PT - JOURNAL ARTICLE AU - Daniels, S AU - Jones, S AU - Dempsey-Hibbert, N AU - Alexander, Y TI - P21 Characterisation of the acute effects of hyperglycaemia on platelet function AID - 10.1136/heartjnl-2016-310696.25 DP - 2016 Oct 01 TA - Heart PG - A8--A8 VI - 102 IP - Suppl 8 4099 - http://heart.bmj.com/content/102/Suppl_8/A8.3.short 4100 - http://heart.bmj.com/content/102/Suppl_8/A8.3.full SO - Heart2016 Oct 01; 102 AB - Background Type 2 Diabetic Mellitus (T2DM) is the most challenging public health problem this century. The most common cause of death and disability in these patients are cardiovascular diseases including myocardial infarction and stroke, in which activated platelets play a pivotal role. Patients with T2DM exhibit platelet hyperreactivity and endothelial dysfunction, which indirectly enhances platelet reactivity through loss of inhibitory molecules. Responses to antiplatelet treatment are also perturbed in these patients increasing their risk of thrombosis. In order to enable a more targeted and stratified antithrombotic approach, a better understanding of the complex mechanisms that underpin platelet hyperreactivity is required. The aim of this study was to establish the effects of acute hyperglycaemia on ADP and collagen-mediated platelet activation.Methods Platelet aggregation and dense granule secretion was measured in response to ADP (2.5 µmol/L) or collagen (1 µg/mL) in whole blood and platelet rich plasma (PRP) from healthy donors using lumi-aggregometry, following 1h incubation with D-glucose (5-30 mmol/L) at 20°C and 37°C.Results Paradoxically, in PRP, increased levels of glucose caused a dose-dependent reduction in ADP-mediated aggregation and dense granule secretion at 37°C, but not at 20°C. In contrast, high levels of glucose had no effect on collagen-induced aggregation or secretion at either temperature. Furthermore, glucose had no effect on platelet aggregation with either stimulant, when using whole blood.Conclusion Acute hyperglycaemia is not responsible for platelet hyperreactivity and the increased risk of thrombosis associated with T2DM. Future studies will focus on the chronic effects of hyperglycaemia and insulin resistance on platelet function.