoid hemorrhage (SAH) who are experiencing intracranial hypertension and/or cerebral vasospasm (CVS). METHODS Of 441 consecutive patients with SAH, 100 developed elevated intracranial pressure and/or symptomatic CVS refractory to conventional treatment. Hypothermia (33–34°C) was induced and maintained until intracranial pressure normalized, CVS resolved, or severe side effects occurred. RESULTS Thirteen patients were treated with hypothermia alone, and 87 were treated with hypothermia in combination with barbiturate coma. Sixty-six patients experienced poor-grade SAH (Hunt and Hess Grades IV and V) and 92 had Fisher Grade 3 and 4 bleedings. The mean duration of hypothermia was 169 ± 104 hours, with a maximum of 16.4 days. The outcome after 1 year was evaluated in 90 of 100 patients. Thirty-two patients (35.6%) survived with good functional outcome (Glasgow Outcome Scale [GOS] score, 4 and 5), 14 (15.5%) were severely disabled (GOS score, 3), 1 (1.1%) was in a vegetative state (GOS score, 2), and 43 (47.8%) died (GOS score, 1). The most frequent side effects were electrolyte disorders (77%), pneumonia (52%), thrombocytopenia (47%), and septic shock syndrome (40%). Of 93 patients with severe side effects, 6 (6.5%) died as a result of respiratory or multi-organ failure. CONCLUSION Prolonged systemic hypothermia may be considered as a last-resort option for a carefully selected group of SAH patients with intracranial hypertension or CVS resistant to conventional treatment. However, complications associated with hypothermia require elaborate protocols in general intensive care unit management.

Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage

2004 ◽  
Vol 101 (3) ◽  
pp. 408-416 ◽  
Author(s):  
Gregory G. Heuer ◽  
Michelle J. Smith ◽  
J. Paul Elliott ◽  
H. Richard Winn ◽  
Peter D. Leroux
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Grade ◽  
Icp Monitoring ◽  
Content Type ◽  
Poor Grade ◽  
Symptomatic Vasospasm ◽  
Increased Icp ◽  
Fine Print

Object. Increased intracranial pressure (ICP) is well known to affect adversely patients with head injury. In contrast, the variables associated with ICP following aneurysmal subarachnoid hemorrhage (SAH) and their impact on outcome have been less intensely studied. Methods. In this retrospective study the authors reviewed a prospective observational database cataloging the treatment details in 433 patients with SAH who had undergone surgical occlusion of an aneurysm as well as ICP monitoring. All 433 patients underwent postoperative ICP monitoring, whereas only 146 (33.7%) underwent both pre- and postoperative ICP monitoring. The mean maximal ICP was 24.9 ± 17.3 mm Hg (mean ± standard deviation). During their hospital stay, 234 patients (54%) had elevated ICP (> 20 mm Hg), including 136 of those (48.7%) with a good clinical grade (Hunt and Hess Grades I–III) and 98 (63.6%) of the 154 patients with a poor grade (Hunt and Hess Grades IV and V) on admission. An increased mean maximal ICP was associated with several admission variables: worse Hunt and Hess clinical grade (p < 0.0001), a lower Glasgow Coma Scale (GSC) motor score (p < 0.0001); worse SAH grade based on results of computerized tomography studies (p < 0.0001); intracerebral hemorrhage (p = 0.024); severity of intraventricular hemorrhage (p < 0.0001); and rebleeding (p = 0.0048). Both intraoperative cerebral swelling (p = 0.0017) and postoperative GCS score (p < 0.0001) were significantly associated with a raised ICP. Variables such as patient age, aneurysm size, symptomatic vasospasm, intraoperative aneurysm rupture, and secondary cerebral insults such as hypoxia were not associated with raised ICP. Increased ICP adversely affected outcome: 71.9% of patients with normal ICP demonstrated favorable 6-month outcomes postoperatively, whereas 63.5% of patients with ICP between 20 and 50 mm Hg and 33.3% with ICP greater than 50 mm Hg demonstrated favorable outcomes. Among 21 patients whose raised ICP did not respond to mannitol therapy, all experienced a poor outcome and 95.2% died. Among 145 patients whose elevated ICP responded to mannitol, 66.9% had a favorable outcome and only 20.7% were dead 6 months after surgery (p < 0.0001). According to results of multivariate analysis, however, ICP was not an independent outcome predictor (odds ratio 1.26, 95% confidence interval 0.28–5.68). Conclusions. Increased ICP is common after SAH, even in patients with a good clinical grade. Elevated ICP post-SAH is associated with a worse patient outcome, particularly if ICP does not respond to treatment. This association, however, may depend more on the overall severity of the SAH than on ICP alone.

