Abstract
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, (ii) the predictors of SLT, (iii) the impact of oral anticoagulant (OAC), platelet inhibition extent and primary haemostasis disorders on SLT. 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. 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 ). 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.
Highlights
Transcatheter aortic valve replacement (TAVR) has become the standard of care in patients with severe symptomatic aortic valve stenosis and who are at intermediate or high surgical risk [1,2]
We sought to investigate (i) the prevalence of Hypoattenuation affecting motion (HAM) and hypoattenuation leaflet thickening (HALT) after TAVR detected by Multidetector computed tomography (MDCT), (ii) predictors of subclinical leaflet thrombosis (SLT), and (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
The salient results of the present study are (1) subclinical leaflet thrombosis is observed in a sizeable proportion of TAVR patients (15%) after a median follow-up of 114 (65–205) days; (2) lack of oral anticoagulant together with elevated Hb levels were evidenced as independent predictors of subclinical leaflet thrombosis; (3) occurrence of subclinical leaflet thrombosis was independent of the extent of platelet inhibition, as measured by the PRI-VASP or the computed tomography (CT)-ADP assay; (4) no impact of subclinical leaflet thrombosis on clinical events could be established
Summary
Transcatheter aortic valve replacement (TAVR) has become the standard of care in patients with severe symptomatic aortic valve stenosis and who are at intermediate or high surgical risk [1,2]. Early stent valve thrombosis after TAVR remains a rare complication, recent reports have emphasized that subclinical leaflet thrombosis (SLT) is detected in a sizeable proportion of patients (7–15%) with normal echocardiographic parameters. Current guidelines recommend the use of DAPT with aspirin and clopidogrel after TAVR to obviate the metallic stent mediated risk of thrombosis/embolization followed by long-term single antiplatelet therapy with aspirin alone. In the last two decades, several studies have emphasized that high platelet reactivity under P2Y12-inhibitors has been associated with increased risk of ischemic events including stent thrombosis and cerebrovascular events [7]. Patients with extremely low platelet reactivity were demonstrated to be at increased risk of bleeding without any further benefit in stent thrombosis [8]. We sought to investigate (i) the prevalence of HAM and HALT after TAVR detected by MDCT, (ii) predictors of SLT, and (iii) the impact of OAC and platelet inhibition extent assessed by platelet reactivity index vasodilator stimulated phosphoprotein (PRI-VASP) and closure time adenosine diphosphate (CT-ADP) on SLT
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