Predictors of high on-aspirin platelet reactivity in elderly patients with coronary artery disease
Authors Zhang JW, Liu WW, McCaffrey TA, He XQ, Liang WY, Chen XH, Feng XR, Fu SW, Liu ML
Received 1 April 2017
Accepted for publication 18 June 2017
Published 10 August 2017 Volume 2017:12 Pages 1271—1279
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Akshita Wason
Peer reviewer comments 3
Editor who approved publication: Dr Wu
JW Zhang,1 WW Liu,1 Timothy A McCaffrey,2 XQ He,1 WY Liang,1 XH Chen,1 XR Feng,1 Sidney W Fu,2 ML Liu1
1Department of Geriatrics, Peking University First Hospital, Beijing, China; 2Department of Medicine, George Washington University Medical Center, Washington, DC, USA
Objectives: Previous studies have illustrated the link between high on-aspirin platelet reactivity (HAPR) with increasing thrombotic risks. The aim of our study was to investigate relative risk factors of HAPR in elderly patients with coronary artery disease.
Methods: Elderly, hospitalized coronary artery disease patients on regular aspirin treatment were enrolled from January 2014 to September 2016. Medical records of each patient were collected, including demographic information, cardiovascular risk factors, concomitant drugs and routine biological parameters. Arachidonic acid (AA, 0.5 mg/mL) and adenosine diphosphate (ADP, 5 µmol/L) induced platelet aggregation were measured via light transmission assay (LTA) to evaluate antiplatelet responses, referred as LTA–AA and LTA–ADP.
Results: A total of 275 elderly patients were included, with mean age of 77.2±8.1 years, and males accounted for 81.8%. HAPR was defined as LTA–AA in the upper quartile of the enrolled population. HAPR patients tended to have lower renal function (P=0.052). Higher serum uric acid (SUA) level, as well as lower platelet count, hemoglobin and hematocrit were observed in HAPR patients, with a higher proportion of diuretics use (P<0.05). Multivariate analysis revealed that SUA (OR: 1.004, 95% CI: 1.000–1.007, P=0.048), platelet count (OR: 0.994, 95% CI: 0.989–1.000, P=0.045), hematocrit (OR: 0.921, 95% CI: 0.864–0.981, P=0.011) and concomitant P2Y12 receptor inhibitors use (OR: 1.965, 95% CI: 1.075–3.592, P=0.028) were correlated with HAPR. Spearman’s correlation analysis demonstrated an inverse association of LTA–AA with hematocrit (r=−0.234, P<0.001), hemoglobin (r=−0.209, P<0.001) and estimated glomerular filtration rate (r=−0.132, P=0.031).
Conclusion: SUA, platelet count, hematocrit and P2Y12 receptor inhibitors use were independently correlated with HAPR. These parameters might provide novel therapeutic targets for optimizing antiplatelet therapy.
Keywords: aspirin, platelet reactivity, elderly, risk factors, coronary artery disease
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