title: The effect of dabigatran and rivaroxaban on platelet reactivity and inflammatory markers.
abstract: The new oral anticoagulants (NOACs) reduce stroke and systemic embolism in patients with non-valvular atrial fibrillation (AF), but dabigatran may increase risk of coronary ischemic events for unclear reasons. Thus, this study assessed the effects of dabigatran and rivaroxaban on platelet reactivity and inflammatory markers in patients with non-valvular AF. Patients with non-valvular AF planned to begin treatment with NOACs were included. Seventeen patients were prescribed dabigatran and ten rivaroxaban. Platelet function (as assessed by multiple-electrode aggregometry, Impact-R shear-induced platelet deposition, P-selectin expression and plasma RANTES levels) and high-sensitivity C-reactive protein (hs-CRP) were measured at enrollment (prior to initiation of NOAC treatment) and at least 7 days into treatment with either dabigratran or rivaroxaban. Seventeen patients treated with dabigatran (mean age 69 ± 7 years, 35 % women, mean CHADS2 score 2.6 ± 1.2), and ten patients treated with rivaroxaban (mean age 73 ± 9 years, 20 % women, mean CHADS2 score 2.7 ± 1.6) completed the study. In both groups, there were no significant differences in platelet reactivity between the baseline and on-anticoagulant treatment time-points, as measured by each of the platelet-specific assays. There was a trend towards increased platelet reactivity in response to arachidonic acid from baseline to on-treatment in both groups, probably as a result of aspirin discontinuation in 33 % of patients. No significant differences were noted between baseline and on-treatment in hs-CRP in both anticoagulant groups. Treatment with dabigatran and rivaroxaban does not appear to be associated with changes in markers of platelet reactivity or systemic inflammation.
authors.affiliation: Department of Cardiology, Rabin Medical Center, Petah-Tikva, and the Sackler Faculty of Medicine, Tel-Aviv University, Tel Aviv, Israel.
authors.forename: Noa
authors.initials: N
authors.lastname: Zemer-Wassercug
authors.forename: Moti
authors.initials: M
authors.lastname: Haim
authors.forename: Dorit
authors.initials: D
authors.lastname: Leshem-Lev
authors.forename: Katia L
authors.initials: KL
authors.lastname: Orvin
authors.forename: Muthiah
authors.initials: M
authors.lastname: Vaduganathan
authors.forename: Ariel
authors.initials: A
authors.lastname: Gutstein
authors.forename: Ehud
authors.initials: E
authors.lastname: Kadmon
authors.forename: Aviv
authors.initials: A
authors.lastname: Mager
authors.forename: Ran
authors.initials: R
authors.lastname: Kornowski
authors.forename: Eli I
authors.initials: EI
authors.lastname: Lev
authors.forename: Eli L
authors.initials: EL
authors.lastname: Lev
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001281:Atrial Fibrillation / Q000097:blood / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000378:metabolism*; D002097:C-Reactive Protein / Q000378:metabolism; D018946:Chemokine CCL5 / Q000097:blood; D000069604:Dabigatran / Q000008:administration & dosage*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects*; D000069552:Rivaroxaban / Q000008:administration & dosage*
chemical_list: D015415:Biomarkers; C483024:CCL5 protein, human; D018946:Chemokine CCL5; D018836:Inflammation Mediators; D019007:P-Selectin; D002097:C-Reactive Protein; D000069552:Rivaroxaban; D000069604:Dabigatran