Why the study?
The prothrombotic state in AF is related to endothelial injury, platelet activation, and the coagulation cascade, but the effects of dabigatran on endothelial- and platelet-derived microparticles required evaluation.
Does dabigatran treatment affect the levels of platelet- and endothelial-derived microparticles in patients with non-valvular atrial fibrillation?
Does dabigatran treatment affect the levels of platelet- and endothelial-derived microparticles in patients with non-valvular atrial fibrillation?
Low concentrations of dabigatran may be associated with platelet activation in patients with non-valvular atrial fibrillation, with coronary and peripheral artery disease exerting distinct effects.
Increased platelet microparticles after dabigatran in AF may signal persistent prothrombotic activity; leaves open clinical relevance and need for prospective validation.
The prothrombotic state in patients with atrial fibrillation (AF) is related to endothelial injury, the activation of platelets and the coagulation cascade. We evaluated the levels of platelet- (CD42b) and endothelial-derived (CD144) microparticles in the plasma patients with non-valvular AF treated with dabigatran at the time of expected minimum and maximum drug plasma concentrations. Following that, we determined the peak dabigatran plasma concentration (c peak ). CD42b increased after taking dabigatran (median [IQR] 36.7 [29.4-53.3] vs. 45.6 [32.3-59.5] cells/µL; p = 0.025). The concentration of dabigatran correlated negatively with the post-dabigatran change in CD42b (ΔCD42b, r = -0.47, p = 0.021). In the multivariate model, the independent predictors of ΔCD42b were: c peak (HR -0.55; with a 95% confidence interval, CI [-0.93, -0.16]; p = 0.007), coronary artery disease (CAD) (HR -0.41; 95% CI [-0.79, -0.02]; p = 0.037) and peripheral artery disease (PAD) (HR 0.42; 95% CI [0.07, 0.74]; p = 0.019). CD144 did not increase after dabigatran administration. These data suggest that low concentrations of dabigatran may be associated with platelet activation. PAD and CAD have distinct effects on CD42b levels during dabigatran treatment.
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Lenart-Migdalska et al. (2020) studied this question.
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