Cerebral haemodynamics with head position changes post-ischaemic stroke: A systematic review and meta-analysis.
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ABSTRACT:
SUBMITTER: Carvalho LB
PROVIDER: S-EPMC7786838 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundIntracerebral haemorrhage (ICH) remains the most devastating yet unpredictable complication of intravenous thrombolysis for acute ischaemic stroke. We performed a systematic review and meta-analysis, to assess whether the presence of cerebral microbleeds (CMBs) on prethrombolysis MRI scans is associated with an increased risk of ICH.MethodsWe searched PubMed for studies assessing ICH risk in patients with acute ischaemic stroke treated with thrombolysis, in relation to the presence of pre-treatment CMBs.ResultsWe identified five studies including 790 patients and pooled data in a meta-analysis. The CMB (+) versus CMB (-) groups were not significantly different in age, gender or stroke severity. The overall prevalence of CMBs was 135/790 (17.1%). Amongst patients with CMBs, 10/135 (7.4%) experienced a symptomatic ICH after thrombolysis, compared to 29/655 (4.4%) patients without CMBs. The pooled relative risk of ICH was 1.90 (95% CI 0.92 to 3.93; p=0.082).ConclusionsThe available evidence does not demonstrate a statistically significant increased risk of symptomatic ICH after thrombolysis for ischaemic stroke in patients with CMBs. However, in view of the methodological limitations of the studies included, the clinical relevance of any potential hazard associated with CMBs remains uncertain. Further studies are warranted to evaluate whether the risk of ICH might outweigh the benefit of thrombolysis, especially in patients with multiple lobar CMBs suggestive of cerebral amyloid angiopathy.
| S-EPMC3905626 | biostudies-literature
Project description:ObjectivesVasodilating antihypertensives prevent stroke and potentially cerebral small vessel disease but their effects on cerebrovascular haemodynamics beyond blood pressure lowering are unclear.MethodsWe searched PubMed, Medline, Embase, Cinahl, Psychinfo, Health Business Elite and Health Management Information Consortium for randomized studies of vasodilating medications, compared to no treatment or nonvasodilators, that reported effects on cerebral blood flow (CBF), mean blood flow velocity (MFV) or cerebrovascular reactivity. Absolute and standardized mean differences (SMD) were combined by inverse-variance weighted fixed or random-effects meta-analysis stratified by study design, population characteristics and vasodilator class.ResultsIn 35 studies reporting 57 comparisons, there was a reduction in SBP (-4.13 mmHg, -7.55 to -0.71, P = 0.018) but no change in MFV (ΔMFV 1.11, confidence interval -0.93 to 3.14, P = 0.29, 23 comparisons). MFV increased in patients with underlying conditions (3.41, 0.24 to 6.57, P = 0.04) but not in healthy study participants (-1.27, -5.18 to 2.64, P = 0.68), with no differences by vasodilating drug class. Cerebral pulsatility index was reduced across all studies (Δ pulsatility index -0.04, -0.07 to -0.02, P = 0.001; Δ pulsatility index -SMD -0.32, -0.47 to -0.16, P < 0.001), except in studies reporting responses to single drug doses (Δ pulsatility index 0.00, -0.09 to -0.08, P = 0.93). Despite evidence of reporting and publication bias, there was an apparent consistent reduction in CBF with vasodilators (CBF-SMD -0.24, -0.46 to -0.02, P = 0.03) with a significant increase in cerebrovascular reactivity-SMD (0.48, 0.13-0.83, P = 0.007).ConclusionsDespite reducing SBP, vasodilators did not significantly impair absolute CBF but improved cerebrovascular pulsatility and reactivity, suggesting therapeutic potential in preventing stroke and cerebral small vessel disease.
