Effect of Prior Statin Use on Functional Outcome and Delayed Vasospasm after Acute Aneurysmal Subarachnoid Hemorrhage: A Matched Controlled Cohort Study

Parra, Augusto; Kreiter, Kurt T.; Williams, Susan E.; Sciacca, Robert R.; Mack, William J.; Naidech, Andrew M.; Commichau, Christopher; Fitzsimmons, Brian‐Fred; Janjua, Nazli; Mayer, Stephan A.; Connolly, E. Sander

doi:10.1227/01.neu.0000153925.96889.8a

Cited by 101 publications

(70 citation statements)

References 59 publications

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“…This concept is supported by the study conducted by Lynch et al 7 The results reported by Ogilvy et al 17 do not support this finding; however, once again, their results did show a trend toward decreased mortality in patients who received statin therapy. This finding does contradict the results of a retrospective cohort study conducted by Parra and colleagues, 18 who found no significant difference in mortality at 14 days between patients who received statins and those who did not. The NNT calculated from our study for this outcome is 6.7, which is very low and strongly supportive of statin use after aneurysmal SAH.…”

Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?contrasting

confidence: 81%

“…One study by McGirt et al 16 (Nϭ115 patients) reported an 11-fold decrease in the incidence of vasospasm among patients who had received statin therapy for at least 1 month before SAH and who continued to receive statin therapy throughout their hospital stay. A second study by Parra et al 18 (Nϭ60 patients) Figure. Forest plot for studies reporting (a) the overall incidence of vasospasm, (b) the incidence of vasospasm-related delayed ischemic deficits, and (c) overall mortality.…”

Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?mentioning

confidence: 91%

“…This is supported by animal as well as human research, which has reported improved neurologic outcomes and functional status in patients who received statins either before or after SAH. 5,18 In randomized, controlled trials, Tseng et al 8 also reported a significant decrease in delayed ischemic deficits for those who received statins; however, preliminary results from the study of Ogilvy et al 17 did not support this finding, although visual examination of their results revealed a trend toward a decreased incidence of vasospasm-related delayed ischemic deficits that did not reach statistical significance. The NNT for this outcome was 5, indicating that statin therapy is required for 5 people to prevent 1 delayed ischemic deficit.…”

Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?mentioning

confidence: 99%

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Do Statins Improve Outcomes and Reduce the Incidence of Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Sillberg

Wells

Perry

2008

Stroke

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Background and Purpose-Subarachnoid hemorrhage (SAH) is a relatively rare cause of stroke with a high rate of morbidity and mortality, primarily due to the occurrence of delayed vasospasm. To date, many therapies have been proposed to help prevent vasospasm, but very few have been proven effective. The initiation of statin therapy after SAH may be effective in reducing the incidence of vasospasm; however, the only studies that have examined this effect have been small. This meta-analysis attempted to determine whether statins reduce morbidity and mortality after aneurysmal SAH. Methods-MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched for randomized, controlled trials relating to the use of statins in SAH. Foreign language and abstract articles were included. Two independent reviewers assessed studies for eligibility, data extraction, and quality. Primary outcome was the incidence of radiographically confirmed clinical vasospasm; secondary outcomes were incidence of delayed ischemic deficits and mortality. Results-The incidence of vasospasm (relative risk [RR]ϭ0.73; 95% CI, 0.54 to 0.99), delayed ischemic deficits (RRϭ0.38; 95% CI, 0.17 to 0.83), and mortality (RRϭ0.22; 95% CI, 0.06 to 0.82) were significantly reduced in the statin group. For these outcomes, we calculated a number needed to treat of 6.25, 5, and 6.7, respectively. Conclusions-Initiation of statin therapy after aneurysmal SAH significantly reduces the incidence of vasospasm, delayed ischemic deficits, and mortality. This is consistent with animal research and retrospective studies and supports the routine use of statins in the care of patients with aneurysmal SAH.

