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A suspected transient ischemic attack should be evaluated urgently in a clinical setting where appropriate specialist expertise and imaging (ideally diffusion-weighted imaging) are available. Management typically includes aspirin (immediately and indefinitely, with clopidogrel for the first 21 days), evaluation to identify the cause and guide intervention as appropriate, and control of risk factors.

A trial involving 11,016 patients showed that the combination of ticagrelor and aspirin after a stroke or high-risk transient ischemic attack was better than aspirin alone in preventing a stroke or death within 30 days. Severe bleeding was rare but occurred more frequently in the dual antiplatelet group.

In this trial, patients with stroke or TIA and atherosclerosis who received a statin with or without ezetimibe were randomly assigned to an LDL cholesterol target of less than 70 mg per deciliter or to a target range of 90 to 110 mg per deciliter. At a median follow-up of 3.5 years, the incidence of a composite cardiovascular end point was 12% lower in the lower-target group than in the higher-target group. The incidence of cerebral hemorrhage did not differ significantly between the two groups.

Despite the inconsistent or weak association between cholesterol and stroke, lowering of cholesterol concentrations with statins reduces the risk of stroke in high-risk populations and in patients with non-cardioembolic stroke or transient ischaemic attack. Statin therapy is the most important advance in stroke prevention since the introduction of aspirin and antihypertensive treatments. Meta-analysis of randomised trials of statins in combination with other preventive strategies, including 165 792 individuals, shows that each 1 mmol/L (39 mg/dL) decrease in LDL cholesterol equates to a reduction in relative risk for stroke of 21·1% (95% CI 6·3–33·5, p=0·009). In secondary prevention of non-cardioembolic stroke, intense reduction of LDL cholesterol by statins also significantly reduced the risk of recurrent stroke (relative risk 0·84, 0·71–0·99, p=0·03) and major cardiovascular events (0·80, 0·69–0·92, p=0·002). Future directions include assessment of a target LDL cholesterol concentration of less than 1·8 mmol/L (70 mg/dL), the effects of triglyceride-lowering therapy alone or in combination with statins, and the effects of treatments to raise HDL cholesterol concentrations.

Up to 12% of patients with stroke have intracranial arterial dolichoectasia (IADE) and the basilar artery is affected in 80% of these cases. Diagnostic criteria and prognosis studies of IADE are based on basilar artery diameter, which is a good quantitative marker for the severity of the disease. The pathophysiology is largely unknown, but IADE can be viewed as a common final pathway of arterial wall response or damage in the tunica media due to various mechanisms, such as matrix metalloproteinase dysfunction or muscle cell or elastic fibre injury. No randomised controlled trials have been undertaken in IADE and thus little high-level evidence is available on which to base treatment guidelines. IADE management depends on clinical presentation and disease severity, and includes blood pressure control, antithrombotic treatments, endovascular procedures, and surgery. Further studies are needed to better define IADE in the general population, to establish its prevalence and pathophysiology, to identify subgroups at risk of life-threatening complications, and to offer effective treatment options.

In this double-blind, randomized trial involving 13,199 patients with ischemic stroke or transient ischemic attack, ticagrelor was not superior to aspirin in reducing the rate of stroke, myocardial infarction, or death at 90 days. Ischemic stroke and transient ischemic attack are common, and the risk of subsequent ischemic events is particularly high during the first 90 days after the index cerebrovascular event. 1 – 4 Aspirin at a dose of 50 to 325 mg daily is commonly used in this context. 5 – 7 However, the benefit of aspirin in the secondary prevention of ischemic stroke is limited; even with concurrent aspirin treatment, the rate of recurrent stroke is 10 to 15% in the first 90 days, and the rate of new ischemic events when aspirin is used in the long term is only 22% lower than the . . .

In this international registry study of patients who had a transient ischemic attack or minor stroke and who were evaluated on an urgent basis by stroke specialists, the 1-year risk of recurrent stroke was 5.1%, which is lower than the risk reported in historical cohorts. Previous studies conducted between 1997 and 2003 estimated that the risk of stroke or an acute coronary syndrome was 12 to 20% during the first 3 months after a transient ischemic attack (TIA) or minor stroke. 1 , 2 Since then, there have been major changes in the management of TIA, including urgent management in specialized units, implementation of immediate investigations, and rapid treatment with antithrombotic agents and other stroke-prevention strategies. 1 – 4 Given these changes, the current prognosis of patients who have had a TIA and the role of risk-scoring systems in patients receiving urgent care are unclear. 5 – 11 Current guidelines recommend . . .

In a randomized trial involving patients who had a first stroke from an embolus of unknown source, rivaroxaban at a daily dose of 15 mg did not result in a lower incidence of recurrent stroke than aspirin at a dose of 100 mg. Bleeding rates were higher with rivaroxaban.

The IMS III trial did not show a clinical benefit of endovascular treatment compared with intravenous alteplase (recombinant tissue plasminogen activator) alone for moderate or severe ischaemic strokes. Late reperfusion of tissue that was no longer salvageable could be one explanation, as suggested by previous exploratory studies that showed an association between time to reperfusion and good clinical outcome. We sought to validate this association in a preplanned analysis of data from the IMS III trial. We used data for patients with complete proximal arterial occlusions in the anterior circulation who received endovascular treatment and achieved angiographic reperfusion (score on Thrombolysis in Cerebral Infarction scale of grade 2–3) during the endovascular procedure (within 7 h of symptom onset). We used logistic regression to model good clinical outcome (defined as a modified Rankin Scale score of 0–2 at 3 months) as a function of the time to reperfusion. We prespecified variables to be considered for adjustment, including age, baseline National Institutes of Health Stroke Scale score, sex, and baseline blood glucose concentration. Of 240 patients who were otherwise eligible for inclusion in our analysis, 182 (76%) achieved angiographic reperfusion. Mean time from symptom onset to reperfusion (ie, procedure end) was 325 min (SD 52). Increased time to reperfusion was associated with a decreased likelihood of good clinical outcome (unadjusted relative risk for every 30-min delay 0·85 [95% CI 0·77–0·94]; adjusted relative risk 0·88 [0·80–0·98]). Delays in time to angiographic reperfusion lead to a decreased likelihood of good clinical outcome in patients after moderate to severe stroke. Rapid reperfusion could be crucial for the success of future acute endovascular trials. US National Institutes of Health and National Institute of Neurological Disorders and Stroke.

In six trials comparing the anti–PCSK9 antibody bococizumab with placebo, the reduction in LDL cholesterol at 12 weeks was 55.2 percentage points lower with bococizumab. However, antidrug antibodies that developed in many patients reduced the magnitude of the reduction. Reducing levels of low-density lipoprotein (LDL) cholesterol with statin therapy is a highly effective method for reducing cardiovascular risk. 1 Trial data, observational studies, and genetic analyses indicate that further reductions in LDL cholesterol levels are likely to confer greater cardiovascular benefits. 2 – 4 Yet, recent studies have shown wide variability in the individual response of patients to statin therapy in terms of the percent reduction in LDL cholesterol levels. 5 , 6 Inhibitors of proprotein convertase subtilisin–kexin type 9 (PCSK9) reduce plasma LDL cholesterol levels by slowing PCSK9-mediated degradation of the LDL receptor. 7 Fully human monoclonal antibodies such as alirocumab and evolocumab that . . .