Correlation of Cardiovascular Risk Factors and Biomarkers With Platelet Reactivity in Coronary Artery Disease.

Abstract

Low response to aspirin, aspirin resistance, and high platelet reactivity on aspirin treatment are similar names for lack of response to block arachidonic acid-induced aggregation with aspirin therapy and have an important role in the evolution of coronary artery disease (CAD) with thromboembolic events. Was to evaluate the correlation between cardiovascular risk factors, biomarkers, and low response to aspirin in patients (pts) with CAD. Four hundred pts with CAD were divided into 8 groups of study, consistent with the type of CAD and low response to aspirin. Cardiovascular risk factors and biomarkers-including some of high platelet reactivity, endothelial dysfunction, hypercoagulability, and oxidative stress-were evaluated in correlation with low response to aspirin, defined as on treatment aspirin test (ASPItest) >30U by multiple electrode platelet aggregometry. In patients with CAD, low response to aspirin was significantly correlated with age older than 65 years, smoking, presence of diabetes mellitus, body mass index >25, hypertension, previous aspirin treatment, low response to clopidogrel, high mean platelets volume and von Willebrand factor activity, low flow-mediated vasodilation, and total antioxidant status (P < 0.01). In unstable angina patients, low response to aspirin was significantly correlated with male sex (P < 0.03). Incidence of other hypercoagulability biomarkers-S Protein, C Protein, Antithrombin III, and V Factor Leiden resistance to activated protein C-was low and not correlated with low response to aspirin. In CAD, low response to aspirin was significantly correlated with age older than 65 years, smoking, presence of diabetes mellitus, body mass index I >25, hypertension, previous aspirin treatment, and only in unstable angina with male sex. Low response to aspirin was also statistically associated with low response to clopidogrel, high mean platelets volume, high von Willebrand factor activity, low flow-mediated vasodilation, and low total antioxidant status values.