Impact of diabetes on immature platelets fraction and its relationship with platelet reactivity in patients receiving dual antiplatelet therapy

M Verdoia, P Pergolini, M Nardin, R Rolla… - Journal of thrombosis …, 2016 - Springer
M Verdoia, P Pergolini, M Nardin, R Rolla, L Barbieri, A Schaffer, P Marino, G Bellomo
Journal of thrombosis and thrombolysis, 2016Springer
Contrasting data have been reported so far on the role of reticulated platelets in suboptimal
response to antiplatelet therapies. In particular, still unexplored is whether they may
contribute to explain the higher risk of thrombotic complications observed in diabetic
patients. Aim of the present study was to evaluate the impact of diabetes on the levels of
reticulated platelets and its relationship with high residual on-treatment platelet reactivity
(HRPR) in patients receiving dual antiplatelet therapy. In patients treated with ASA (100–160 …
Abstract
Contrasting data have been reported so far on the role of reticulated platelets in suboptimal response to antiplatelet therapies. In particular, still unexplored is whether they may contribute to explain the higher risk of thrombotic complications observed in diabetic patients. Aim of the present study was to evaluate the impact of diabetes on the levels of reticulated platelets and its relationship with high residual on-treatment platelet reactivity (HRPR) in patients receiving dual antiplatelet therapy. In patients treated with ASA (100–160 mg) and clopidogrel (75 mg daily) or ticagrelor (90 mg twice a day) platelet reactivity and the reticulated platelets fraction (immature platelets fraction, IPF) were assessed at 30–90 days post-discharge for an acute coronary syndrome or elective PCI. Aggregation was assessed by multiple-electrode aggregometry. We included 386 patients, 158 (40.9%) diabetics. The percentage of IPF was similar in diabetic and non diabetic patients, both at baseline (3.5±2.5 vs 3.6±2.7%, p= 0.91) and at 30–90 days re-assessment (3.3±2.1 vs 3.5±2.5%, p= 0.30), with diabetes not emerging as an independent predictor of IPF above III tertile (adjusted OR [95% CI]= 0.58 [0.30–1.09], p= 0.10). Diabetic patients displayed an enhanced platelet reactivity and a higher rate of HRPR with ADP antagonists (32.8 vs 22.5%, p= 0.009). However, no association was found between the percentage of IPF and platelet function (r=− 0.004; p= 0.95 for ASPI test, r=− 0.04; p= 0.59 for ADP-mediated aggregation), or the rate of HRPR for ADP antagonsist across IPF tertiles. Results were similar for diabetics both receiving clopidogrel and ticagrelor. Diabetic patients display a higher platelet reactivity and suboptimal response to ADP-antagonists. However, the rate of reticulated platelets is neither influenced by diabetic status nor associated with an increased platelet reactivity among diabetic patients receiving dual antiplatelet therapy for a recent acute coronary syndrome or PCI.
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