Urinary tract infection after acute stroke: Impact of indwelling urinary catheterization and assessment of catheter-use practices in French stroke centers

Introduction

Urinary catheterization and acute urinary retention increase the risk of urinary tract infection (UTI). Our study aimed to investigate the incidence of UTI following acute stroke at our stroke center (SC) and to assess urinary catheter-care practices among French SCs.

Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial

The aim of the study was to assess the safety and feasibility of a clinical trial on the effect of vinpocetine, a synthetic ethyl ester of apovincamine, in acute ischaemic stroke. Thirty consecutive patients with computed tomography verified diagnosis of acute ischaemic stroke, who could receive drug treatment within 72 h of stroke onset, were enrolled. The patients were randomly allocated to receive either low-molecular weight dextran alone or in combination with vinpocetine. Poor outcome was defined as being dead or having a Barthel index of < 70 or a Rankin score of 3--5. Intention-to-treat analysis was applied. One-tenth of all hospitalized patients with acute ischaemic stroke were eligible for the trial. Thirty eligible patients were treated with either low-molecular weight dextran alone (mean age 57.9 +/- 11.6 years, n = 15) or in combination with vinpocetine (mean age 60.8 +/- 6.6 years, n = 15). The two treatment groups were comparable with respect to major prognostic variables. A relative risk (RR) reduction of poor outcome at 3 months follow-up was 30% (RR = 0.7; 95% confidence interval [CI] 0.1--3.4), as defined by the modified Barthel Index, and 60% as defined by the modified Ranking score (RR = 0.4, 95% CI: 0.1--1.7). The National Institute of Health (NIH--NINDS) Stroke Scale score was marginally significantly better in the vinpocetine treated group at 3 months of follow-up (P = 0.05, ANOVA). No significant adverse effects were seen. This pilot study shows that a full-scale randomized double-blind, placebo-controlled trial of vinpocetine treatment in acute ischaemic stroke is feasible and warranted.     

Efficacy and safety of ginsenoside-Rd for acute ischaemic stroke: a randomized, double-blind, placebo-controlled, phase II multicenter trial

Background and purpose:  Ginsenoside-Rd is a selective competitive Ca²⁺ receptor antagonist. A phase II randomized, double-blind, placebo-controlled, multicenter study was conducted to examine the efficacy and safety of ginsenoside-Rd in patients with acute ischaemic stroke.
Methods:  A total of 199 patients were randomized equally to receive a 14-day infusion of placebo (group B), ginsenoside-Rd 10 mg (group A) or ginsenoside-Rd 20 mg (group C). Primary end-points were National Institutes of Health Stroke Scale (NIHSS) scores at 15 days. Secondary end-points were NIHSS scores and the Barthel Index at 8 days, the Barthel Index and the modified Rankin scale at 15 days and 90 days. The safety end-points included serious and non-serious adverse events, laboratory values and vital signs. Analysis was by intention to treat.
Results:  For the primary study outcome, there is significant difference amongst the three groups at 15 days in NIHSS scores ( P  = 0.0003). Comparing group A with B and group B with C, the difference in the mean for NIHSS was significant in statistics ( P  = 0.0004, P  = 0.0009 respectively). This is no significant difference between group A and C ( P  = 0.9640). For the secondary study outcome, ginsenoside-Rd did not improve neurological functioning. Incidence of serious and non-serious adverse events was similar amongst the three groups.
Conclusions:  Ginsenoside-Rd may be of some benefit in acute ischaemic stroke.     

Ginsenoside-Rd improves outcome of acute ischaemic stroke - a randomized, double-blind, placebo-controlled, multicenter trial

Background and purpose: Ginsenoside‐Rd is a receptor‐operated calcium channel antagonist and has shown promise as a neuroprotectant in our phase II study. As an extended work, we sought to confirm its efficacy and safety of Ginsenoside‐Rd in patients with acute ischaemic stroke. Methods: We conducted a randomized, double‐blind, placebo‐controlled trial involving 390 patients with acute ischaemic stroke in a 3:1 ratio to receive a 14‐day intravenous infusion of Ginsenoside‐Rd or placebo within 72 h after the onset of stroke. Our primary end‐point was the distribution of disability scores on the modified Rankin scale (mRs) at 90 days. Results: The efficacy analysis was based on 386 patients (Ginsenoside‐Rd group: 290; placebo group: 96). Ginsenoside‐Rd significantly improved the overall distribution of scores on the mRs, as compared with the placebo (P = 0.02; odds ratios [OR], 1.74; 95% confidence interval [CI], 1.08–2.78). There were significant differences between the two groups when we categorized the scores into 0–1 vs. 2–5 (P = 0.01; OR, 2.32; 95% CI, 1.23–4.38; 66.8% vs. 53.1%). It also improved the National Institutes of Health Stroke Scale (NIHSS) at 15 days [P < 0.01; least squares mean (LSM), ?0.77; 95% CI, ?1.31 to ?0.24]. Mortality and rates of adverse events were similar in the two groups. Conclusions: Ginsenoside‐Rd improved the primary outcome of acute ischaemic stroke and had an acceptable adverse‐event profile.     