| S-EPMC6513078 | biostudies-literature
Project description:IntroductionInsulin resistance is an independent risk factor for atherosclerosis, coronary artery disease and ischaemic stroke. Currently, insulin resistance is not usually included in post-stroke risk stratification. This systematic review and meta-analysis intends to determine if available scientific knowledge supports an association between insulin resistance and post-stroke outcomes in patients without diabetes.Methods and analysisThe authors will conduct a literature search in Medline, Embase, Web of Science and Cochrane Central. The review will include studies that assess the association between elevated insulin homeostasis model of insulin resistance (HOMA-IR) and post-stroke outcome (functional outcome and recurrent stroke). The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines will be used. The primary outcome will be post-stroke functional outcome (Modified Rankin Scale), and the secondary outcome will be recurrent ischaemic stroke. Comparison of outcome will be made between highest and lowest HOMA-IR range (as defined in each article included in this systematic review). Risk of bias will be assessed qualitatively. Meta-analysis will be performed if sufficient homogeneity exists between studies. Heterogeneity of outcomes will be assessed by I².Ethics and disseminationNo human or animal subjects or samples were/will be used. The results will be published in a peer-reviewed journal, and will be disseminated at local and international neurology conferences.Prospero registration numberCRD42020173608.
| S-EPMC8006852 | biostudies-literature
Project description:Central and cerebral haemodynamic parameters can vary under similar brachial blood pressure (BP). We aimed to investigate the effects of antihypertensive agents on central and cerebral haemodynamic parameters in hypertensive patients with ischaemic stroke. The Fimasartan, Atenolol, and Valsartan On haemodynamic paRameters (FAVOR) study was conducted in a prospective, double-blinded manner. One hundred five patients were randomly administered atenolol, valsartan, or fimasartan during 12 weeks. We measured brachial, central, cerebral haemodynamic parameters and plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) levels at baseline and after 12-week. Baseline haemodynamic parameters were balanced among the three groups. Even with similar brachial BP reduction, significantly lower central systolic BP (atenolol; 146.5?±?18.8 vs. valsartan; 133.5?±?20.7 vs. fimasartan; 133.6?±?19.8?mmHg, p?=?0.017) and augmentation index values (89.8?±?13.2 vs. 80.6?±?9.2 vs. 79.2?±?11.6%; p?=?0.001) were seen in the angiotensin receptor blockers (ARBs) groups. The pulsatility index on transcranial Doppler was significantly reduced in valsartan (p?=?0.002) and fimasartan group (p?=?0.008). Plasma NT-proBNP level was also significantly decreased in ARB groups, especially for the fimasartan group (37.8?±?50.6 vs. 29.2?±?36.9 vs.19.2?±?27.8?pg/mL; p?=?0.006). These findings suggest that short-term ARB administration would be favourable for ischaemic stroke patients with hypertension, permitting effective reduction of central pressure and dampening of cerebral pulsatility.
| S-EPMC5784025 | biostudies-literature
Project description:Microglia, the major endogenous immune cells of the central nervous system, mediate critical degenerative and regenerative responses in ischaemic stroke. Microglia become "activated", proliferating, and undergoing changes in morphology, gene and protein expression over days and weeks post-ischaemia, with deleterious and beneficial effects. Pro-inflammatory microglia (commonly referred to as M1) exacerbate secondary neuronal injury through the release of reactive oxygen species, cytokines and proteases. In contrast, microglia may facilitate neuronal recovery via tissue and vascular remodelling, through the secretion of anti-inflammatory cytokines and growth factors (a profile often termed M2). This M1/M2 nomenclature does not fully account for the microglial heterogeneity in the ischaemic brain, with some simultaneous expression of both M1 and M2 markers at the single-cell level. Understanding and regulating microglial activation status, reducing detrimental and promoting repair behaviours, present the potential for therapeutic intervention, and open a longer window of opportunity than offered by acute neuroprotective strategies. Pharmacological modulation of microglial activation status to promote anti-inflammatory gene expression can increase neurogenesis and improve functional recovery post-stroke, based on promising preclinical data. Cell-based therapies, using preconditioned microglia, are of interest as a method of therapeutic modulation of the post-ischaemic inflammatory response. Currently, there are no clinically-approved pharmacological options targeting post-ischaemic inflammation. A major developmental challenge for clinical translation will be the selective suppression of the deleterious effects of microglial activity after stroke whilst retaining (or enhancing) the neurovascular repair and remodelling responses of microglia.
