Change in mitral regurgitation severity impacts survival after transcatheter aortic valve replacement.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 11 2019
Historique:
received: 07 04 2019
revised: 20 06 2019
accepted: 23 07 2019
pubmed: 11 8 2019
medline: 26 5 2020
entrez: 11 8 2019
Statut: ppublish

Résumé

The impact of a change in mitral regurgitation (MR) following TAVR is unknown. We studied the impact of baseline MR and early post-procedural change in MR on survival following TAVR. The SWEDEHEART registry included all TAVRs performed in Sweden. Patients were dichotomized into no/mild and moderate/severe MR groups. Vital status, echocardiographic data at baseline and within 7 days after TAVR were analyzed. 1712 patients were included. 1404 (82%) had no/mild MR and 308 (18%) had moderate/severe MR. Baseline moderate/severe MR conferred a higher mortality rate at 5-year follow-up (adjusted HR 1.29, CI 1.01-1.65, p = 0.04). Using persistent ≤mild MR as the reference, when moderate/severe MR persisted or if MR worsened from ≤mild at baseline to moderate/severe after TAVR, higher 5-year mortality rates were seen (adjusted HR 1.66, CI 1.17-2.34, p = 0.04; adjusted HR 1.97, CI 1.29-3.00, p = 0.002, respectively). If baseline moderate/severe MR improved to ≤mild after TAVR no excess mortality was seen (HR 1.09, CI 0.75-1.58, p = 0.67). Paravalvular aortic regurgitation (PVL) was inversely associated with MR improvement after TAVR (OR 0.4, 95%: CI 0.17-0.94; p = 0.034). Atrial fibrillation (OR 2.1, 95% CI: 1.27-3.39, p = 0.004), self-expanding valve (OR 3.8, 95% CI: 2.08-7.14, p < 0.0001), and PVL (4.3, 95% CI 2.32-7.78. p < 0.0001) were associated with MR worsening. Moderate/severe baseline MR in patients undergoing TAVR is associated with a mortality increase during 5 years of follow-up. This risk is offset if MR improves to ≤mild, whereas worsening of MR after TAVR is associated with a 2-fold mortality increase.

Sections du résumé

BACKGROUND
The impact of a change in mitral regurgitation (MR) following TAVR is unknown. We studied the impact of baseline MR and early post-procedural change in MR on survival following TAVR.
METHODS
The SWEDEHEART registry included all TAVRs performed in Sweden. Patients were dichotomized into no/mild and moderate/severe MR groups. Vital status, echocardiographic data at baseline and within 7 days after TAVR were analyzed.
RESULTS
1712 patients were included. 1404 (82%) had no/mild MR and 308 (18%) had moderate/severe MR. Baseline moderate/severe MR conferred a higher mortality rate at 5-year follow-up (adjusted HR 1.29, CI 1.01-1.65, p = 0.04). Using persistent ≤mild MR as the reference, when moderate/severe MR persisted or if MR worsened from ≤mild at baseline to moderate/severe after TAVR, higher 5-year mortality rates were seen (adjusted HR 1.66, CI 1.17-2.34, p = 0.04; adjusted HR 1.97, CI 1.29-3.00, p = 0.002, respectively). If baseline moderate/severe MR improved to ≤mild after TAVR no excess mortality was seen (HR 1.09, CI 0.75-1.58, p = 0.67). Paravalvular aortic regurgitation (PVL) was inversely associated with MR improvement after TAVR (OR 0.4, 95%: CI 0.17-0.94; p = 0.034). Atrial fibrillation (OR 2.1, 95% CI: 1.27-3.39, p = 0.004), self-expanding valve (OR 3.8, 95% CI: 2.08-7.14, p < 0.0001), and PVL (4.3, 95% CI 2.32-7.78. p < 0.0001) were associated with MR worsening.
CONCLUSIONS
Moderate/severe baseline MR in patients undergoing TAVR is associated with a mortality increase during 5 years of follow-up. This risk is offset if MR improves to ≤mild, whereas worsening of MR after TAVR is associated with a 2-fold mortality increase.

Identifiants

pubmed: 31399298
pii: S0167-5273(19)31687-0
doi: 10.1016/j.ijcard.2019.07.075
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

32-36

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Kari Feldt (K)

Department of Medicine, Unit of Cardiology, Karolinska Institutet, Stockholm, Sweden; Heart and Vascular Theme, Department of Cardiology, Karolinska University Hospital, 171 76 Stockholm, Sweden. Electronic address: kari.feldt@ki.se.

Rodney De Palma (R)

Buckinghamshire NHS Trust, Buckinghamshire, United Kingdom; Department of Medicine, Unit of Cardiology, Karolinska Institutet, 171 76 Stockholm, Sweden.

Henrik Bjursten (H)

Lund University Hospital, Lund University, 222 42 Lund, Sweden.

Petur Petursson (P)

Sahlgrenska University Hospital, Dept. of Medicine, Gothenburg University, 413 45 Göteborg, Sweden.

Niels Erik Nielsen (NE)

Linkoping University Hospital, 581 85 Linköping, Sweden.

Thomas Kellerth (T)

Örebro University Hospital, 701 85 Orebro, Sweden.

Anders Jönsson (A)

University Hospital, 751 85 Uppsala, Sweden.

Johan Nilsson (J)

Umea University Hospital, Umea, Sweden.

Andreas Rück (A)

Department of Medicine, Unit of Cardiology, Karolinska Institutet, Stockholm, Sweden; Heart and Vascular Theme, Department of Cardiology, Karolinska University Hospital, 171 76 Stockholm, Sweden.

Magnus Settergren (M)

Department of Medicine, Unit of Cardiology, Karolinska Institutet, Stockholm, Sweden; Heart and Vascular Theme, Department of Cardiology, Karolinska University Hospital, 171 76 Stockholm, Sweden. Electronic address: magnus.settergren@ki.se.

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