Association between seropositivity to Chlamydia pneumoniae and acute ischaemic stroke

Recent studies suggest an association between Chlamydia pneumoniae infection with atherosclerosis, including cerebrovascular disease. We investigated the prevalence of Chlamydial seropositivity in patients with acute ischaemic stroke syndrome compared with age- and sex-matched control subjects. Specific antibodies (IgA) to C. pneumoniae were measured by microimmunofluorescence in both the clinical group (n=91) and the control group (n=112). Forty patients (43.9%) and 34 controls (30.3%) had positive IgA titres (P < 0.05). The pooled data from this and previous series yielded 45% of seropositivity in cerebrovascular patients vs. 19% in control subjects (P < 0.001). In conclusion, we suggest an association between chronic infection by C. pneumoniae and acute ischaemic stroke.     

Body temperature and response to thrombolytic therapy in acute ischaemic stroke

Objective: To determine the relationship between body temperature (BT), arterial recanalization, functional outcome, and hemorrhagic transformation (HT) of cerebral infarction in patients treated with i.v. tissue plasminogen activator (tPA). Methods: We studied 254 patients treated with tPA within 3 h from stroke onset. National Institute of Health Stroke Scale score, BT, and transcranial Doppler ultrasound (n = 99) on admission and at 24 h were recorded. Hypodensity volume and HT were evaluated on CT at 24–36 h. Poor outcome (Rankin Scale > 2) was evaluated at 3 months. Results: Arterial recanalization at 24 h was found in 70.7% of patients, HT in 24.8% (symptomatic in 4.7%) and poor outcome in 44.1%. Baseline BT was not associated with greater stroke severity at admission or at 24 h, HT or poor outcome. However, BT at 24 h correlated to stroke severity (P < 0.001) and hypodensity volume (P < 0.001) at 24 h, and was higher in patients who did not recanalize (P = 0.001), had symptomatic HT (P = 0.063) and poor outcome (P < 0.001). The adjusted odds ratio of poor outcome for patients with BT at 24 h ≥ 37°C was 2.56 (1.19–5.50, P = 0.016). Conclusion: Body temperature ≥37°C at 24 h, but not at baseline, is associated with a lack of recanalization, greater hypodensity volume and worse outcome in stroke patients treated with tPA.     

Lipid profile,statin use,and outcome after intravenous thrombolysis for acute ischaemic stroke

BACKGROUND: Low cholesterol levels have been associated with an increased risk of haemorrhagic stroke. This study investigated whether lipid levels or prior statin use influence outcome in patients with acute ischaemic stroke treated with IV thrombolysis. METHODS: The relation between admission lipid levels or statin use and both the development of symptomatic intracerebral haemorrhage (sICH) and 3-months functional outcome was assessed in a prospective hospital-based stroke registry comprising 252 patients treated with IV tissue plasminogen activator (tPA). The fasting status of the patients was unknown. Favourable outcome at 3 months was defined as a modified Rankin scale score 相似文献   

Revascularization in acute ischaemic stroke using the penumbra system: the first single center experience

Background and purpose:  This is the first single center experience illustrating the effectiveness of the penumbra system (PS) in the treatment of large vessel occlusive disease in the arena of acute ischaemic stroke. The PS is an innovative mechanical thrombectomy device, employed in the revascularization of large cerebral vessel occlusions in patients via the utilization of an aspiration platform.
Methods:  This is a prospective, non-randomized controlled trial evaluating the clinical and functional outcome in 29 patients with acute intra-cranial occlusions consequent to mechanical thrombectomy by the PS either as mono-therapy or as an adjunct to current standard of care. Patients were evaluated by a neurologist and treated by our in house interventional neuro-radiologists. Primary end-points were revascularization of the occluded target vessel to TIMI grade 2 or 3 and neurological outcome as measured by an improvement in the NIH Stroke Scale (NIHSS) score after the procedure.
Results:  Complete revascularization (TIMI 3) was achieved in 21/29 (72.4%) of patients. Partial revascularization (TIMI 2) was established in 4/29 (13.8%) of patients. Revascularization failed in four (13.8%) patients. Nineteen (19) patients (65.5%) had at least a four-point improvement in NIHSS scores. Modified Rankin scale scores of ≤2 were seen in 37.9% of patients. There were no device-related adverse events. Symptomatic intra-cranial hemorrhage occurred in 7% of patients.
Conclusions:  The PS has the potential of exercising a significant impact in the interventional treatment of ischaemic stroke in the future.     

