Vitamin K antagonists versus antiplatelet therapy after transient ischaemic attack or minor ischaemic stroke of presumed arterial origin
Department of Neurology, Rijnland Ziekenhuis Leiderdorp, Netherlands.Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 09/2012; 9(9):CD001342. DOI: 10.1002/14651858.CD001342.pub3
People who have a stroke due to a blockage of an artery have a higher risk of having another possibly fatal stroke, or a heart attack. Treatment with antiplatelet drugs (like aspirin) definitely reduces this risk. Blood thinning treatment (anticoagulation by vitamin K antagonists) was believed to provide added protection. We reviewed eight trials involving 5762 participants that compared anticoagulants with antiplatelet agents for preventing recurrent stroke and found no benefit of low intensity anticoagulation over aspirin, and an increased risk of bleeding with high intensity anticoagulation.
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ABSTRACT: Vitamin K antagonists are widely used for the prevention of stroke due to atrial fibrillation, treatment and secondary prevention of venous thromboembolism, prevention of valvular thromboembolism in patients with prosthetic heart valves, and secondary prevention of acute myocardial infarction. The most common adverse event experienced by patients receiving anticoagulant therapy is major bleeding. The incidence of major bleeding in patients receiving long-term anticoagulation with a vitamin K antagonist in contemporary studies is 1-3% per year. To determine if the benefits of anticoagulant therapy outweigh the risk of bleeding in an individual patient, physicians must be aware of the risk factors associated with major bleeding. This narrative review will provide an overview of the incidence of major bleeding in patients receiving therapeutic anticoagulant therapy with vitamin K antagonists, discuss the risk factors for bleeding, and outline the most commonly used clinical prediction rules for bleeding.
Article: Secondary stroke prevention[Show abstract] [Hide abstract]
ABSTRACT: Survivors of stroke and transient ischaemic attacks are at risk of a recurrent stroke, which is often more severe and disabling than the index event. Optimum secondary prevention of recurrent stroke needs rapid diagnosis and treatment and prompt identification of the underlying cardiovascular cause. Effective treatments include organised acute assessment and intervention with antithrombotic therapy, carotid revascularisation, and control of causal risk factors, as appropriate. However, effective treatments are not implemented optimally in clinical practice. Recurrent strokes continue to account for 25-30% of all strokes and represent unsuccessful secondary prevention. Immediate and sustained implementation of effective and appropriate secondary prevention strategies in patients with first-ever stroke or transient ischaemic attack has the potential to reduce the burden of stroke by up to a quarter.
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ABSTRACT: Peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists are insulin-sensitising drugs used for the treatment of insulin resistance. In addition to lowing glucose in diabetes, these drugs may also protect against hyperlipidaemia and arteriosclerosis, which are risk factors for stroke. To assess the efficacy and safety of PPAR-γ agonists in the secondary prevention of stroke and related vascular events for people with stroke or transient ischaemic attack (TIA). We searched the Cochrane Stroke Group Trials Register (August 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2013, Issue 9), MEDLINE (1949 to October 2013), EMBASE (1980 to October 2013), CINAHL (1982 to October 2013), AMED (1985 to October 2013) and 11 Chinese databases (October 2013). In an effort to identify further published, unpublished and ongoing trials we searched ongoing trials registers, reference lists and relevant conference proceedings, and contacted authors and pharmaceutical companies. There were no language restrictions. We included randomised controlled trials (RCTs) evaluating PPAR-γ agonists versus placebo for the secondary prevention of stroke and related vascular events in people with stroke or TIA, with the outcomes of recurrent stroke, vascular events and adverse events. Two review authors independently screened the titles and abstracts of identified records, selected studies for inclusion, extracted eligible data, cross-checked the data for accuracy and assessed the methodological quality. We identified four eligible studies with 1163 participants; only one study had a low risk of bias for all domains. The participants in different studies were heterogeneous. The number of participants with recurrent stroke was evaluated in two studies, where PPAR-γ agonists reduced the recurrence of stroke compared with placebo (risk ratio (RR) 0.52, 95% confidence interval (CI) 0.34 to 0.80). PPAR-γ agonists given over a mean duration of 34.5 months in a single trial were found to reduce a composite outcome of total events of cardiovascular death, non-fatal myocardial infarction or non-fatal stroke (RR 0.73, 95% CI 0.54 to 0.99). Data on additional composite outcomes reflecting serious adverse events (all-cause death and other major vascular events; all-cause mortality, non-fatal myocardial infarction or non-fatal stroke) were similar although the confidence intervals were wider and the effects were not statistically significant. In addition, two studies respectively measured insulin sensitivity and the ubiquitin-proteasome activity in carotid plaques with significant differences in these outcomes between PPAR-γ agonists and placebo. None of the studies reported the number of participants with disability due to vascular events or improvement in quality of life. Three RCTs reported information about adverse events. Frequent adverse events included oedema, cardiac failure and anaemia. Evidence that adverse events occurred more frequently in participants treated with PPAR-γ agonists when compared with placebo was imprecise and inconsistent (risk difference (RD) 10%, 95% CI -8% to 28%, I² = 86%). PPAR-γ agonists were demonstrated to reduce recurrent stroke and total events of cardiovascular death, non-fatal myocardial infarction or non-fatal stroke, and improve insulin sensitivity and the stabilisation of carotid plaques. There is evidence of limited quality that they are well-tolerated. However, the conclusions should be interpreted with caution considering the small number and the quality of the included studies. In future, well-designed, double-blind RCTs with large samples are required to test the efficacy and safety of PPAR-γ agonists in the secondary prevention of stroke and related vascular events in people with stroke or TIA.
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