Calcium antagonists for acute ischemic stroke

Zhang, Jing; Yang, Jie; Zhang, Canfei; Jiang, Xian; Zhou, Huijie; Liu, Ming

doi:10.1002/14651858.cd001928.pub2

Cited by 51 publications

(35 citation statements)

References 42 publications

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“…A meta-analysis of clinical trials assessing the calcium channel blocker nimodipine showed no neuroprotective effect in patients with acute ischemic stroke. 23 Two of these trials reported that nimodipine therapy within 48 hours of stroke onset was associated with worse clinical outcomes in patients with acute ischemic stroke. 24,25 Recently, a few preliminary randomized trials of blood pressure reduction in acute ischemic stroke have been published.…”

Section: Discussionmentioning

confidence: 99%

Effects of Immediate Blood Pressure Reduction on Death and Major Disability in Patients With Acute Ischemic Stroke

Zhang

et al. 2014

JAMA

382

289

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IMPORTANCE Although the benefit of reducing blood pressure for primary and secondary prevention of stroke has been established, the effect of antihypertensive treatment in patients with acute ischemic stroke is uncertain.OBJECTIVE To evaluate whether immediate blood pressure reduction in patients with acute ischemic stroke would reduce death and major disability at 14 days or hospital discharge. DESIGN, SETTING, AND PARTICIPANTS The China Antihypertensive Trial in Acute IschemicStroke, a single-blind, blinded end-points randomized clinical trial, conducted among 4071 patients with nonthrombolysed ischemic stroke within 48 hours of onset and elevated systolic blood pressure. Patients were recruited from 26 hospitals across China between August 2009 and May 2013.INTERVENTIONS Patients (n = 2038) were randomly assigned to receive antihypertensive treatment (aimed at lowering systolic blood pressure by 10% to 25% within the first 24 hours after randomization, achieving blood pressure less than 140/90 mm Hg within 7 days, and maintaining this level during hospitalization) or to discontinue all antihypertensive medications (control) during hospitalization (n = 2033). MAIN OUTCOMES AND MEASURESPrimary outcome was a combination of death and major disability (modified Rankin Scale score Ն3) at 14 days or hospital discharge.RESULTS Mean systolic blood pressure was reduced from 166.7 mm Hg to 144.7 mm Hg (−12.7%) within 24 hours in the antihypertensive treatment group and from 165.6 mm Hg to 152.9 mm Hg (−7.2%) in the control group within 24 hours after randomization (difference, −5.5% [95% CI, −4.9 to −6.1%]; absolute difference, −9.1 mm Hg [95% CI, −10.2 to −8.1]; P < .001). Mean systolic blood pressure was 137.3 mm Hg in the antihypertensive treatment group and 146.5 mm Hg in the control group at day 7 after randomization (difference, −9.3 mm Hg [95% CI, −10.1 to −8.4]; P < .001). The primary outcome did not differ between treatment groups (683 events [antihypertensive treatment] vs 681 events [control]; odds ratio, 1.00 [95% CI, 0.88 to 1.14]; P = .98) at 14 days or hospital discharge. The secondary composite outcome of death and major disability at 3-month posttreatment follow-up did not differ between treatment groups (500 events [antihypertensive treatment] vs 502 events [control]; odds ratio, 0.99 [95% CI, 0.86 to 1.15]; P = .93).CONCLUSION AND RELEVANCE Among patients with acute ischemic stroke, blood pressure reduction with antihypertensive medications, compared with the absence of hypertensive medication, did not reduce the likelihood of death and major disability at 14 days or hospital discharge.

