The relation between platelet reactivity and glycemic control in diabetic patients with cardiovascular disease on maintenance aspirin and clopidogrel therapy

Background High platelet reactivity (HPR) during aspirin and clopidogrel therapy in patients with diabetes has been reported and may affect outcomes. However, the relation of platelet reactivity to glycemic control is less studied in patients on dual antiplatelet therapy. Methods Platelet aggregation (PA) in response to 5 and 20 mu mol/L adenosine diphosphate (ADP) was compared in type 2 diabetic (n = 36) and nondiabetic patients in = 35) undergoing elective stenting on aspirin and clopidogrel maintenance therapy. The relation of glycosylated hemoglobin (HbA(1c)) <7 g/dL (n = 16) and HbA(1c) >= 7 g/dL (n = 20) on PA was examined. High platelet reactivity was defined as >46% for 5 mu mol/L ADP-induced and >59% for 20 mu mol/L ADP-induced PA. Results Diabetic patients had higher 5 and 20 mu mol/L ADP-induced PA than nondiabetic patients (45 +/- 17 vs 33 12, P = .009 and 52 +/- 19 vs 40 +/- 12, P = .004, respectively). Diabetic patients with HbA(1c) >= 7.0 g/dL had significantly higher 5 and 20 mu mol/L ADP-induced PA versus patients with diabetes with HbA(1c) <7.0 g/dL (54 +/- 15 vs 34 +/- 14, P < .001 and 62 +/- 14 vs 40 +/- 17, P < .001, respectively). Among diabetic patients with HbA(1c) >= 7 g/dL, the prevalence of HPR was 65% and 60%; and among diabetic patients with HbA(1c) <7 g/dL, the prevalence of HPR was 19% and 13% as measured by 5 and 20 mu mol/L ADP-induced PA, respectively. A correlation was present between 5 and 20 mu mol/L ADP-induced PA and HbA(1c) (r = 0.60 and 0.62, P = .0001, respectively). Conclusion An important relation exists between glycemic control and platelet reactivity in patients with type 2 diabetes mellitus treated with dual antiplatelet therapy. Poorly controlled patients with diabetes have the greatest platelet reactivity and may require alternative antiplatelet strategies, and further clinical investigations are warranted. (Am Heart J 20091-158:784.e1-784.e6.)