Leukocytosis as an independent risk factor for cerebral vasospasm following aneurysmal subarachnoid hemorrhage

2003 ◽  
Vol 98 (6) ◽  
pp. 1222-1226 ◽  
Author(s):  
Matthew J. McGirt ◽  
John C. Mavropoulos ◽  
Laura Y. McGirt ◽  
Michael J. Alexander ◽  
Allan H. Friedman ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Leukocyte Count ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Increased Risk ◽  
Grade 3 ◽  
Fine Print

Object. The identification of patients at an increased risk for cerebral vasospasm after subarachnoid hemorrhage (SAH) may allow for more aggressive treatment and improved patient outcomes. Note, however, that blood clot size on admission remains the only factor consistently demonstrated to increase the risk of cerebral vasospasm after SAH. The goal of this study was to assess whether clinical, radiographic, or serological variables could be used to identify patients at an increased risk for cerebral vasospasm. Methods. A retrospective review was conducted in all patients with aneurysmal or spontaneous nonaneurysmal SAH who were admitted to the authors' institution between 1995 and 2001. Underlying vascular diseases (hypertension or chronic diabetes mellitus), Hunt and Hess and Fisher grades, patient age, aneurysm location, craniotomy compared with endovascular aneurysm stabilization, medications on admission, postoperative steroid agent use, and the occurrence of fever, hydrocephalus, or leukocytosis were assessed as predictors of vasospasm. Two hundred twenty-four patients were treated for SAH during the review period. One hundred one patients (45%) developed symptomatic vasospasm. Peak vasospasm occurred 5.8 ± 3 days after SAH. There were four independent predictors of vasospasm: Fisher Grade 3 SAH (odds ratio [OR] 7.5, 95% confidence interval [CI] 3.5–15.8), peak serum leukocyte count (OR 1.09, 95% CI 1.02–1.16), rupture of a posterior cerebral artery (PCA) aneurysm (OR 0.05, 95% CI 0.01–0.41), and spontaneous nonaneurysmal SAH (OR 0.14, 95% CI 0.04–0.45). A serum leukocyte count greater than 15 × 109/L was independently associated with a 3.3-fold increase in the likelihood of developing vasospasm (OR 3.33, 95% CI 1.74–6.38). Conclusions. During this 7-year period, spontaneous nonaneurysmal SAH and ruptured PCA aneurysms decreased the odds of developing vasospasm sevenfold and 20-fold, respectively. The presence of Fisher Grade 3 SAH on admission or a peak leukocyte count greater than 15 × 109/L increased the odds of vasospasm sevenfold and threefold, respectively. Monitoring of the serum leukocyte count may allow for early diagnosis and treatment of vasospasm.

