کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2837109 | 1164888 | 2011 | 5 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Platelet reactivity in diabetic patients subjected to acute exercise stress test Platelet reactivity in diabetic patients subjected to acute exercise stress test](/preview/png/2837109.png)
BackgroundPrevious studies have reported ambiguous results regarding the effect of acute exercise on platelet reactivity in healthy and cardiac patients.ObjectivesWe aimed to assess platelet reactivity among diabetic patients before and immediately after an acute exercise stress test.MethodsPatients (controls: mean age 53.1±12.1 years; four males; body mass index 27.0±5.7 kg/m2; HbA1c 6.0±1.1%, n=8) and diabetic patients (52.9±11.3; six males; body mass index 30.7±2.2 kg/m2; HbA1c 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.ResultsAlthough 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%).ConclusionPlatelet stimulation in diabetic patients is blunted and might be explained by the prolonged exposure of platelets to multiple diabetic risk factors.
Journal: Cardiovascular Revascularization Medicine - Volume 12, Issue 1, January–February 2011, Pages 20–24