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Background: There is growing evidence that inflammation plays an important role in atherogenesis. Previous studies show that C-reactive protein (CRP), an inflammatory marker, is associated with stroke outcomes and future vascular events. It is not clear whether this is due a direct dose-response effect or rather an epiphenomenon. We studied the effect of CRP measured within 24 hours after stroke onset on functional outcome, mortality and future vascular events.

Background: Animal studies show a neuroprotective effect of serum albumin in ischemic stroke. The neuroprotective effect of albumin in ischemic stroke in humans is not well studied. This study was aimed to determine the association of serum albumin with outcome and mortality after ischemic stroke. Methods: In a prospective study, we included 444 patients with ischemic stroke. Serum albumin was measured at the time of admission. Stroke severity was measured at the time of admission with the National Institutes of Health Stroke Scale (NIHSS). Functional outcome was measured with the modified Rankin scale (mRS) on day 7. Multiple logistic regression analysis was used to assess the independent association between variables and outcome. Survival was analyzed by Cox regression analysis after adjusting for age, sex and NIHSS score on admission. Results: The mean age (SD) of the patients was 70.4 (14.4) years. The median NIHSS score (interquartile range) on admission was 4 (1–8) and the median mRS score (interquartile range) on day 7 was 2 (1–3). Sixty patients (13%) died during a median follow-up period of 2 years. High serum albumin was independently associated with a better outcome (OR = 1.12, 95% CI = 1.05–1.20, p = 0.001). After adjusting for age, sex and NIHSS score on admission, high serum albumin was associated with lower mortality (OR = 0.88, 95% CI = 0.83–0.93, p < 0.0001). Conclusions: The current study indicates that high serum albumin is associated with better outcome and lower mortality in ischemic stroke patients. High serum albumin may be neuroprotective in ischemic stroke in humans.

Our study suggests that the effect of high body temperature on clot lysis is more important than the neuroprotective effect of low body temperature in the early phase after cerebral infarction treated with tPA.

BackgroundA possible synergic role of serum uric acid (SUA) with thrombolytic therapies is controversial and needs further investigations. We therefore evaluated association of admission SUA with clinical improvement and clinical outcome in patients receiving rt-PA, early admitted patients not receiving rt-PA, and patients admitted after time window for rt-PA.MethodsSUA levels were obtained at admission and categorized as low, middle and high, based on 33° and 66° percentile values. Patients were categorized as patients admitted within 3 hours of symptom onset receiving rt-PA (rt-PA group), patients admitted within 3 hours of symptom onset not receiving rt-PA (non-rt-PA group), and patients admitted after time window for rt-PA (late group). Short-term clinical improvement was defined as the difference between NIHSS on admission minus NIHSS day 7. Favorable outcome was defined as mRS 0 - 3 and unfavorable outcome as mRS 4 - 6.ResultsSUA measurements were available in 1136 patients. Clinical improvement was significantly higher in patients with high SUA levels at admission. After adjustment for possible confounders, SUA level showed a positive correlation with clinical improvement (r = 0.012, 95% CI 0.002-0.022, p = 0.02) and was an independent predictor for favorable stroke outcome (OR 1.004; 95% CI 1.0002-1.009; p = 0.04) only in the rt-PA group.ConclusionsSUA may not be neuroprotective alone, but may provide a beneficial effect in patients receiving thrombolysis.

BackgroundAlteplase is the only approved thrombolytic agent for acute ischaemic stroke. The overall benefit from alteplase is substantial, but some evidence indicates that alteplase also has negative effects on the ischaemic brain. Tenecteplase may be more effective and less harmfull than alteplase, but large randomised controlled phase 3 trials are lacking. The Norwegian Tenecteplase Stroke Trial (NOR-TEST) aims to compare efficacy and safety of tenecteplase vs. alteplase.Methods/DesignNOR-TEST is a multi-centre PROBE (prospective randomised, open-label, blinded endpoint) trial designed to establish superiority of tenecteplase 0.4 mg/kg (single bolus) as compared with alteplase 0.9 mg/kg (10% bolus + 90% infusion/60 minutes) for consecutively admitted patients with acute ischaemic stroke eligible for thrombolytic therapy, i.e. patients a) admitted <4½ hours after symptoms onset; b) admitted <4½ hours after awakening with stroke symptoms c) receiving bridging therapy before embolectomy.Randomisation tenecteplase:alteplase is 1:1. The primary study endpoint is favourable functional outcome defined as modified Rankin Scale 0–1 at 90 days. Secondary study endpoints are: 1) haemorrhagic transformation (haemorrhagic infarct/haematoma); 2) symptomatic cerebral haemorrhage on CT 24–48 hours; 3) major neurological improvement at 24 hours; 4) recanalisation at 24–36 hours; 5) death.DiscussionNOR-TEST may establish a novel approach to acute ischaemic stroke treatment. A positive result will lead to a more effective, safer and easier treatment for all acute ischaemic stroke pasients.NOR-TEST is reviewed and approved by the Regional Committee for Medical and Health Research Ethics (2011/2435), and The Norwegian Medicines Agency (12/01402). NOR-TEST is registered with EudraCT No 2011-005793-33 and in ClinicalTrials.gov (NCT01949948).

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