Impact of anti-thrombotic regimen and platelet inhibition extent on leaflet thrombosis detected by cardiac MDCT after transcatheter aortic-valve replacement

Background The impact of antithrombotic regimen and platelet inhibition extent on subclinical leaflet thrombosis (SLT) detected by cardiac multidetector computed tomography (MDCT) after transcatheter aortic-valve replacement (TAVR) is not well established. Hypoattenuation affecting motion (HAM) has been proposed as a surrogate marker of SLT and is characterized by hypoattenuated leaflet thickening (HALT) and concomitant reduction in leaflet motion (RELM). Purpose We sought to investigate (i) the prevalence of HAM and HALT, (ii) the predictors of SLT, (iii) the impact of oral anticoagulant (OAC), platelet inhibition extent and primary haemostasis disorders on SLT. Methods Of 187 consecutive patients who underwent TAVR from August 1st 2017 to March 31th 2018, 90 of them had cardiac CT at relevant follow-up. Clinical, biological, echocardiographic, procedural characteristics and treatments were collected before, at discharge and 1 year after TAVR. P2Y12 platelet inhibition extent and primary haemostasis disorders were investigated using platelet PRI-VASP and CT-ADP point of care assays. Results Eighty five post-TAVR CTs out of 90 were ranked for clarity. HAM was evidenced in 13 patients (15%) and HALT in 30 patients (35%). No impact of P2Y12 inhibition nor primary haemostasis disorders on SLT could be evidenced. No impact of SLT on valve deterioration evaluated by transthorac echocardiography (TTE) and clinical events could be established at 12 months follow-up. By multivariate analysis, lack of oral anticoagulant therapy at discharge (HR 12.130 CI 95% [1.394–150.582]; P = 0.028) and higher haemoglobin levels were evidenced as independent predictors of SLT. In 4 patients with HAM, MDCT follow-up after initiation of OAC therapy showed a complete regression of HAM ( Fig. 1 ). Conclusion SLT was evidenced in a sizeable proportion of patients after TAVR and was mainly determined by the lack of oral anticoagulant therapy. No impact of platelet inhibition extent on SLT could be evidenced.