Leaflet Thrombosis in Surgically Explanted or Post-Mortem TAVR Valves

Mangione, Fernanda Marinho; Jatene, Tannas; Gonçalves, Alexandra; Fishbein, Gregory A.; Mitchell, Richard N.; Pelletier, Marc; Kaneko, Tsuyoshi; Shah, Pinak; Nyman, Charles; Shook, Douglas C.; Blankstein, Ron; Padera, Robert F.; Bhatt, Deepak L.

doi:10.1016/j.jcmg.2016.11.009

Cited by 44 publications

(22 citation statements)

References 1 publication

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“…As pointed at by Midha et al [17] supra-annular position of the neosinus may reduce thrombotic potential owing to the reduction of blood stasis. Another important factor relies on the under expansion of the prosthesis as underlined in Sapiens 3 valves or in autopsy studies [18]. Moreover, the possible contribution of valve injury mediated by balloon valvuloplasty or inflammatory response in thrombosis onset remains to be determined [19].…”

Section: Discussionmentioning

confidence: 99%

Impact of Antithrombotic Regimen and Platelet Inhibition Extent on Leaflet Thrombosis Detected by Cardiac MDCT after Transcatheter Aortic Valve Replacement

Jimenez

Ohana

Marchandot

et al. 2019

JCM

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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.

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Section: Discussionmentioning

confidence: 99%

Impact of Antithrombotic Regimen and Platelet Inhibition Extent on Leaflet Thrombosis Detected by Cardiac MDCT after Transcatheter Aortic Valve Replacement

Jimenez

Ohana

Marchandot

et al. 2019

JCM

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“…One report suggested the possibility of association of hypersensitive reaction to metal 19. The following patients are also reported to be likely to have thrombosis: patients with large valves,2 4 patients with an ejection fraction of 35% or lower,7 patients with a valve-in-valve placement,17 20 males,4 patients with a large sinus of Valsalva,4 patients not receiving anticoagulants2 and patients in whom incomplete or asymmetrical expansion occurred 20. These facts suggest the involvement of blood flow stagnation near the valve, regional low flow rates and other factors important for thrombus formation, but these have not definitively been established as risk factors.…”

Section: Why Does Subclinical Leaflet Thrombosis Occur?mentioning

confidence: 99%

Subclinical leaflet thrombosis after transcatheter aortic valve implantation

Nakatani

2017

Heart

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Although clinically significant valve thrombosis after transcatheter aortic valve implantation (TAVI) is rare, the incidence of subclinical leaflet thrombosis has been reported to be up to about 10%-15%. It is mostly found 1-3 months after procedure in any type of transcatheter heart valve. Leaflet thrombosis is detected by high-resolution CT in the form of limited valve opening/closure and hypoattenuated leaflet thickening. Transthoracic or transesophageal echocardiography is capable of detecting limitations of valve motion, leaflet thickening, increased flow velocity across the valve. However, CT seems to be more sensitive than echocardiography to detect leaflet thrombosis. It can occur under dual antiplatelet therapy with aspirin and a thienopyridine but rarely occurs with anticoagulation with a vitamin K antagonist. A vitamin K antagonist is also helpful to resolve leaflet thrombosis. Several studies are ongoing to determine the effect of new oral anticoagulants (NOACs) in preventing major cardiovascular events. They will also provide useful information on whether NOACs prevent leaflet thrombosis.

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“…Transcatheter aortic valve implantation (TAVI) is a minimally invasive intervention whereby a bioprosthetic valve mounted on a stent is delivered and deployed on a stenotic valve. Although TAVI has recently been approved for low-surgical risk patients [1], its wide use is still constrained by the increasing evidence of subclinical leaflet thrombosis post-TAVI [2][3][4]. Subclinical leaflet thrombosis has been suggested as the underlying reason for hypoattenuated leaflet thickening (HALT) [5], leading to a reduced leaflet motion [2].…”

Section: Introductionmentioning

confidence: 99%

Numerical models for assessing the risk of leaflet thrombosis post-transcatheter aortic valve-in-valve implantation

Mayo

Yaakobovich

Finkelstein³

et al. 2020

R. Soc. open sci.

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Leaflet thrombosis has been suggested as the reason for the reduced leaflet motion in cases of hypoattenuated leaflet thickening of bioprosthetic aortic valves. This work aimed to estimate the risk of leaflet thrombosis in two post-valve-in-valve (ViV) configurations, using five different numerical approaches. Realistic ViV configurations were calculated by modelling the deployments of the latest version of transcatheter aortic valve devices (Medtronic Evolut PRO, Edwards SAPIEN 3) in the surgical Sorin Mitroflow. Computational fluid dynamics simulations of blood flow followed the dry models. Lagrangian and Eulerian measures of near-wall stagnation were implemented by particle and concentration tracking, respectively, to estimate the thrombogenicity and to predict the risk locations. Most of the numerical approaches indicate a higher leaflet thrombosis risk in the Edwards SAPIEN 3 device because of its intra-annular implantation. The Eulerian approaches estimated high-risk locations in agreement with the wall sheer stress (WSS) separation points. On the other hand, the Lagrangian approaches predicted high-risk locations at the proximal regions of the leaflets matching the low WSS magnitude regions of both transcatheter aortic valve implantation models and reported clinical and experimental data. The proposed methods can help optimizing future designs of transcatheter aortic valves with minimal thrombotic risks.

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Leaflet Thrombosis in Surgically Explanted or Post-Mortem TAVR Valves

Cited by 44 publications

References 1 publication

Impact of Antithrombotic Regimen and Platelet Inhibition Extent on Leaflet Thrombosis Detected by Cardiac MDCT after Transcatheter Aortic Valve Replacement

Impact of Antithrombotic Regimen and Platelet Inhibition Extent on Leaflet Thrombosis Detected by Cardiac MDCT after Transcatheter Aortic Valve Replacement

Subclinical leaflet thrombosis after transcatheter aortic valve implantation

Numerical models for assessing the risk of leaflet thrombosis post-transcatheter aortic valve-in-valve implantation

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