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Background and purpose Recurrent ischemic stroke (IS) or TIA is frequent with a considerable variation in incidence and mortality across populations. Current data on stroke recurrence and mortality are useful to examine trends, risk factors, and treatment effects. In this study, we calculated the incidence of recurrent IS or TIA in a hospital‐based stroke population in Western Norway, investigated recurrence factors, and estimated the effect of recurrence on all‐cause mortality. Methods This prospective cohort study registered recurrence and mortality among 1872 IS and TIA survivors admitted to the stroke unit at Haukeland University Hospital between July 2007 and December 2013. Recurrence and death until September 1, 2016, were identified by medical chart review. Cumulative incidences of recurrence were estimated with a competing risks Cox model. Multivariate Cox models were used to examine recurrence factors and mortality. Results During follow‐up, 220 patients had 277 recurrent IS or TIAs. The cumulative recurrence rate was 5.4% at 1 year, 11.3% at 5 years, and 14.2% at the end of follow‐up. Hypertension (HR = 1.65, 95% CI 1.21‐2.25), prior symptomatic stroke (HR = 1.63, 95% CI 1.18‐2.24), chronic infarcts on MRI (HR = 1.48, 95% CI 1.10‐1.99), and age (HR 1.02/year, 95% CI 1.00‐1.03) were independently associated with recurrence. A total of 668 (35.7%) patients died during follow‐up. Recurrence significantly increased the all‐cause mortality (HR = 2.55, 95% CI 2.04‐3.18). Conclusions The risk of recurrent IS stroke or TIA was modest in our population and was associated with previously established risk factors. Recurrence more than doubled the all‐cause mortality.

The prevalence of prior cancer is higher in ISP than in the general population. ISPs with prior cancer are more prone to cardioembolism.

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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.

Given that alteplase has been the only approved thrombolytic agent for acute ischemic stroke for almost two decades, there has been intense interest in more potent and safer agents over the last few years. Tenecteplase is a bioengineered mutation of alteplase with advantageous pharmacodynamics and pharmacokinetics. The superiority of tenecteplase over alteplase has been proven by in vitro and animal studies, and it was approved for use in myocardial infarction more than a decade ago. In patients with acute ischemic stroke, tenecteplase has shown promise in randomized phase II trials and the drug is currently being tested in four phase III clinical trials that will start delivering definite results in the near future: NOR-TEST (NCT01949948), TASTE (ACTRN12613000243718), TEMPO-2 (NCT02398656), and TALISMAN (NCT02180204).

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).

Background. Stroke aetiology may affect the risk and causes of readmission after ischaemic stroke (IS) and transient ischaemic attack (TIA) due to differences in risk factors, functional outcome, and treatment. We aimed to examine frequencies, causes, and risk of 30-day readmission by stroke subtype, determine predictors of 30-day readmission, and study the impact of 30-day readmissions on one-year mortality. Methods. All surviving patients admitted with IS or TIA from July 2007 to December 2013 were followed by review of medical records for all unplanned readmissions within 30 days after discharge. Stroke subtype was classified as largeartery atherosclerosis (LAA), cardioembolism (CE), small vessel occlusion (SVO), stroke of other determined aetiology (SOE), or stroke of undetermined aetiology (SUE). Cox regression analyses were performed to assess the risk of 30-day readmission for the stroke subtypes and identify predictors of 30-day readmission, and its impact on one-year mortality. Results. Of 1874 patients, 200 (10.7%) were readmitted within 30 days [LAA 42/244 (17.2%), CE 75/605 (12.4%), SVO 12/205 (5.9%), SOE 6/32 (18.8%), SUE 65/788 (8.3%)]. The most frequent causes of readmissions were stroke-related event, infection, recurrent stroke/ TIA, and cardiac disease. After adjusting for age, sex, functional outcome, length of stay, and the risk factor burden, patients with LAA and SOE subtype had significantly higher risks of readmission for any cause, recurrent stroke or TIA, and stroke-related events. Predictors of 30-day readmission were higher age, peripheral arterial disease, enteral feeding, and LAA subtype. Thirty-day readmission was an independent predictor of one-year mortality. Conclusions. Patients with LAA or SOE have a high risk of 30-day readmission, possibly caused by an increased risk of recurrent stroke and stroke-related events. Awareness of the risk of readmission for different causes and appropriate handling according to stroke subtype may be useful for preventing some readmissions after stroke.