London, United Kingdom 2013 26 Meta-analysis and reviews Targeted use of heparin, heparinoids or low molecular weight heparin to improve outcome af-ter acute ischaemic stroke: individual patient data from 22,655 patients in 5 randomised con-trolled E-Poster Session Blue Cerebrovasc Dis 2013; 35 (suppl 3)1-854 579 trials W.N. Whiteley1, H.P. Adams Jr.2, P.M.W. Bath3, E. Berge4, P.M. Sandset5, M.S. Dennis6, G. Mur-ray7, K-S Wong8, P.A.G. Sandercock9 Division of Clinical Neurosciences, Western General Hospital, University of Edinburgh, Ed-inburgh, UNITED KINGDOM1, Department of Neurology, University of Iowa, Iowa City, Iowa City, USA2, Division of Stroke, University of Nottingham, Nottingham, UNITED KINGDOM3, Oslo University Hospital, Department of Haematology, and University of Oslo, Institute of Clinical Medicine, Oslo, NORWAY4, Oslo University Hospital, Department of Haematology, and Univer-sity of Oslo, Institute of Clinical Medicine, Oslo, NORWAY5, Division of Clinical Neurosciences, Western General Hospital, University of Edinburgh, Edinburgh, UNITED KINGDOM6, Centre for Population Health Sciences, University of Edinburgh, Edinburgh, UNITED KINGDOM7, Division of Neurology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong, HONG-KONG8, Division of Clinical Neurosciences, Western General Hospital, Uni-versity of Edinburgh, Edinburgh, UNITED KINGDOM9 BACKGROUND Many international guidelines on the prevention of venous thromboembolism recommend targeting heparin treatment on the stroke patients with a high risk of venous thrombotic events or a low risk of haemorrhagic events. We sought to identify reliable methods to target anticoagulant treatment and so improve the chance of avoiding death or dependence after stroke. METHODS We obtained individual patient data from the 5 largest randomised controlled trials in acute isch-aemic stroke which compared a heparin with aspirin or placebo. We developed and evaluated statis-tical models for the prediction of thrombotic events (myocardial infarction, stroke, deep vein throm-bosis or pulmonary embolism) and haemorrhagic events (symptomatic intracranial or significant extracranial) in the first 14 days after stroke. We calculated the absolute risk difference for the out-come ‘dead or dependent’ in patients grouped by quarters of predicted risk of thrombotic and haem-orrhagic events with random effect meta-analysis. RESULTS Ischaemic stroke patients who: were older, had more neurological impairment, or had atrial fibril-lation, had a higher risk of both post-stroke thrombotic and haemorrhagic events. In addition brain scan evidence of recent cerebral ischaemia increased the risk of thrombotic events. In evaluation datasets, the area under a receiver operator curve for prediction models for thrombotic events was 0.63 (95%CI:0.59-0.67) and for haemorrhagic events was 0.60 (95%CI:0.55-0.64). We found no ev-idence that the net benefit from heparin increased with either increasing risk of thrombotic events or decreasing risk of haemorrhagic events. CONCLUSIONS There was no evidence that the ischaemic stroke patients at higher risk of thrombotic events or low-er risk of haemorrhagic events benefited from heparins. We were therefore unable to define a tar-geted approach to select the ischaemic stroke patients who would benefit from treatment with early anticoagulant therapy. 25 Stroke prevention Antiplatelet profiles of the fixed-dose combination of extended-release dipyridamole and low-dose aspirin compared with aspirin in patients after ischemic stroke H. Magerova1, B. Urbanova2, O. Chudomel3, J. Schwabova4, M. Šrámek5, I. Šarbochová6, I. Ha-davová7, M. Bojar8, A. Tomek9 Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Mo-tol Hospital, Prague, CZECH REPUBLIC1, Stroke Unit, Department of Neurology, Charles Uni-versity, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH REPUBLIC2, Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH REPUBLIC3, Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH REPUBLIC4, Stroke Unit, Department of Neurolo-gy, Kladno Hospital, Kladno, CZECH REPUBLIC5, Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH REPUBLIC6, Department of Clinical Haematology, Motol Hospital, Prague, CZECH REPUBLIC7, Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH RE-PUBLIC8, Stroke Unit, Department of Neurology, Charles University, 2nd Faculty of Medicine and Motol Hospital, Prague, CZECH REPUBLIC9 Background: Dipyridamole (DIP) inhibits adenosine uptake into platelets, endothelial cells and erythrocytes. Elevation of cAMP lowers ability of platelets to be aggregated by collagen and ade-nosine diphosphate (ADP). Clinical efficacy of combination aspirin (ASA) and DIP (ASA/DIP) is well established but only minimal in-vitro aggregometry data are available. The aim of our study was to determine the effect of DIP on platelet aggregometry and the difference of ASA/DIP versus ASA alone. Methods: Light transmittance aggregometry (LTA) was performed in 112 subjects taking ASA and 92 ASA/DIP. Platelet aggregation was measured as the maximum percentage of light transmittance change (% max) from baseline at the end of recording time using standard platelet agonists - ADP, arachidonic acid (ARA), collagen and ristocetin. Poor response was defined as a % max of >/= 70% with ADP and >/= 20% with ARA. Results: % max LTA did not differ in groups taking ASA and ASA/DIP when induced by ARA (mean(ASA)=14.86%, mean(ASA/DIP)=18.02%), collagen (53.15%, resp. 60.31%) or ristocetin (72.58%, resp. 70.74%) (p>0.05). Difference in ADP-induced LTA approached statistical signifi-cance (mean(ASA)=44.53%, mean(ASA/DIP)=50.74%; p=0.056). There was a tendency for unre-sponsiveness in ASA/DIP group; in ADP-induced LTA (ASA=11.7%, ASA/DIP=20.7%; p=0.082) as well as in ARA-induced LTA (ASA=15.2%, ASA/DIP=19.6%; p=0.408). There was fair agreement between ADP and ARA induced resistance (kappa 0.169 for ASA, 0.288 for ASA/DIP). Conclusion: Our data indicate that DIP does not markedly change aggregometry response. However, a trend can be observed using ADP. On the contrary, patients taking ASA/DIP show more frequent unresponsiveness that is supposedly caused by lower dose of ASA. We are aware of limitations of platelet responsiveness assessment; nevertheless higher platelet reactivity identifies high-risk pa-tients at the time of the acute stroke for which a tailored antiplatelet therapy might be useful.
Karger_ESC London_2013
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