4.3 Article

Do statins influence platelet reactivity on acetylsalicylic acid therapy in patients with type 2 diabetes?

Journal

CARDIOLOGY JOURNAL
Volume 19, Issue 5, Pages 494-500

Publisher

VIA MEDICA
DOI: 10.5603/CJ.2012.0090

Keywords

acetylsalicylic acid; platelet reactivity; statins; tumor necrosis factor-alpha; coronary artery disease

Funding

  1. Polish Pharmaceutical Company ADAMED for a Young Scientist Award [1WR DAR1/2007]

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Background: Type 2 diabetes (T2DM) patients are at increased risk of cardiovascular events despite long-term acetylsalicylic acid (ASA) therapy. This study was performed to establish the prevalence of high platelet reactivity (HPR) on ASA in T2DM and to identify its predictors. Methods: The study included 185 T2DM on chronic ASA therapy and to assess platelet reactivity during long-term ASA therapy, we applied the point-of-care method VerifyNow (R) aspirin test (Accumetrics, San Diego, CA, USA). Results: Compared with the low platelet reactivity (LPR) group, patients with HPR had higher triglyceride levels (145 vs. 118 mg/dL, p = 0.041), were less frequently treated with statins (57.1% vs. 75.3%;p = 0.038) and tumor necrosis factor-alpha (TNF-alpha) concentrations were higher (2.15 vs. 1.74 pg/mL; p = 0.052). In a multivariate analysis only statin therapy (OR 0.375; 95% CI 0.15-0.91; p = 0.030) and lower concentrations of TNF-alpha (for each 1.0 pg/mL: OR 1.3; 95% CI 1.00-1.72; p = 0.046) were predictive of LPR. Conclusions: Our study provides indirect evidence that the beneficial effect of statins on platelet activity may be related to their non-lipid-mediated, pleiotropic mechanisms of action. This might have been partly related to decreased platelet reactivity in patients receiving statin therapy. In our study in patients with T2DM, platelet reactivity on ASA therapy measured with VerifyNow was associated with TNF-alpha concentrations and statin therapy. These results may imply a role for subclinical systemic inflammation and a beneficial effect of statins in the development of HPR in T2DM. (Cardiol J 2012; 19,5: 494-500)

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