TY - JOUR
T1 - The relation between platelet reactivity and glycemic control in diabetic patients with cardiovascular disease on maintenance aspirin and clopidogrel therapy
AU - Singla, Anand
AU - Antonino, Mark J.
AU - Bliden, Kevin P.
AU - Tantry, Udaya S.
AU - Gurbel, Paul A.
N1 - Funding Information:
The study is supported by a grant from the Sinai Hospital of Baltimore.
PY - 2009/11
Y1 - 2009/11
N2 - 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 μmol/L adenosine diphosphate (ADP) was compared in type 2 diabetic (n = 36) and nondiabetic patients (n = 35) undergoing elective stenting on aspirin and clopidogrel maintenance therapy. The relation of glycosylated hemoglobin (HbA1c) <7 g/dL (n = 16) and HbA1c ≥7 g/dL (n = 20) on PA was examined. High platelet reactivity was defined as >46% for 5 μmol/L ADP-induced and >59% for 20 μmol/L ADP-induced PA. Results: Diabetic patients had higher 5 and 20 μmol/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 HbA1c ≥7.0 g/dL had significantly higher 5 and 20 μmol/L ADP-induced PA versus patients with diabetes with HbA1c <7.0 g/dL (54 ± 15 vs 34 ± 14, P < .001 and 62 ± 14 vs 40 ± 17, P < .001, respectively). Among diabetic patients with HbA1c ≥7 g/dL, the prevalence of HPR was 65% and 60%; and among diabetic patients with HbA1c <7 g/dL, the prevalence of HPR was 19% and 13% as measured by 5 and 20 μmol/L ADP-induced PA, respectively. A correlation was present between 5 and 20 μmol/L ADP-induced PA and HbA1c (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.
AB - 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 μmol/L adenosine diphosphate (ADP) was compared in type 2 diabetic (n = 36) and nondiabetic patients (n = 35) undergoing elective stenting on aspirin and clopidogrel maintenance therapy. The relation of glycosylated hemoglobin (HbA1c) <7 g/dL (n = 16) and HbA1c ≥7 g/dL (n = 20) on PA was examined. High platelet reactivity was defined as >46% for 5 μmol/L ADP-induced and >59% for 20 μmol/L ADP-induced PA. Results: Diabetic patients had higher 5 and 20 μmol/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 HbA1c ≥7.0 g/dL had significantly higher 5 and 20 μmol/L ADP-induced PA versus patients with diabetes with HbA1c <7.0 g/dL (54 ± 15 vs 34 ± 14, P < .001 and 62 ± 14 vs 40 ± 17, P < .001, respectively). Among diabetic patients with HbA1c ≥7 g/dL, the prevalence of HPR was 65% and 60%; and among diabetic patients with HbA1c <7 g/dL, the prevalence of HPR was 19% and 13% as measured by 5 and 20 μmol/L ADP-induced PA, respectively. A correlation was present between 5 and 20 μmol/L ADP-induced PA and HbA1c (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.
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U2 - 10.1016/j.ahj.2009.08.013
DO - 10.1016/j.ahj.2009.08.013
M3 - Article
C2 - 19853698
AN - SCOPUS:70350056868
SN - 0002-8703
VL - 158
SP - 784.e1-784.e6
JO - American Heart Journal
JF - American Heart Journal
IS - 5
ER -