Cigarette smoking—induced increase in the risk of symptomatic vasospasm after aneurysmal subarachnoid hemorrhage

1997 ◽  
Vol 87 (3) ◽  
pp. 381-384 ◽  
Author(s):  
Todd M. Lasner ◽  
Robert J. Weil ◽  
Howard A. Riina ◽  
Joseph T. King ◽  
Eric L. Zager ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Alcohol Abuse ◽  
Cigarette Smoking ◽  
Cerebral Vasospasm ◽  
Odds Ratio ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
World Federation ◽  
Symptomatic Vasospasm ◽  
Fisher Grade ◽  
Grade 3

✓ Vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is correlated with the thickness of blood within the basal cisterns on the initial computerized tomography (CT) scan. To identify additional risk factors for symptomatic vasospasm, the authors performed a prospective analysis of 75 consecutively admitted patients who were treated for aneurysmal SAH. Five patients who died before treatment or were comatose postoperatively were excluded from the study. Of the remaining 70 patients, demographic (age, gender, and race) and clinical (hypertension, diabetes, coronary artery disease, smoking, alcohol abuse, illicit drug use, sentinel headache, Fisher grade, Hunt and Hess grade, World Federation of Neurological Surgeons grade, and ruptured aneurysm location) parameters were evaluated using multivariate logistic regression to determine factors independently associated with cerebral vasospasm. All patients were treated with hypervolemic therapy and administration of nimodipine as prophylaxis for vasospasm. Cerebral vasospasm was suspected in cases that exhibited (by elevation of transcranial Doppler velocities) neurological deterioration 3 to 14 days after SAH with no other explanation and was confirmed either by clinical improvement in response to induced hypertension or by cerebral angiography. The mean age of the patients was 50 years. Sixty-three percent of the patients were women, 74% were white, 64% were cigarette smokers, and 46% were hypertensive. Ten percent of the patients suffered from alcohol abuse, 19% from sentinel bleed, and 49% had a Fisher Grade 3 SAH. Twenty-nine percent of the patients developed symptomatic vasospasm. Multivariate analysis demonstrated that cigarette smoking (p = 0.033; odds ratio 4.7, 95% confidence interval [CI] 2.4–8.9) and Fisher Grade 3, that is, thick subarachnoid clot (p = 0.008; odds ratio 5.1, 95% CI 2–13.1), were independent predictors of symptomatic vasospasm. The authors make the novel observation that cigarette smoking increases the risk of symptomatic vasospasm after aneurysmal SAH, independent of Fisher grade.

Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial

2013 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Nobuo Senbokuya ◽  
Hiroyuki Kinouchi ◽  
Kazuya Kanemaru ◽  
Yasuhiro Ohashi ◽  
Akira Fukamachi ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Control Group ◽  
Fisher Exact Test ◽  
Exact Test ◽  
Symptomatic Vasospasm ◽  
Angiographic Vasospasm ◽  
Significant Difference ◽  
Length Of Hospitalization

Object Cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is a major cause of subsequent morbidity and mortality. Cilostazol, a selective inhibitor of phosphodiesterase 3, may attenuate cerebral vasospasm because of its antiplatelet and vasodilatory effects. A multicenter prospective randomized trial was conducted to investigate the effect of cilostazol on cerebral vasospasm. Methods Patients admitted with SAH caused by a ruptured anterior circulation aneurysm who were in Hunt and Kosnik Grades I to IV and were treated by clipping within 72 hours of SAH onset were enrolled at 7 neurosurgical sites in Japan. These patients were assigned to one of 2 groups: the usual therapy group (control group) or the add-on 100 mg cilostazol twice daily group (cilostazol group). The group assignments were done by a computer-generated randomization sequence. The primary study end point was the onset of symptomatic vasospasm. Secondary end points were the onset of angiographic vasospasm and new cerebral infarctions related to cerebral vasospasm, clinical outcome as assessed by the modified Rankin scale, and length of hospitalization. All end points were assessed for the intention-to-treat population. Results Between November 2009 and December 2010, 114 patients with SAH were treated by clipping within 72 hours from the onset of SAH and were screened. Five patients were excluded because no consent was given. Thus, 109 patients were randomly assigned to the cilostazol group (n = 54) or the control group (n = 55). Symptomatic vasospasm occurred in 13% (n = 7) of the cilostazol group and in 40% (n = 22) of the control group (p = 0.0021, Fisher exact test). The incidence of angiographic vasospasm was significantly lower in the cilostazol group than in the control group (50% vs 77%; p = 0.0055, Fisher exact test). Multiple logistic analyses demonstrated that nonuse of cilostazol is an independent factor for symptomatic and angiographic vasospasm. The incidence of new cerebral infarctions was also significantly lower in the cilostazol group than in the control group (11% vs 29%; p = 0.0304, Fisher exact test). Clinical outcomes at 1, 3, and 6 months after SAH in the cilostazol group were better than those in the control group, although a significant difference was not shown. There was also no significant difference in the length of hospitalization between the groups. No severe adverse event occurred during the study period. Conclusions Oral administration of cilostazol is effective in preventing cerebral vasospasm with a low risk of severe adverse events. Clinical trial registration no. UMIN000004347, University Hospital Medical Information Network Clinical Trials Registry.

