The influence of aspirin dose and glycemic control on platelet inhibition in patients with type 2 diabetes mellitus

摘要

Background: Low-dose aspirin seems to offer no benefit in the primary prevention of cardiovascular disease in type 2 diabetes mellitus (DM2). The anti-platelet effect may be diminished by poor glycemic control or inadequate dosing of aspirin. Objectives: To study the effects of both glycemic control and increasing aspirin dose on platelet response to aspirin in DM2 patients and matched controls. Patients/methods: Platelet effects of increasing doses of aspirin (30, 100 and 300mg daily) were prospectively assessed in 94 DM2 patients and 25 matched controls by measuring thromboxane levels in urine (11-dhTxB2) and platelet aggregation using VerifyNow ? and light transmission aggregometry (LTA). DM2 patients were stratified for glycemic control (hemoglobin-A1c [HbA1c] ≤53, 53-69, ≥69mmolmol -1). Results: At baseline, median 11-dhTxB2 excretion was higher in the poorly controlled patients (77ngmmol -1), and the moderately controlled (84ngmmol -1) compared with the well-controlled patients (64ngmmol -1) and controls (53ngmmol -1), P0.01. Next, 30mg of aspirin reduced 11-dhTxB2 excretion to 31, 29 and 24ngmmol -1 in the poorly, moderately and well-controlled patients, respectively, and to 19ngmmol -1 in controls, P0.001. VerifyNow ? and LTA were also incompletely suppressed in DM2 patients using 30mg of aspirin, but 100mg resulted in similar platelet suppression in all groups, with no additional effect of 300mg. Conclusions: DM2 patients with inadequate glycemic control (HbA1c53mmolmol -1) have higher baseline platelet activity and incomplete suppression of platelet activity with 30mg of aspirin. However, 100mg of aspirin leads to optimal inhibition irrespective of glycemic control, and 300mg does not further improve platelet suppression.