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Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?contrasting

confidence: 81%

Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?mentioning

confidence: 91%

Section: Sillberg Et Al Do Statins Improve Outcome After Aneurysmal Sah?mentioning

confidence: 99%

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Do Statins Improve Outcomes and Reduce the Incidence of Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Sillberg

Wells

Perry

2008

Stroke

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“…Perhaps its fibrinolytic 201 or anti-platelet 202 properties account for its success. Statins protect against DID 203,204 and have also been found to reduce microclot formation after brain injury 205,206 .…”

Section: Proximately 30% Of Patients Develop Signs Of Cerebral Ischemiamentioning

confidence: 99%

Brain Ischemia in Patients with Intracranial Hemorrhage: Pathophysiological Reasoning for Aggressive Diagnostic Management

et al. 2013

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“…Statins have pleiotropic effects targeting many processes in the pathogenesis of vasospasm and reduce post-SAH vasospasm in animal models 1 and pilot human studies. [2][3][4] We conducted a prospective, randomized, double-blind study of the safety and feasibility of simvastatin treatment after SAH.…”

mentioning

confidence: 99%

A Randomized, Double-Blind, Placebo-Controlled Pilot Study of Simvastatin in Aneurysmal Subarachnoid Hemorrhage

Chou

Smith

Badjatia

et al. 2008

Stroke

130

190

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Background and Purpose-Studies suggest statins ameliorate aneurysmal subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and ischemic complications. We tested safety and feasibility of simvastatin 80 mg/d for vasospasm prevention in SAH patients. Methods-Thirty-nine statin-naïve Fisher grade 3 SAH subjects were double-blind randomized to receive simvastatin 80 mg/d (nϭ19) or placebo (nϭ20), stratified by Hunt and Hess grade. Primary end points were death and drug morbidity. Results-Mortality was 3/20 in the placebo and 0/19 in the simvastatin group. Study drug was withdrawn in 1 subject in each treatment group for reversible liver enzyme or creatine phosphokinase elevation. MethodsThirty-nine adults (age Ͼ18) with Fisher grade 3 SAH were included. Subjects were eligible if their ruptured aneurysm(s) were secured and if study drug can be started within 96 hours of aneurysm rupture. Patients at high risk for early mortality (Hunt and Hess grade V, or intracranial pressure Ͼ30 cm H 2 O for Ͼ30 minutes) were excluded. Other exclusion criteria were abnormal baseline serum creatine phosphokinase (CPK), alanine aminotransferase (ALT), or aspartate aminotransferase (AST), prior statin use, and contraindication for statin use. The institutional review board approved this study (ClinicalTrials.gov Identifier: NCT00235963).After informed consent from patient or health-care proxy, subjects were double-blind randomized to receive placebo or simvastatin 80 mg/d (until discharge from neurointensive care unit, or a maximum of 21 days), stratified by Hunt and Hess scores (I-II versus III-IV) to ensure an even distribution of this important outcome predictor. Plasma CPK, ALT and AST were monitored every 7 days. Study drug was stopped on unexplained 3-fold elevation of CPK or ALT/AST on 2 consecutive measurements 24 hours apart.Primary end points of this study were death and incidence of drug morbidity defined as CK/AST/ALT elevation. Secondary outcomes included incidence of transcranial Doppler (TCD), angiographic or clinical vasospasm, vasospasm-related infarcts, clinical outcomes at discharge, and cardiac and infectious morbidities.Angiographic vasospasm was defined as focal or generalized reduction of cerebral arterial caliber on conventional cerebral angiogram confirmed by a neuroradiologist and a neurocritical care physician. TCD vasospasm was defined as any peak systolic middle cerebral artery velocity (PSV MCA ) Ͼ200 cm/s and a Lindegaard ratio of Ͼ3. Clinically, delayed ischemic neurological deficit (DIND) was defined as any 2 or more point fall in modified Glasgow Coma Scale or unaccountable new focal neurological deficit lasting Ն2 hours. Vasospasm-related ischemic infarct was defined as the development of a new lesion consistent with infarction on CT or MRI in the vascular territory of angiographic or TCD vasospasm.All patients received nimodipine and an anticonvulsant, were kept euthermic, euvolemic, and euglycemic, and had daily TCD monitoring per standardized protocols. Patients with abnormal TCD velocities or...

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Effect of Prior Statin Use on Functional Outcome and Delayed Vasospasm after Acute Aneurysmal Subarachnoid Hemorrhage: A Matched Controlled Cohort Study

Cited by 101 publications

References 59 publications

Do Statins Improve Outcomes and Reduce the Incidence of Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Do Statins Improve Outcomes and Reduce the Incidence of Vasospasm After Aneurysmal Subarachnoid Hemorrhage

Brain Ischemia in Patients with Intracranial Hemorrhage: Pathophysiological Reasoning for Aggressive Diagnostic Management

A Randomized, Double-Blind, Placebo-Controlled Pilot Study of Simvastatin in Aneurysmal Subarachnoid Hemorrhage

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