Simvastatin for the prevention of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage: a single-institution prospective cohort study

2009 ◽  
Vol 110 (5) ◽  
pp. 968-974 ◽  
Author(s):  
Matthew J. McGirt ◽  
Giannina L. Garces Ambrossi ◽  
Judy Huang ◽  
Rafael J. Tamargo
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Hospital Mortality ◽  
Cerebral Vasospasm ◽  
Glasgow Outcome Scale ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Poor Outcome ◽  
Symptomatic Vasospasm ◽  
Scale Scores ◽  
Length Of Hospitalization

Object Vasospasm is the major cause of disability and death after aneurysmal subarachnoid hemorrhage (aSAH). Although the results of 2 randomized clinical trials demonstrated that statin decreases the incidence of symptomatic cerebral vasospasm after aSAH, retrospective studies have failed to confirm this. The authors conducted a prospective observational study to determine whether a standardized regimen of simvastatin would reduce the incidence of cerebral vasospasm and improve neurological outcomes in patients with aSAH. Methods Since 1991, all patients with aSAH admitted to the authors' institution have been prospectively followed up with standardized outcomes recording. Starting in September 2005, all patients admitted with aSAH were given enteral simvastatin (80 mg/day for 14 days) in addition to the standard care. The incidence of symptomatic cerebral vasospasm, length of hospitalization, in-hospital mortality rate, and discharge Glasgow Outcome Scale scores in these 170 patients were compared to data obtained in 170 consecutive patients who underwent treatment in our unit prior to the introduction of statin therapy. Results The 5-year study period included 340 consecutively treated patients (170 who received statins and 170 who did not). Patients who received simvastatin therapy were more frequently male (29 vs 20%) and had a smaller median aneurysm diameter (6 vs 7 mm). Baseline characteristics were otherwise similar between the cohorts. There were no differences in the incidence of symptomatic vasospasm (25.3 vs 30.5%; p = 0.277), in-hospital mortality rate (18 vs 15%; p = 0.468), length of hospitalization (21 ± 15 vs 19 ± 12 days; p = 0.281), or poor outcome at discharge (Glasgow Outcome Scale Scores 1–2: 21.7 vs 18.2%; p = 0.416) between the simvastatin and nonstatin cohorts. There were no statin-related complications. Conclusions The uniform introduction of simvastatin did not reduce the incidence of symptomatic cerebral vasospasm, death, or poor outcome in patients with aSAH. Simvastatin was well tolerated, but its benefit may be less than has been previously reported.

