Statins may not protect against vasospasm in subarachnoid haemorrhage

Kern, Michael J.; Lam, Mark; Knuckey, Neville W.; Lind, Christopher R. P.

doi:10.1016/j.jocn.2008.08.001

Cited by 39 publications

(28 citation statements)

References 23 publications

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“…Two have only been published as abstracts [22,23]. Observational studies assessed 1,542 patients, of whom 386 were treated with a statin [24][25][26][27][28][29]. Six studies administered simvastatin at a dose of 80 mg per day for 14-21 days.…”

Section: Resultsmentioning

confidence: 99%

Statins in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Kramer

Fletcher

2009

Neurocrit Care

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Section: Resultsmentioning

confidence: 99%

Statins in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Kramer

Fletcher

2009

Neurocrit Care

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“…Patients who are treated with statins prior to aSAH tend to have a lower incidence of subsequent CVS (17). However, other studies have shown that simvastatin does not exert a beneficial effect on patients with aSAH (8,9). Kramer et al (11) pointed out that if there is a benefit to statin use, it may be smaller than suggested by previous studies.…”

Section: Introductionmentioning

confidence: 96%

Effect of statins on aneurysmal subarachnoid hemorrhage: a meta-analysis of randomized controlled trials

Zhang¹,

Song²,

Wang³

et al. 2014

Turkish Neurosurgery

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AIm:The role of statins for treating aneurysmal subarachnoid hemorrhage (aSAH) remains uncertain. In this study, the relevance of different end points was evaluated in order to clarify the action and efficacy of statins. mAterIAl and methOds: A systematic literature retrieval was carried out to obtain randomized controlled trials (RCTs) from before March 2013 on the use of statins for aSAH. Data extraction and quality evaluation of the studies were performed by 2 investigators. A meta-analysis was performed using Review Manager (RevMan) software version 5.2.3. results:Seven randomized controlled trials comprising 347 patients that met the inclusion criteria were included in this meta-analysis. Results showed that, in aSAH, statins did not reduce vasospasm on transcranial Doppler (RR=0.80; 95% CI, 0.53-1.21; p=0.29) or improve outcomes (RR=0.92; 95% CI, 0.71-1.20; p=0.54). However, statins were able to decrease delayed ischemic neurological deficits (RR=0.56; 95% CI, 0.41-0.75; p=0.0001) and mortality (RR=0.54; 95% CI, 0.32-0.91; p=0.02) compared with placebo.COnClusIOn: Acute statin treatment might not be a good choice for cerebral vasospasm after aSAH. Further large-scale, well-designed RCTs on this topic are still needed. BulGulAr: Bu meta analize çalışmaya alma kriterlerini karşılayan 347 hastalık yedi randomize kontrollü çalışma dahil edilmiştir. Sonuçlar aSAK durumunda statinlerin transkraniyal Doppler'de vazospazmı azaltmadığını (RR=0,80; %95 GA, 0,21; p=0,29) veya sonuçları daha iyi hale getirmediğini (RR=0,92; %95CI, 0,20; p=0,54) göstermiştir. Ancak statinler plaseboyla karşılaştırıldığında gecikmiş iskemik nörolojik defisitleri (RR=0,56; %95 GA, 0,41-0,75; p=0,0001) ve mortaliteyi (RR=0,54; %95 GA, 0,32-0,91; p=0,02) azaltmıştır. sOnuÇ: Akut statin tedavisi aSAK sonrasında serebral vazospazm için iyi bir tercih olmayabilir. Bu konuda daha büyük ölçekli ve iyi tasarlanmış randomize kontrollü çalışmalar gereklidir.

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“…It is also interesting to note that animals that are either pretreated or given multiple statins (increases eNOS protein expression) treatment extending from phase I to III develop little delayed vasospasm after SAH [56,57]. That, this observation could not be repeated in clinical SAH may represent delay in initiation of this therapy due to reasons mentioned above [58,59].…”

Section: Phase I (0-60 Min After Sah)mentioning

confidence: 99%

Nitric Oxide in Early Brain Injury After Subarachnoid Hemorrhage

Sehba

Bederson

2011

Early Brain Injury or Cerebral Vasospasm

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Nitric Oxide (NO) is the major regulator of cerebral blood flow. In addition, it inhibits platelet adherence and aggregation, reduces adherence of leukocytes to the endothelium, and suppresses vessel injury. NO is produced on demand by nitric oxide synthase and has a very short half life. Hence maintenance of its cerebral level is crucial for normal vascular physiology. Time dependent alterations in cerebral NO level and the enzymes responsible for its synthesis are found after subarachnoid hemorrhage (SAH). Cerebral NO level decreases, recovers and increases within the first 24 h after SAH. Each change in cerebral NO level elicits a different pathological response form already compromised brain. These response range from constriction, platelet aggregation and vascular injury that occurs during the early hours and delayed occurring vasospasm, neuronal and axonal damage. This review summarizes the underlying mechanism and the consequence of alteration in cerebral NO level on brain during the first 72 h after SAH.

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Statins may not protect against vasospasm in subarachnoid haemorrhage

Cited by 39 publications

References 23 publications

Statins in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Statins in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Effect of statins on aneurysmal subarachnoid hemorrhage: a meta-analysis of randomized controlled trials

Nitric Oxide in Early Brain Injury After Subarachnoid Hemorrhage

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