Different roles of matrix metalloproteinases-2 and -9 after human ischaemic stroke

Accumulating data suggest that matrix metalloproteinases (MMPs), in particular MMP-2 and MMP-9, are deleterious after acute ischaemic stroke. A beneficial effect of MMPs in the repairing phases of cerebral ischaemia has also been proposed. This study investigated the relationship between MMP-2 and MMP-9 and stroke subtypes, clinical recovery and haemorrhagic transformation (HT). We measured MMP-9 and MMP-2 plasma levels in 29 patients with ischaemic stroke at days one and seven. MMP-2 levels increased only in lacunar strokes, whilst MMP-9 increased only in patients with more severe stroke. Basal MMP-2 levels were higher in patients with stable or recovering symptoms whilst MMP-9 values at day seven were correlated with worse clinical outcome. No differences related to the presence of HT were found. This study sustains a different behaviour of MMPs after ischaemic stroke. MMP-2 seems to be expressed early and related to better outcome, whilst MMP-9 seems to be late and related to more severe stroke.     

Positron emission tomography in ischaemic stroke: cerebral perfusion and metabolism after stroke onset

PET studies were performed in 37 patients up to 1 month after ischaemic stroke to observe the relationships between cerebral blood flow (CBF), rate of cerebral oxygen metabolism (CMRO(2)) and oxygen extraction fraction (OEF) with time. PET findings were classified as misery perfusion (two patients), luxury perfusion (15 patients), matched hypoperfusion-hypometabolism (17 patients) or normal (nine patients). Misery perfusion was seen up to 3 days post-stroke, suggesting an extended time window during which at least some tissue may be salvageable. Luxury perfusion, an indication of non-nutritional flow, was seen as early as 30 h and as late as 23 days, but more commonly between 3 and 7 days. A matched reduction of CBF and CMRO(2) was seen during all time periods, but as early as 27 hours. Since this was associated with severely impaired CBF, presumably from the onset of stroke, it can be assumed that the duration of cerebral tissue survival is less than 27 h under these conditions. We inferred that, for maximal tissue recovery, therapy will need to be introduced within 27 h after stroke, but that at least some potential for recovery exists up to 3 days.     

Correlation between genetic polymorphisms and stroke recovery: analysis of the GAIN Americas and GAIN International Studies

Background and purpose: Recovery after stroke occurs on the basis of specific molecular events. Genetic polymorphisms associated with impaired neural repair or plasticity might reduce recovery from stroke and might also account for some of the intersubject variability in stroke recovery. This study hypothesized that the ApoE ε4 polymorphism and the val⁶⁶met polymorphism for brain‐derived neurotrophic factor (BDNF) are each associated with poorer outcome after stroke. Associations with mitochondrial genotype were also explored. Methods: Genotypes were determined in 255 stroke patients who also received behavioral evaluations in the Glycine Antagonist In Neuroprotection (GAIN) clinical trials. The primary outcome measure was recovery during the first month post‐stroke, as this is the time when neural repair is at a maximum and so when genetic influences might have their largest impact. Two secondary outcome measures at 3 months post‐stroke were also examined. Results: Genotype groups were similar acutely post‐stroke. Presence of the ApoE ε4 polymorphism was associated with significantly poorer recovery over the first month post‐stroke (P = 0.023) and with a lower proportion of subjects with minimal or no disability (modified Rankin score 0–1, P = 0.01) at 3 months post‐stroke. Indeed, those with this polymorphism were approximately half as likely to achieve minimal or no disability (18.2%) versus those with polymorphism absent (35.5%). Findings were confirmed in multivariate models. Results suggested possible effects from the val⁶⁶met BDNF polymorphism and from the R0 mitochondrial DNA haplotype. Conclusions: Genetic factors, particularly the ApoE ε4 polymorphism, might contribute to variability in outcomes after stroke.