Coronary artery diseaseInfluence of Aspirin Resistance on Platelet Function Profiles in Patients on Long-Term Aspirin and Clopidogrel After Percutaneous Coronary Intervention
Section snippets
Study population
A total of 135 patients who had previously undergone elective percutaneous coronary intervention and were on ASA (100 mg/day) and clopidogrel (75 mg/day) therapy for ≥1 month were included. Patients were screened during their routine clinical follow-up visits at our outpatient clinic. All patients were clinically stable after percutaneous coronary intervention. Patient compliance to antiplatelet treatment was assessed by interview and pill counting. Patients were enrolled consecutively if these
Results
In the overall study population, 60 of 135 patients (44%) were ASA resistant and 75 (56%) were ASA sensitive. The rate of ASA resistance was even higher among diabetics (57%). The characteristics of ASA-resistant and -sensitive patients are shown in Table 1. No differences were observed between groups, except for a higher number of diabetic patients in the ASA-resistant group (p = 0.001).
Hematocrit, platelet count, and mean platelet volume values were similar between the groups (Table 1).
Discussion
This is the first study to investigate the influence of ASA resistance on platelet function profiles of patients concomitantly treated with clopidogrel. In particular, ASA-resistant patients showed increased platelet activation and aggregation compared with ASA-sensitive patients, regardless of the concomitant use of clopidogrel. In addition, the results of the present study also demonstrated the presence of a significant patient variability in platelet response in ASA-resistant and -sensitive
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Cardiovascular Protection in People With Diabetes
2018, Canadian Journal of DiabetesAntiplatelet Therapy in Diabetes
2018, Endocrinology and Metabolism Clinics of North AmericaPlatelets and diabetes mellitus
2015, Prostaglandins and Other Lipid MediatorsCitation Excerpt :Patients with diabetes are typically characterized by platelet hyperreactivity. Although ASA may lead to complete blockade of COX-1 as assessed by assays specific to this target, high residual platelet reactivity may persist in these patients as a result of upregulation of other signaling pathways, which are not blocked by ASA [125]. Diabetic individuals are characterized by increased platelet reactivity and an increased level and activity of prothrombotic clotting factors, which may explain their predisposition to inadequate ASA-induced effects.