Increased exercise-related platelet activation assessed by impedance aggregometry in diabetic patients despite aspirin therapy.

Aspirin is widely used for the prevention of thromboembolic diseases, but inhibition of platelet aggregation (PA) is not uniform. Additionally, aspirin has been shown to be ineffective in blunting PA in response to exercise in patients with coronary artery disease (CAD). Limited data exists about platelet function following acute exercise in diabetics taking aspirin. In our study, we aimed to investigate PA before and after exercise stress test in type-2 diabetic patients taking aspirin. Forty-three patients with type-2 diabetes mellitus (DM) and 36 subjects (age- and sex-matched) as control group were included prospectively. All participants were under aspirin (100 mg/day) therapy for at least 1 week. The measures of PA were assessed by impedance aggregometry using arachidonic acid as an agonist (ASPI test). Blood samplings were undertaken before and immediately after treadmill exercise test. At rest, diabetic and control groups had comparable pre-exercise PA (22.97 ± 14.57 versus 22.11 ± 12.71 AU min, p = NS, respectively). After treadmill exercise, both groups showed significantly higher absolute increase (9.02 ± 13.08 and 3.66 ± 5.87 AU min, p < 0.01, p < 0.01, respectively) and percent (%) increase (45.67 ± 49.34 and 24.04 ± 46.59 AU min, p < 0.01, p = 0.01, respectively) in PA. Both absolute increase (p < 0.05) and % increase (p < 0.05) in PA were significantly higher in DM group compared to the control group. Multiple regression analysis revealed that high-sensitive C-reactive protein (p = 0.014) was independent predictor of absolute increase PA. Our study showed that aspirin has limited effect in inhibiting exercise-induced PA, even in the absence of documented CAD. The increase in PA following exercise was significantly greater in patients with DM compared with controls.