SynthesisThe Cochrane database of systematic reviews2000
Vasoactive drugs for acute stroke.
Synthesis in The Cochrane database of systematic reviews, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 3 syntheses or guidelines pooled it, 11 citations in OpenAlex.
- Cerebrolysin for acute ischaemic stroke.The Cochrane database of systematic reviews · 2017Pooled it
- Cerebrolysin for acute ischaemic stroke.The Cochrane database of systematic reviews · 2016Pooled it
- Naftidrofuryl for acute stroke.The Cochrane database of systematic reviews · 2007Pooled it
- Control of blood pressure in hypertensive neurological emergencies.Current hypertension reports · 2014Review
- Elevated blood pressure in the acute phase of stroke and the role of Angiotensin receptor blockers.International journal of hypertension · 2013Article
- Blood pressure management in acute stroke.Journal of human hypertension · 2009Review
- Treatment of hypertension in acute ischemic stroke.Current treatment options in neurology · 2009Article
- New insights into hypertension management in acute stroke: let the CHHIPS fall where they may.Journal of clinical hypertension (Greenwich, Conn.) · 2008Article
- Management of arterial hypertension in patients with acute stroke.Current treatment options in neurology · 2006Article
- What do we (not) know about the management of blood pressure in acute stroke?Current neurology and neuroscience reports · 2004Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIt is unclear whether blood pressure should be managed after acute stroke and if so whether it is best to reduce or increase blood pressure.
objectivesThe objective of this review was to assess the effect of lowering or elevating blood pressure in people with acute stroke, and the effect of different vasoactive drugs on blood pressure in acute stroke. SEARCH STRATEGY: We searched the Cochrane Library (1999 Issue 1) using the CDSR and the CCTR databases, MEDLINE (from 1966), EMBASE (from 1980), BIDS ISI (Science Citation Index from 1981), and existing review articles. We contacted researchers in the field and pharmaceutical companies. SELECTION CRITERIA: Randomised trials of interventions that would be expected, on pharmacological grounds, to alter blood pressure in patients within two weeks of the onset of acute ischaemic or haemorrhagic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the trial inclusion criteria, assessed trial quality, and extracted the data. MAIN
resultsSixty five trials were identified involving in excess of 11,500 patients; a further 5 trials are ongoing. Data were obtained for 32 trials (5,368 patients). Significant imbalances in baseline blood pressure were present across trials of intravenous calcium channel blockers and prostacyclin. Major imbalances in baseline blood pressure between treatment and control groups have made the interpretation of these results difficult. Intravenous calcium channel blockers (CCBs) and oral CCBs significantly lowered late blood pressure as compared to controls. (systolic/diastolic BP): iv CCBs -8.2/-6.7 mm Hg (95% CI -12.6 to -3.8)/ (95% CI -9.2 to -4.3); oral CCBs -3.2/-2.1 mm Hg (95% CI -5.0 to -1.3)/ (95% CI -3.0 to -1.0). Beta blockers significantly lowered late diastolic blood pressure but not significantly late systolic blood pressure; -5.0/-4.5 mm Hg (95% CI -10.2 to 0.4)/(95% CI -7.8 to -1.15). Angiotensin converting enzyme inhibitors and prostacyclin non-significantly reduced late BP as compared to the controls by -5.4/-3.0 mm Hg (95% CI -16.5 to 5.8)/(95% CI -11.1 to 5.0) and -7.4/-3.9 mmHg (95% CI -15.6 to 0.2)/(95% CI -8.1 to 0.4) respectively. Magnesium, naftidrofuryl and piracetam had no significant effect on blood pressure. Oral CCBs and beta blockers each significantly reduced late heart rate (beats per minute (bpm)): CCBs -2.8 bpm (95%CI -3.9 to -1.7); beta blockers -9.3 bpm (95% CI -12.0 to -6.6). Prostacyclin significantly increased late heart rate by +5.6 bpm (95% CI 0.8 to 10.4). None of the drug classes significantly altered outcome apart from beta blockers and streptokinase which increased early case fatality (odds ratio 1.77, 95%CI, 1.05 to 3.00) and 2.27 (95% CI 1.4 to 3.67). REVIEWER'S
conclusionsThere is not enough evidence reliably to evaluate the effect of altering blood pressure on outcome after acute stroke. CCBs, beta blockers, and probably ACE-inhibitors, prostacyclin and nitric oxide, each lowered BP during the acute phase of stroke. In contrast, magnesium, naftidrofuryl and piracetam had little or no effect on BP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.