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Review
. 2025 Jul;14(13):e041505.
doi: 10.1161/JAHA.125.041505. Epub 2025 Jun 18.

Transcatheter Aortic Valve Durability: Focus on Structural Valve Deterioration

Affiliations
Review

Transcatheter Aortic Valve Durability: Focus on Structural Valve Deterioration

Antonin Trimaille et al. J Am Heart Assoc. 2025 Jul.

Abstract

Transcatheter aortic valve replacement has emerged as a valuable alternative to surgical aortic valve replacement in patients with severe aortic stenosis. Given the expansion of transcatheter aortic valve replacement to lower-risk and younger populations with longer life expectancy, the durability of transcatheter heart valves (THVs) has become an important issue that may impact cardiovascular outcomes. THVs share similarities with surgical valves but have unique features, including a trend to larger effective orifice area and less prosthesis-patient mismatch, interactions with the native valve, and crimping process, that may all potentially influence a THV's life span. Multiple mechanisms may lead to bioprosthetic valve dysfunction, including structural valve deterioration, thrombosis, endocarditis, and nonstructural valve deterioration. With an incidence of up to 12.3% 5 years after transcatheter aortic valve replacement, structural valve deterioration represents the ultimate consequence of fibrotic remodeling and calcification within the bioprosthesis, driven by thrombotic and inflammatory processes involving the native aortic valve and influenced by patient and procedural factors. Understanding these mechanisms is crucial for improving THV durability.

Keywords: bioprosthetic valve failure; durability; structural valve deterioration; transcatheter aortic valve replacement; transcatheter heart valve.

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Conflict of interest statement

A.T. has received a fellowship grant from Edwards Lifesciences. S.K. has received a grant from the Japan Heart Foundation/Bayer Yakuhin Research Grant Abroad. K.M. received a grant from Edwards Lifesciences (THV‐F20–142). V.S.K. has received research grants from Boehringer‐Ingelheim, Nugerontix, and Servier. J.R.C. has received institutional grants and consultant/speaker fees from Edwards Lifesciences and Medtronic. O.M. declared grants from AstraZeneca, Medtronic, and Boehringer Ingelheim. The other authors declare that they have no competing interest relevant to the manuscript.

Figures

Figure 1
Figure 1. Summary of the main definition of structural valve deterioration.
AR indicates aortic regurgitation; BVF, bioprosthetic valve failure; EOA, effective orifice area; HALT, hypoattenuated leaflet thickening; LV, left ventricular; RLM, reduced leaflet motion; and SVD, structural valve deterioration.
Figure 2
Figure 2. Pathomechanisms involved in structural valve deterioration after transcatheter aortic valve replacement.
MDCT indicates multidetector computed tomography; SLT, subclinical leaflet thrombosis; SVD, structural valve deterioration; TAVR, transcatheter aortic valve replacement; and THV, transcatheter heart valve.
Figure 3
Figure 3. Current guidelines on antithrombotic treatment after transcatheter aortic valve replacement (A) and in patients with subclinical leaflet thrombosis (B).
CT indicates computed tomography; DAPT, dual antiplatelet therapy; HALT, hypoattenuated leaflet thickening; INR, international normalized ratio; OAC, oral anticoagulant; PCI, percutaneous coronary intervention; RLM, reduced leaflet motion; SAPT, single antiplatelet therapy; SLT, subclinical leaflet thrombosis; TAVR, transcatheter aortic valve replacement; THV, transcatheter heart valve; and TTE, transthoracic echocardiography.
Figure 4
Figure 4. Diagnosis, exploration, and management of structural valve deterioration after TAVR.
BVD indicates bioprosthetic valve dysfunction; CABG, coronary artery bypass grafting; CT, computed tomography; MRI, magnetic resonance imaging; PCI, percutaneous coronary intervention; PET, positon emission tomography; TAVR, transcatheter aortic valve replacement; THV, transcatheter heart valve; and TTE, transthoracic echocardiography.

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