| S-EPMC7139954 | biostudies-literature
Project description:OBJECTIVE: To explore the association between migraine and risk of ischaemic stroke. DESIGN: Systematic review and meta-analysis. DATA SOURCES: Observational studies published between 1966 and June 2004 (identified through Medline and Embase) that examined the association between migraine and risk of ischaemic stroke. RESULTS: 14 studies (11 case-control studies and 3 cohort studies) were identified. These studies suggest that the risk of stroke is increased in people with migraine (relative risk 2.16, 95% confidence interval 1.89 to 2.48). This increase in risk was consistent in people who had migraine with aura (relative risk 2.27, 1.61 to 3.19) and migraine without aura (relative risk 1.83, 1.06 to 3.15), as well as in those taking oral contraceptives (relative risk 8.72, 5.05 to 15.05). CONCLUSIONS: Data from observational studies suggest that migraine may be a risk factor in developing stroke. More studies are needed to explore the mechanism of this potential association. In addition, the risk of migraine among users of oral contraceptives must be further investigated.
| S-EPMC543862 | biostudies-other
Project description:BackgroundWe have previously shown that recurrent arterial ischaemic stroke (AIS) in children with cerebral arteriopathy is associated with increased circulating endothelial cells and endothelial microparticles, consistent with ongoing endothelial injury. To date, however, little is known about endothelial repair responses in childhood AIS. We examined the relationship between the number and function of circulating endothelial progenitor cells (EPC), the levels of brain-derived neurotrophic factor (BDNF) and AIS recurrence.MethodsFlow cytometry was used to identify peripheral blood mononuclear cells positive for CD34/kinase insert domain-containing receptor (KDR). In a subgroup of patients (5 in each group selected at random), monocytic EPC function was assessed by colony-forming unit (EPC-CFU) capacity and incorporation into endothelial cell networks in Matrigel. BDNF was measured using ELISA.ResultsThirty-five children, aged 12 years (range: 5-16.5; 9 males), with AIS and cerebral arteriopathy were studied; 10 had recurrent AIS. CD34+/KDR+ cells were significantly higher in recurrent AIS compared to non-recurrent AIS patients (p = 0.005) and controls (p = 0.0002). EPC-CFU and EPC incorporation into endothelial cell networks were significantly reduced in recurrent compared to non-recurrent AIS patients (p = 0.04 and p = 0.01, respectively). Levels of BDNF were significantly higher in recurrent compared to non-recurrent AIS patients (p = 0.0008) and controls (p = 0.0002).ConclusionsChildren with recurrent AIS and cerebral arteriopathy had increased circulating CD34+/KDR+ cells and BDNF consistent with an endothelial repair response. However, EPC function was impaired. Future studies are needed to examine whether suboptimal endothelial repair contributes to childhood AIS recurrence.
| S-EPMC4478301 | biostudies-literature
Project description:Backgroundstroke is the main cause of disability in high-income countries, and ranks second as a cause of death worldwide. Patients with acute stroke are at risk for infections, but reported post-stroke infection rates vary considerably. We performed a systematic review and meta-analysis to estimate the pooled post-stroke infection rate and its effect on outcome.MethodsMEDLINE and EMBASE were searched for studies on post-stroke infection. Cohort studies and randomized clinical trials were included when post-stroke infection rate was reported. Rates of infection were pooled after assessment of heterogeneity. Associations between population- and study characteristics and infection rates were quantified. Finally, we reviewed the association between infection and outcome.Results87 studies were included involving 137817 patients. 8 studies were restricted to patients admitted on the intensive care unit (ICU). There was significant heterogeneity between studies (P < 0.001, I(2) = 97%). The overall pooled infection rate was 30% (24-36%); rates of pneumonia and urinary tract infection were 10% (95% confidence interval [CI] 9-10%) and 10% (95%CI 9-12%). For ICU studies, these rates were substantially higher with 45% (95% CI 38-52%), 28% (95%CI 18-38%) and 20% (95%CI 0-40%). Rates of pneumonia were higher in studies that specifically evaluated infections and in consecutive studies. Studies including older patients or more females reported higher rates of urinary tract infection. Pneumonia was significantly associated with death (odds ratio 3.62 (95%CI 2.80-4.68).ConclusionsInfection complicated acute stroke in 30% of patients. Rates of pneumonia and urinary tract infection after stroke were 10%. Pneumonia was associated with death. Our study stresses the need to prevent infections in patients with stroke.