Primary results of the Vesalio NeVa VS for the Treatment of Symptomatic Cerebral Vasospasm following Aneurysm Subarachnoid Hemorrhage (VITAL) Study

2021 ◽  
pp. neurintsurg-2021-017859
Author(s):  
Rishi Gupta ◽  
Keith Woodward ◽  
David Fiorella ◽  
Henry H Woo ◽  
David Liebeskind ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Primary Endpoint ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vessel Diameter ◽  
Multicenter Trial ◽  
Neurological Outcomes ◽  
Non Invasive ◽  
Before And After ◽  
Pre Treatment

BackgroundCerebral vasospasm (CV) after aneurysmal subarachnoid hemorrhage (aSAH) is linked to worse neurological outcomes. The NeVa VS is a novel cerebral dilation device based on predicate stent retrievers. We report the results of the Vesalio NeVa VS for the Treatment of Symptomatic Cerebral Vasospasm following aSAH (VITAL) Study.MethodsThis was a single-arm prospective multicenter trial to assess the safety and probable benefit of the NeVa VS device to treat CV. Patients were screened and treated if they had CV >50% on non-invasive imaging confirmed by cerebral angiography. The vessel diameters were measured before and after treatment by an independent core laboratory. The primary endpoint was ≥50% vessel diameter immediately after treatment with the NeVa VS device.ResultsThirty patients with a mean age of 52±11 years and mean Hunt–Hess grade of 3.1±0.9 were enrolled. A total of 74 vessels were treated with an average of 1.3 deployments per vessel (95 deployments total). The mean pre-treatment narrowing of the target vessel (n=74) was 65.6% with reduction of the narrowing to 29.4% after treatment. The primary endpoint was achieved in 64 of 74 vessels (86.5%). In three of 95 total deployments (3.2%), thrombus at the site of deployment was observed during the procedure without apparent neurological sequelae.ConclusionsThe NeVa VS device appears to be a safe treatment to regain vessel diameter in severely narrowed intracranial arteries secondary to CV associated with aSAH. This treatment offers a new tool that allows for controlled vessel expansion to treat CV.

Endovascular treatment for cerebral vasospasm following aneurysmal subarachnoid hemorrhage: predictors of outcome and retreatment

2017 ◽  
Vol 10 (4) ◽  
pp. 367-374 ◽  
Author(s):  
Jennifer D Sokolowski ◽  
Ching-Jen Chen ◽  
Dale Ding ◽  
Thomas J Buell ◽  
Daniel M Raper ◽  
...  
Keyword(s):  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Initial Treatment ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Smoking Status ◽  
Functional Independence ◽  
Study Cohort ◽  
Good Outcome ◽  
Symptomatic Vasospasm

ObjectiveAlthough endovascular therapy has been widely adopted for the treatment of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH), its effect on clinical outcomes remains incompletely understood. The aims of this retrospective cohort study are to evaluate the outcomes of endovascular intervention for post-aSAH vasospasm and identify predictors of functional independence at discharge and repeat endovascular vasospasm treatment.MethodsWe assessed the baseline and outcomes data for patients with aSAH who underwent endovascular vasospasm treatment at our institution, including intra-arterial (IA) vasodilator infusion and angioplasty. Statistical analyses were performed to determine factors associated with good outcome at discharge (modified Rankin Scale 0–2) and repeat endovascular vasospasm treatment.ResultsThe study cohort comprised 159 patients with a mean age of 52 years. Good outcome was achieved in 17% of patients at discharge (26/150 patients), with an in-hospital mortality rate of 22% (33/150 patients). In the multivariate analysis, age (OR 0.895; p=0.009) and positive smoking status (OR 0.206; p=0.040) were negative independent predictors of good outcome. Endovascular retreatment was performed in 34% (53/156 patients). In the multivariate analysis, older age (OR 0.950; p=0.004), symptomatic vasospasm (OR 0.441; p=0.046), initial treatment with angioplasty alone (OR 0.096; p=0.039), and initial treatment with combined IA vasodilator infusion and angioplasty (OR 0.342; p=0.026) were negative independent predictors of retreatment.ConclusionWe found a modest rate of functional independence at discharge in patients with aSAH who underwent endovascular vasospasm treatment. Older patients and smokers had worse functional outcomes at discharge. Initial use of angioplasty appears to decrease the need for subsequent retreatment.

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