Lack of oral anticoagulant therapy at discharge was an independent predictor of subclinical leaflet thrombosis after TAVR (HR 12.130; 95% CI 1.394-150.582; p=0.028).
Cohort (n=187)
Does oral anticoagulant therapy or platelet inhibition extent prevent subclinical leaflet thrombosis detected by MDCT after TAVR?
Oral anticoagulant therapy, but not the extent of platelet inhibition, is associated with a reduced risk of subclinical leaflet thrombosis after TAVR.
Hazard Ratio: 12.13 (95% CI 1.394–150.582)
p-value: p=0.028
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). We sought to investigate (i) the prevalence of HAM and HALT after TAVR detected by MDCT, (ii) the predictors of SLT, (iii) the impact of oral anticoagulant (OAC) and platelet inhibition extent assessed by platelet reactivity index vasodilator stimulated phosphoprotein (PRI-VASP) and closure time adenosine diphosphate (CT-ADP) on SLT. Of 187 consecutive patients who underwent TAVR from 1 August 2017 to 31 March 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. Eighty-five post-TAVR CTs out of 90 were ranked for clarity and assessed with sufficient diagnostic quality. HAM was evidenced in 13 patients (15.3%) and HALT in 30 patients (35%). Procedural characteristics, including aortic valve calcium score, annulus size, or procedural heparin regimens, were equivalent between groups. Likewise, no impact of P2Y12 inhibition (PRI-VASP) nor primary haemostasis disorders (CT-ADP) on SLT could be evidenced. No impact of SLT on valve deterioration evaluated by transthoracic 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 the sole independent predictors of SLT. In four patients with HAM, MDCT follow-up was obtained after initiation of OAC therapy and showed a complete regression of HAM. SLT was evidenced in a sizeable proportion of patients treated by TAVR and was mainly determined by the lack of oral anticoagulant therapy. Conversely, no impact of platelet inhibition extent on SLT could be evidenced.
Jimenez et al. (Fri,) conducted a cohort in Subclinical leaflet thrombosis after TAVR (n=187). Lack of oral anticoagulant therapy vs. Oral anticoagulant therapy was evaluated on Subclinical leaflet thrombosis (SLT) (HR 12.130, 95% CI 1.394-150.582, p=0.028). Lack of oral anticoagulant therapy at discharge was an independent predictor of subclinical leaflet thrombosis after TAVR (HR 12.130; 95% CI 1.394-150.582; p=0.028).