Abstract 17186: In Vivo Platelet Activation in Impaired Glucose Tolerance and During Progression of Type 2 Diabetes: a Cross-sectional and Longitudinal Study
Introduction: Impaired glucose tolerance (IGT) reflects the progression from normoglycemia to type 2 diabetes mellitus (DM). IGT and DM are associated with high cardiovascular disease (CVD) morbidity and mortality.
Hypothesis: Enhanced platelet activation has been previously reported in DM, but whether this pertains to IGT is unknown.
Methods: We investigated in vivo platelet activation, as reflected by the urinary excretion of 11-dehydro-TXB2 (TXM), in IGT and DM patients with a diagnosis documented either <12 months (new-DM) or ≥12 months (established-DM) from study entry. Patients were studied repeatedly up to 46 months to assess changes in platelet activation over time. Some patients were given standard 500 kcal meals at 8am, 1 and 6pm and TXM was measured repeatedly during a 12-hr period.
Results: We enrolled 49 IGT patients (19M, age 56±9 yrs), 59 new-DM (36M, 61±10 yrs) and 61 established-DM (34M, 62±7 yrs, DM duration 9.7±6.1 yrs) patients diagnosed according to the ADA criteria, not on antiplatelet drugs. Median TXM values at study entry were comparably enhanced in the 3 groups (1,189 [897-1,503], 1,277 [897-1,870], and 1,217 [885-1,494] pg/mg creatinine in IGT, new- and established-DM, respectively; p=0.39). Urinary TXM excretion showed limited intra-subject variability over time, as shown in the Figure. There was no convincing evidence of a circadian variation in TXM excretion. Two-hour, post-meal glucose variations (8-10am or 1-3pm) did not affect subsequent TXM values.
Conclusions: We conclude that the potential benefits and risks of antiplatelet therapy should be considered in IGT management, because persistent platelet activation might contribute to CVD progression and its thrombotic complications. Given the stability of high TXM excretion in DM, this non-invasive biomarker of platelet activation should be tested as a predictor of vascular events during long-term follow-up.
Author Disclosures: F. Ciaffardini: None. G. Davì: None. P. Di Fulvio: None. G. Formoso: None. R. Liani: None. F. Pagliaccia: None. C. Patrono: Other Research Support; Modest; Institutional grant for investigator-initiated research from Bayer. Speakers Bureau; Modest; Speaker fees from Bayer, Eli Lilly and Merck. Consultant/Advisory Board; Modest; Consultant fees from Bayer, Eli Lilly and Merck. G. Petrucci: None. D. Pitocco: None. B. Rocca: None. F. Santilli: None. P. Simeone: None. L. Tanese: None. R. Tripaldi: None. N. Vazzana: None. F. Zaccardi: None.
- © 2014 by American Heart Association, Inc.