Clinical and Hemodynamic Outcomes of Balloon-Expandable Mitral Valve-in-Valve Positioning and Asymmetric Deployment: The VIVID Registry.

Background: Mitral valve-in-valve (ViV) is associated with suboptimal hemodynamics and rare left ventricular outflow tract (LVOT) obstruction.
Objectives: This study aimed to determine whether device position and asymmetry are associated with these outcomes.
Methods: Patients undergoing SAPIEN 3 (Edwards Lifesciences) mitral ViV included in the VIVID (Valve-in-Valve International Data) Registry were studied. Clinical endpoints are reported according to Mitral Valve Academic Research Consortium definitions. Residual mitral valve stenosis was defined as mean gradient ≥5 mm Hg. Depth of implantation (percentage of transcatheter heart valve [THV] atrial to the bioprosthesis ring) and asymmetry (ratio of 2 measures of THV height) were evaluated.
Results: A total of 222 patients meeting the criteria for optimal core lab evaluation were studied (age 74 ± 11.6 years; 61.9% female; STS score = 8.3 ± 7.1). Mean asymmetry was 6.2% ± 4.4%. Mean depth of implantation was 19.0% ± 10.3% atrial. Residual stenosis was common (50%; mean gradient 5.0 ± 2.6 mm Hg). LVOT obstruction occurred in 7 cases (3.2%). Implantation depth was not a predictor of residual stenosis (OR: 1.19 [95% CI: 0.92-1.55]; P = 0.184), but more atrial implantation was protective against LVOT obstruction (0.7% vs 7.1%; P = 0.009; per 10% atrial, OR: 0.48 [95% CI: 0.24-0.98]; P = 0.044). Asymmetry was found to be an independent predictor of residual stenosis (per 10% increase, OR: 2.30 [95% CI: 1.10-4.82]; P = 0.027).
Conclusions: Valve stenosis is common after mitral ViV. Asymmetry was associated with residual stenosis. Depth of implantation on its own was not associated with residual stenosis but was associated with LVOT obstruction. Technical considerations to reduce postdeployment THV asymmetry should be considered.
Competing Interests: Funding Support and Author Disclosures Dr Whisenant is a consultant for Edwards Lifesciences. Dr Unbehaun is a proctor for Edwards Lifesciences. Dr Erlebach has received speaker honoraria from Medtronic and Abbott; and is a proctor for Abbott. Dr Guerrero has received institutional research grant support from Edwards Lifesciences. Dr Bruschi is a consultant for Abbott. Dr Rudolph has received speaker honoraria from Edwards Lifesciences; and is a proctor for Edwards Lifesciences. Dr Andreas is a consultant for Edwards Lifesciences, Abbott, Medtronic, Boston Scientific, Zoll, and AbbVie; and has received institutional research grants from Edwards Lifesciences, Abbott, Medtronic, and LSI. Dr Dvir is a consultant for Edwards Lifesciences. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)