Impact of platelet reactivity on subclinical valve thrombosis in patients treated with TAVR

Abstract

Abstract Background and introduction High residual platelet reactivity (HPR) in patients undergoing percutaneous coronary intervention with dual antiplatelet therapy (DAPT) is associated with an increased risk of thrombotic events. The relationship between HPR and the presence of subclinical valve thrombosis (SVT) following transcatheter aortic valve replacement (TAVR) is unknown. Purpose The aim of this study was to determine whether HPR is associated with the occurrence of SVT in patients undergoing TAVR treated with DAPT and to determine independent predictors of SVT. Methods This is a prospective, multicentre study. Patients with symptomatic aortic stenosis successfully treated with TAVR followed by DAPT (aspirin + clopidogrel) for 3 months were included. Patients with monotherapy, oral anticoagulation, or severe renal impairment were excluded. For the purpose of the study, platelet reactivity was measured either with Multiplate analyzer or VerifyNow point-of-care assay at baseline, at 1-2 days post, and 1-3 months post-TAVR. HPR was defined as ≥ 468AU, or ≥208PRU, respectively. The primary endpoint was the incidence of SVT measured by multi-slice CT at 3-months post TAVR in relation to HPR. Secondary objectives included the relationship between HPR following TAVR and the incidence of major adverse cardiac and cerebral clinical events (MACCE), to determine whether a pro-thrombotic inflammatory response is associated with the appearance of SVT and to evaluate factors associated with the occurrence of SVT. Results A total of 169 patients were included, the mean age was 81.5±5 and 51% were female. The overall rate of SVT was 22%. Patients with HPR demonstrated a similar incidence of SVT to those without (23,7% vs 33,6%: p=0,29). The overall bleeding rate was 4,9%. No differences in the rate of stroke at 1-year follow-up were observed (no SVT group 1.5% vs SVT group 2.6%: p=0.6). Independent predictors of SVT, were: dyslipemia OR 0,38 (0,15-0,96) p=0,039, creatinine clearance 0.98 (0.96.1.0, p=0.04), self-expandable valve OR 3,57 (1,40-9,06); p=0,006 and prosthesis size 0,78 (0,64-0,96): p=0,009. Patients with SVT expressed increased inflammatory parameters at 6 months compared to those without SVT CD14+ CD16-: 76,6±9,9 vs 70,7±13,9: p=0.02. Conclusion In contrast to coronary interventions, for the first time we have demonstrated that HPR does not appear to be associated with the development of SVT in TAVR patients treated with DAPT.