| S-EPMC3185266 | biostudies-literature
Project description:Pre-intervention CT imaging-based biomarkers, such as hyperdense middle cerebral artery sign (HMCAS) may have a role in acute ischaemic stroke prognostication. However, the clinical utility of HMCAS in settings of reperfusion therapy and the level of prognostic association is still unclear. This systematic review and meta-analysis investigated the association of HMCAS sign with clinical outcomes and its prognostic capacity in acute ischaemic stroke patients treated with reperfusion therapy. Prospective and retrospective studies from the following databases were retrieved from EMBASE, MEDLINE and Cochrane. Association of HMCAS with functional outcome, symptomatic intracerebral haemorrhage (sICH) and mortality were investigated. The random effect model was used to calculate the risk ratio (RR). Subgroup analyses were performed for subgroups of patients receiving thrombolysis (tPA), mechanical thrombectomy (EVT) and/or combined therapy (tPA + EVT). HMCAS significantly increased the rate of poor functional outcome by 1.43-fold in patients (RR 1.43; 95% CI 1.30-1.57; p < 0.0001) without any significant differences in sICH rates (RR 0.91; 95% CI 0.68-1.23; p = 0.546) and mortality (RR 1.34; 95% CI 0.72-2.51; p = 354) in patients with positive HMCAS as compared to negative HMCAS. In subgroup analyses, significant association between HMCAS and 90 days functional outcome was observed in patients receiving tPA (RR 1.53; 95% CI 1.40-1.67; p < 0.0001) or both therapies (RR 1.40; 95% CI 1.08-1.80; p = 0.010). This meta-analysis demonstrated that pre-treatment HMCAS increases risk of poor functional outcomes. However, its prognostic sensitivity and specificity in predicting long-term functional outcome, mortality and sICH after reperfusion therapy is poor.
| S-EPMC8180356 | biostudies-literature
Project description:ObjectivesTo evaluate the efficacy and safety of endovascular treatment, particularly adjunctive intra-arterial mechanical thrombectomy, in patients with ischaemic stroke.DesignSystematic review and meta-analysis.Data sourcesMedline, Embase, Cochrane Central Register of Controlled Trials, Web of Science, SciELO, LILACS, and clinical trial registries from inception to December 2015. Reference lists were crosschecked.Eligibility criteria for selecting studiesRandomised controlled trials in adults aged 18 or more with ischaemic stroke comparing endovascular treatment, including thrombectomy, with medical care alone, including intravenous recombinant tissue plasminogen activator (rt-PA). Trial endpoints were functional outcome (modified Rankin scale scores of ?2) and mortality at 90 days after onset of symptoms. No language or time restrictions applied.Results10 randomised controlled trials (n=2925) were included. In pooled analysis endovascular treatment, including thrombectomy, was associated with a higher proportion of patients experiencing good (modified Rankin scale scores ?2) and excellent (scores ?1) outcomes 90 days after stroke, without differences in mortality or rates for symptomatic intracranial haemorrhage, compared with patients randomised to medical care alone, including intravenous rt-PA. Heterogeneity was high among studies. The more recent studies (seven randomised controlled trials, published or presented in 2015) proved better suited to evaluate the effect of adjunctive intra-arterial mechanical thrombectomy on its index disease owing to more accurate patient selection, intravenous rt-PA being administered at a higher rate and earlier, and the use of more efficient thrombectomy devices. In most of these studies, more than 86% of the patients were treated with stent retrievers, and rates of recanalisation were higher (>58%) than previously reported. Subgroup analysis of these seven studies yielded a risk ratio of 1.56 (95% confidence interval 1.38 to 1.75) for good functional outcomes and 0.86 (0.69 to 1.06) for mortality, without heterogeneity among the results of the studies. All trials were open label. Risk of bias was moderate across studies. The full results of two trials are yet to be published.ConclusionsModerate to high quality evidence suggests that compared with medical care alone in a selected group of patients endovascular thrombectomy as add-on to intravenous thrombolysis performed within six to eight hours after large vessel ischaemic stroke in the anterior circulation provides beneficial functional outcomes, without increased detrimental effects.Systematic review registrationPROSPERO CRD42015019340.
| S-EPMC4834754 | biostudies-literature