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Section: Discussionmentioning

confidence: 99%

Effects of Immediate Blood Pressure Reduction on Death and Major Disability in Patients With Acute Ischemic Stroke

Zhang

et al. 2014

JAMA

382

289

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“…Many drugs show the neuroprotective effects such as NMDA receptor antagonist, calcium antagonists and histone deacetylases (HDACs) [18][19][20]. Nowadays, pharmacodynamic constituents from natural medicines have been regarded as the focus in pharmaceutical development.…”

Section: Discussionmentioning

confidence: 99%

Baicalin attenuates proinflammatory cytokine production in oxygen–glucose deprived challenged rat microglial cells by inhibiting TLR4 signaling pathway

Hou

Wang

Zhang

et al. 2012

International Immunopharmacology

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“…A number of pharmacological treatments such as mitochondria potassium channel openers, calcium channel blockers, anti-oxidative agents, anti-inflammatory drugs, estrogens, progesterone, iron chelators, stem cells, etc. (Bi and Song, 2011; Hao et al, 2014; Ma et al, 2012; Mangoni et al, 2010; Shao et al, 2012; Sun and Feng, 2013; Tewari et al, 2014; Wali et al, 2014; Zhang et al, 2012) have shown potential in animal stroke models, but most of these failed to function effectively (Bi and Song, 2011; Wali et al, 2014), or caused unwanted side effects in human clinical practice. Considering the unpredictability of the time of a stroke attack, it is of extreme importance to find effective neuroprotective strategies to be delivered (Hahn et al, 2011) either before, during, or after blood flow stoppage to the brain.…”

Section: Introductionmentioning

confidence: 99%

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

Wang

Reis

Applegate

et al. 2015

Experimental Neurology

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In the area of brain injury and neurodegenerative diseases, a plethora of experimental and clinical evidence strongly indicates the promise of therapeutically exploiting the endogenous adaptive system at various levels like triggers, mediators and the end-effectors to stimulate and mobilize intrinsic protective capacities against brain injuries. It is believed that ischemic pre- or post-conditioning are actually the strongest known interventions to stimulate the innate neuroprotective mechanism to prevent or reverse neurodegenerative diseases including stoke and traumatic brain injury. Recently, studies showed the effectiveness of ischemic per-conditioning in some organs. Therefore the term ischemic conditioning, including all interventions applied pre-, per- and post- ischemia, which spans therapeutic windows in 3 time periods, has recently been broadly accepted by scientific communities. In addition, it is extensively acknowledged that ischemia-mediated protection not only affects the neurons but also all the components of the neurovascular network (consisting of neurons, glial cells, vascular endothelial cells, pericytes, smooth muscle cells, and venule/veins). The concept of cerebroprotection has been widely used in place of neuroprotection. Intensive studies on the cellular signaling pathways involved in ischemic conditioning have improved the mechanistic understanding of tolerance to cerebral ischemia. This has added impetus to exploration for potential pharmacologic mimetics, which could possibly induce and maximize inherent protective capacities. However, most of these studies were performed in rodents, and the efficacy of these mimetics remains to be evaluated in human patients. Several classical signaling pathways involving apoptosis, inflammation, or oxidation have been elaborated in the past decades. Newly characterized mechanisms are emerging with the advances in biotechnology and conceptual renewal. In this review we are going to focus on those recently reported methodological and mechanistic discoveries in the realm of ischemic conditioning. Due to the varied time differences of ischemic conditioning in different animal models and clinical trials, it is important to define optimal timing to achieve the best conditioning induced neuroprotection. This brings not only an opportunity in treatment of stroke, but challenges as well, as data is just becoming available and the procedures are not yet optimized. The purpose of this review is to shed light on exploiting these ischemic conditioning modalities to protect the cerebrovascular system against diverse injuries and neurodegenerative disorders.

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Calcium antagonists for acute ischemic stroke

Cited by 51 publications

References 42 publications

Effects of Immediate Blood Pressure Reduction on Death and Major Disability in Patients With Acute Ischemic Stroke

Effects of Immediate Blood Pressure Reduction on Death and Major Disability in Patients With Acute Ischemic Stroke

Baicalin attenuates proinflammatory cytokine production in oxygen–glucose deprived challenged rat microglial cells by inhibiting TLR4 signaling pathway

Ischemic conditioning-induced endogenous brain protection: Applications pre-, per- or post-stroke

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