22. European Stroke Conference 578 © 2013 S. Karger AG, Basel Scientific Programme 24 Stroke prevention Low-dose Aspirin therapy and Silent Brain Infarcts (SBI): an observational study. V. Di Piero1, M. Altieri2 on behalf of SILENCE Investigators Dept. Neurology and Psychiatry, Sapienza University of Rome, Roma, ITALY1, Dept. Neurolo-gy and Psychiatry, Sapienza University of Rome, Roma, ITALY2 Background: SBI show the same characteristics of cerebral infarctions without acute clinical pre-sentation. SBI are frequently seen on MRI in healthy adults and associated with subsequent clinical stroke as well as cognitive decline. The balance of risks and benefits of low-dose ASA therapy has not been established in healthy subjects with SBI. Our aim was to assess if ASA treatment might re-duce the risk of further SBI, stroke or MI. Methods: We performed an observational study on ASA 100 mg/day for the prevention of SBI and stroke. We recruited subjects with at least one SBI, aged ≥45 years, without previous occurrence of clinical cerebrovascular (CVD) event and without contra-indications to ASA. Subjects were followed for a year assessing the incidence of CVD and new SBI assessed by MRI (primary endpoint) and incidence of new vascular events, and adverse events (sec-ondary endpoints). Results: We enrolled 83 subjects (57 F and 26 M, mean age 65.3+9 years), who had completed a year follow-up. Hypertension occurred in 55.4%, dyslipidemia in 66.2% and diabe-tes in 3.6%; 24% were alcohol drinkers and 15.6% smokers. Subjects received ASA therapy (n=36) or no antiplatelets agents (n=47). No difference in age, sex and routine vascular risk factors were observed between the two groups. In the ASA group occurred 1 new SBI, 1 stroke and 1 myocardi-al infarction whereas in the untreated one there were 2 strokes, 6 new SBI, 1 TIA and 1 myocardial infarction. In the ASA group, a subject had peptic ulcer while in the untreated group there were 1 epistaxis and 1 gastrointestinal hemorrhage. Although significance was not reached, in the untreated group there were 9 (19.1%) major events vs. 2 (5.6%) in the ASA one (p=0.10). Discussion: These data show an increase of new CVD events in the untreated group. Despite the study limitations, SBI seems to be a negative prognostic factor for CVD diseases. ASA preventive treatment might contrib-ute to ameliorate SI prognosis. 23 Stroke prevention Allopurinol reduces carotid artery intima-media thickness progression amongst stroke survi-vors P. Higgins1, M.R. Walters2, K.R. Lees3, A. McConnachie4, H. Murray5, K. McArthur6, J. Dawson7 University of Glasgow, Glasgow, UNITED KINGDOM1, University of Glasgow, Glasgow, UNIT-ED KINGDOM2, University of Glasgow, Glasgow, UNITED KINGDOM3, University of Glasgow, Glasgow, UNITED KINGDOM4, University of Glasgow, Glasgow, UNITED KINGDOM5, Uni-versity of Glasgow, Glasgow, UNITED KINGDOM6, University of Glasgow, Glasgow, UNITED KINGDOM7 Background Novel strategies are needed to reduce recurrent stroke risk. Allopurinol, traditionally used in gout prophylaxis, reduces both circulating uric acid levels and oxidative stress through xanthine oxidase inhibition (XOI). It confers beneficial effects on a range of surrogate measures of cardiovascular health in non-stroke patients. We sought to gather evidence of a beneficial and sustained effect of allopurinol on robust markers of vascular health after stroke. Methods We performed a randomised, double-blind placebo controlled study, examining the effect of one year’s treatment with allopurinol 300 mg daily, on carotid artery intima-media thickness (IMT) pro-gression. Patients aged over 18 years with previous ischaemic stroke or TIA were eligible. The primary efficacy endpoint was change in carotid IMT over one year. Secondary endpoints included change in arterial stiffness at one year and change in endothelial function and circulating levels of endothelial progenitor cells, vWF, s-ICAM-1, E-selectin & s-thrombomodulin, at 6 months. Results Eighty participants, with a mean age of 67.8 years (SD 9.4) were recruited. Mean common carot-id IMT was a significantly reduced at one year following allopurinol use compared with placebo (between group treatment difference -0.057mm (95% CI -0.108, -0.006), p < 0.05). There was no statistically significant difference between groups for secondary endpoints of arterial stiffness or circulating markers of endothelial function. Central aortic systolic blood pressure fell following al-lopurinol treatment (between group difference -6.65 mmHg (95% CI -13.03), -0.27, p < 0.05) at 12 months. Conclusions These findings confirm the potential for XOI as a preventative measure after stroke and are consis-tent with recent studies in other vascular disease populations in which LVH regression was demon-strated. Future studies should explore the effect of allopurinol on clinical outcomes after ischaemic stroke.
Karger_ESC London_2013
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