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Review
. 2023 May 29;13(11):1908.
doi: 10.3390/diagnostics13111908.

Imaging of Bioprosthetic Valve Dysfunction after Transcatheter Aortic Valve Implantation

Affiliations
Review

Imaging of Bioprosthetic Valve Dysfunction after Transcatheter Aortic Valve Implantation

Louhai Alwan et al. Diagnostics (Basel). .

Abstract

Transcatheter aortic valve implantation (TAVI) has become the standard of care in elderly high-risk patients with symptomatic severe aortic stenosis. Recently, TAVI has been increasingly performed in younger-, intermediate- and lower-risk populations, which underlines the need to investigate the long-term durability of bioprosthetic aortic valves. However, diagnosing bioprosthetic valve dysfunction after TAVI is challenging and only limited evidence-based criteria exist to guide therapy. Bioprosthetic valve dysfunction encompasses structural valve deterioration (SVD) resulting from degenerative changes in the valve structure and function, non-SVD resulting from intrinsic paravalvular regurgitation or patient-prosthesis mismatch, valve thrombosis, and infective endocarditis. Overlapping phenotypes, confluent pathologies, and their shared end-stage bioprosthetic valve failure complicate the differentiation of these entities. In this review, we focus on the contemporary and future roles, advantages, and limitations of imaging modalities such as echocardiography, cardiac computed tomography angiography, cardiac magnetic resonance imaging, and positron emission tomography to monitor the integrity of transcatheter heart valves.

Keywords: TAVI; bioprosthetic valve dysfunction; bioprosthetic valve failure; multimodality imaging; structural valve deterioration.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Multimodality imaging can be used to depict underlying causes (i.e., structural valve deterioration marked with red arrows on the left panel, non-structural valve deterioration, thrombus marked with yellow arrows, hypoattenuated leaflet thickening, pannus and infective endocarditis marked with red arrows on the right panel) of bioprosthetic valve dysfunction after TAVI. These changes may ultimately lead to bioprosthetic valve failure.
Figure 2
Figure 2
Demonstration of paravalvular leak (PVR) after TAVI by transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE).
Figure 3
Figure 3
Different clinical scenarios of suspected bioprosthesis dysfunction after TAVI. Adapted from Pibarot P. et al., 2019 [37]. Gd = gradient; DVI = Doppler velocity index; AT = acceleration time; AT/ET = quotient acceleration time on ejection time; EF = ejection fraction; FU = follow-up; VTI = velocity time integral. * Improper high LVOT VTI (septum bulge, measurement done in the valve)/underestimation of TAVI gradient due to improper CW–Doppler placement. ** Improper low LVOT VTI (measurement done in LV/big LVOT).
Figure 4
Figure 4
In panel (AC), echocardiographic findings of leaflet thickening and thrombosis after TAVI 29 mm Edwards Sapien are depicted. Panel (DF) shows hypoattenuated leaflet thickening (HALT) and valve thrombosis (asterisk).
Figure 5
Figure 5
In panel (AC), transthoracic echocardiography images are depicted and show increased peak velocity, mean gradient, and acceleration time and reduced Doppler velocity index, without obvious leaflet thickening (due to impaired image quality, impaired echocardiographic window). Panel (D,E) shows hypoattenuated leaflet thickening (HALT) with impaired motion as the underlying cause of increased gradient on the TAVI bioprosthesis and is therefore considered subclinical leaflet thrombosis.

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