HMG-CoA Reductase Inhibitors Improve Acute Ischemic Stroke Outcome

Moonis, Majaz; Kane, Kevın; Schwiderski, Ute; Sandage, Bobby W.; Fisher, Marc

doi:10.1161/01.str.0000165920.67784.58

Cited by 119 publications

(79 citation statements)

References 7 publications

(2 reference statements)

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“…Although some trials have failed to find lipid lowering effects of other policosanol tablets [27][28][29], the cholesterollowering effects here seen are consistent with previous experimental [30][31][32][33][34] and clinical [35][36][37][38] data of policosanol. Since statins may improve outcomes in acute ischemic stroke [39,40], these effects of poli + AS treatment could have contributed to the neurological recovery of study patients.…”

Section: Discussionmentioning

confidence: 99%

Effects of policosanol on the recovery of ischemic stroke: a randomized controlled study

Sánchez¹

2012

iosrphr

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Background. Antiplatelet therapy lowers the risk of recurrent stroke. Policosanol, a mixture of 8 high molecular weight sugar cane wax alcohols, has shown to reduce platelet aggregation. Objectives. To investigate whether the therapy with policosanol plus aspirin (AS) could improve the neurological outcome as compared to placebo + AS in patients with a recent ischemic stroke. Methods. Ninety-two (92) patients with a modified Rankin Scale score (mRSs) ≥2 -≤4 after suffering an ischemic stroke within 30 days before enrollment were randomized to placebo or policosanol (20 mg/day) + AS (125 mg/day) (pla + AS or poli + AS) for 24 weeks. The primary efficacy variable was to obtain a better stroke outcome (mRSs ≤1) as compared to pla +AS. Reduction of platelet aggregation was a secondary variable. Results. After 12 and 24 weeks on therapy, the rates of patients treated with poli + AS (10/46, 21.7% and 32/46, 69.6%, respectively) who achieved mRSs ≤1 were significantly (p0.01 and p0.0001, respectively) greater than those treated with pla + AS (0/46, 0.0% and 7/46, 15.2%, respectively). Poli + AS treatment given for 6 weeks reduced significantly (p0.00001 vs baseline, p0.01 vs pla + AS) the mean mRSs value (24.1%), and this effect improved thereafter, so that it was reduced by 31.0% and 55.2% after 12 and 24 weeks on therapy, respectively. Poli + AS treatment also reduced significantly arachidonic acid-and adenosine diphosphateinduced platelet aggregation by 41.0% and 24.8%, respectively. Treatments were well tolerated. There were not withdrawals due to adverse experiences. Conclusions. In patients with recent ischemic stroke, poli + AS treatment improved the neurological recovery and decreased platelet aggregation as compared to pla + AS.

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Section: Discussionmentioning

confidence: 99%

Effects of policosanol on the recovery of ischemic stroke: a randomized controlled study

Sánchez¹

2012

iosrphr

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“…49,50 Treatment of patients within 4 weeks after acute ischemic stroke with statins significantly increased favorable outcome at 12 weeks. 51 In addition, the efficacy, safety, and tolerability of statins have been confirmed in randomized, controlled, multicenter trials involving large numbers of patients aged Ն65 years. 52 Elderly patients taking lipid-lowering agents, such as statins, at the time of an ischemic stroke have lower poststroke mortality and a lower risk of worsening during hospitalization.…”

Section: Pharmacological Treatment Of Stroke Statinsmentioning

confidence: 95%

Neurorestorative treatment of stroke: Cell and pharmacological approaches

Chen

Chopp

2006

NeuroRX

153

114

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Summary:There is a compelling need to develop cell and pharmacological therapeutic approaches to be administered beyond the hyperacute phase of stroke. These therapies capitalize on the capacity of the brain for neuroregeneration and neuroplasticity and are designed to reduce neurological deficits after stroke. This review provides an update of bone marrowderived mesenchymal stem cells (MSCs) and select pharmacological agents in clinical use for other indications that promote the recovery process in the subacute and chronic phases after stroke. Among these agents are 3-hydroxy-3-methylglutarylcoenzyme A reductase inhibitors (statins), erythropoietin (EPO), and phosphodiesterase type 5 (PDE-5) inhibitors and nitric oxide (NO) donors. Both the MSCs and the pharmacologic agents potentiate brain plasticity and neurobehavioral recovery after stroke.

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“…Additional studies shown that, besides the lipid-lower effect, at the same time lovastatin could stabilize the atherosclerotic plaque and have beneficial effects on cerebral circulation and brain parenchyma during ischemic stroke and reperfusion [34]. We measured the plaque thickness and volume of patients in three groups and found that lovastatin could significantly decreased plaque thickness and volume.…”

Section: Discussionmentioning

confidence: 91%

The effect of high-dose lovastatin therapy on patients with acute cerebral infarction

Guo¹,

Chen²,

Ye³

et al. 2017

Gastroenterol Hepatol Endosc

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Cerebrovascular disease (CVD) is the third most common cause of death worldwide and responsible for stroke and transient ischemic attack. This study aimed to investigate the clinical efficacy of high-dose lovastatin on patients with acute cerebral infarction. 150 patients with acute cerebral infarction were randomized divided into control group (n=50), 80 mg/d lovastatin (80 L) group (n=50) and 20 mg/d lovastatin (20 L) group (n=50). Control group, 80 L group and 20 L group received conventional treatment, conventional treatment together with lovastatin 80 mg/d and conventional treatment as well as lovastatin 20 mg/d respectively for 3 months. Biochemical indices, neurological deficit and plaque thickness and volume were assessed and recorded after treatment. After lovastatin treatment, the plasma levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) were significantly decreased in 80 L group and 20 L group, and highdensity lipoprotein (HDL) were significantly increased in 80 L group and 20 L group (p<0.05). Moreover, lovastatin could also decrease MMP-9 and hs-CRP levels (p<0.05). Furthermore, improved neurological deficit were found in lovastatin treatment groups. In addition, lovastatin treatment also improved plaque states include plaque thickness and volume in 80 L group and 20 L group (p<0.05). What's more, high-dose lovastatin a better ability in regulated plasma lipid levels, inflammation, neurological deficit and plaque thickness and volume than low-dose of lovastatin. Lovastatin could improve acute cerebral infarction and high-dose lovastatin treatment was better than low-dose lovastatin treatment.

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HMG-CoA Reductase Inhibitors Improve Acute Ischemic Stroke Outcome

Cited by 119 publications

References 7 publications

Effects of policosanol on the recovery of ischemic stroke: a randomized controlled study

Effects of policosanol on the recovery of ischemic stroke: a randomized controlled study

Neurorestorative treatment of stroke: Cell and pharmacological approaches

The effect of high-dose lovastatin therapy on patients with acute cerebral infarction

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