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Updated: Jun 5, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Platelet reactivity in diabetic patients subjected to acute exercise stress test
Mickey Scheinowitz1, Rajbabu Pakala, Itsik Ben-Dor
1Division of Cardiology, Washington Hospital Center, Washington, DC 20010, USA.
Background:
Previous studies have reported ambiguous results regarding the effect of acute exercise on platelet reactivity in healthy and cardiac patients.
Objectives:
We aimed to assess platelet reactivity among diabetic patients before and immediately after an acute exercise stress test.
Methods:
Patients (controls: mean age 53.1 ± 12.1 years; four males; body mass index 27.0 ± 5.7 kg/m(2); HbA(1c) 6.0 ± 1.1%, n = 8) and diabetic patients (52.9 ± 11.3; six males; body mass index 30.7 ± 2.2 kg/m(2); HbA(1c) 7.8 ± 1.7%, n = 8) referred for diagnostic nuclear exercise stress test were recruited. Blood samples obtained at rest and immediately post-exercise were stimulated with adenosine diphosphate (ADP), collagen and arachidonic acid. Expression of CD41 (pan-platelet marker) and CD62p (platelet stimulation marker) were measured by flow cytometry. Aspirin responsiveness was measured using VerifyNow.
Results:
Although peak systolic blood pressure was significantly higher in the diabetics compared with nondiabetics (186.3 ± 25.4 vs. 157.1 ± 19.1, respectively, P = .028), peak exercise heart rate was similar (156.5 ± 8.3 vs. 155.5 ± 12.1 for diabetics and nondiabetics, respectively). No differences were observed between groups for aspirin resistance. Platelet stimulation with ADP exhibited significantly lower CD62p-positive cell population (%) in the diabetic patients both prior to and following the exercise stress test (P = .03). In addition, although not significant, platelet stimulation was higher post-exercise in the diabetic patients (6.3 ± 4.7% vs. 12.0 ± 5.6%, for pre- and post-exercise, respectively, P = .2) with no difference in controls (9.2 ± 5.5% vs. 8.9 ± 5.9%).
Conclusion:
Platelet stimulation in diabetic patients is blunted and might be explained by the prolonged exposure of platelets to multiple diabetic risk factors.
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