Platelet non-responsiveness to dual antiplatelet therapy and relation to coronary disease among diabetes patients

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Aggregation to ADP 20 μmol/L (%) 4 [0,10] 0 [0,0] b0.001 Aggregation to collagen 5 μmol/L (%) 22 [16,40] 16 [10,32] b0.001 Plasma P-selectin (pg/mL) 62.2±25.7 60.7±20.4 0.78 Random blood glucose (mm Hg) 8.3±4.3 9.0±4.2 0.54 Platelet count (10/mm) 276±71 274±59 0.83 Patients with Type II diabetes mellitus have higher rates of first and recurrent cardiovascular events and greater tendency towards diffuse and small vessel coronary artery disease (CAD). A key factor in the development and pathogenesis of both diffuse vessel disease and increased rate of cardiovascular events may be higher platelet reactivity compared to non-diabetics [1,2]. Biochemical studies and in vitro platelet aggregation tests of diabetes patients have shown platelet activity and reactivity to vary with poor metabolic control, presence of hypertension and smoking [3–7]. Aspirin therapy alone may not be effective in reducing platelet activation and aggregation. So would a dual antiplatelet regime be more effective in reducing platelet activation and aggregation? Around 10–20% of the general non-diabetic population are presumed to be non-responsive, or resistant, to dual aspirin– clopidogrel therapy who were more likely to suffer severe angina pectoris, recurrent atherothrombotic events following acute MI and increased in-stent thrombosis post-coronary stenting [8–15]. We conducted a pilot study to investigate the prevalence of resistance to clopidogrel as add-on antiplatelet therapy among type II diabetes patients, and the association of double antiplatelet resistance to extent of coronary disease. 35 Type II diabetes patients were recruited consecutively from a single out-patient cardiology clinic along with 19 nondiabetes patients who acted as controls. All patients had