Left ventricular remodelling in mitral valve prolapse patients: implications of apical papillary muscle insertion.


Journal

European heart journal. Cardiovascular Imaging
ISSN: 2047-2412
Titre abrégé: Eur Heart J Cardiovasc Imaging
Pays: England
ID NLM: 101573788

Informations de publication

Date de publication:
20 09 2021
Historique:
received: 12 04 2021
accepted: 22 06 2021
pubmed: 20 7 2021
medline: 21 10 2021
entrez: 19 7 2021
Statut: ppublish

Résumé

Mitral valve prolapse (MVP) causes left ventricular (LV) remodelling even in the absence of significant mitral regurgitation. To evaluate whether apical insertion of the papillary muscle (PM) influences the pattern and severity of MVP-related LV remodelling. All MVP patients who underwent CMR at our institution between December 2008 and December 2019 were included, thoroughly reviewed and grouped according to apical/non-apical PM insertion. Apical PM insertion was found in 53/92 patients (58%) and associated with mitral leaflet thickening (P < 0.01) and a trend towards higher prevalence of mitral annular disjunction (P = 0.05). Whereas no differences in ventricular volumes or ejection fraction were found, patients with apical PM insertion showed more lateral wall remodelling with mid lateral wall thinning [2.1 (1.8-2.5) vs. 4.0 (3.5-5.0) mm, P < 0.01], increased LV eccentricity and a lower GCS at this level (15 ± 3% vs. 20 ± 3%, P < 0.01). In long-axis direction, increased end-diastolic mid lateral wall angulation was found (i.e. angle <155° measured in the thinnest point of the mid lateral wall in four-chamber view) with a higher angle variation during systole (25 ± 11° vs. 17 ± 8°, P < 0.01). Remarkably, PM fibrosis was significantly more frequent in patients with apical PM insertion (i.e. 66% vs. 28%, P < 0.01). Finally, a higher burden of premature ventricular complexes (>5%) and non-sustained ventricular tachyarrhythmias was found in patients with apical PM insertion: 53% vs. 25% (P = 0.04) and 38% vs. 18% (P = 0.04), respectively. Apical PM insertion is part of the phenotypic spectrum of MVP, impacts significantly LV remodelling, and potentially may be related to increased ventricular arrhythmogenicity.

Identifiants

pubmed: 34279022
pii: 6323678
doi: 10.1093/ehjci/jeab134
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1119-1128

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions, please email: journals.permissions@oup.com.

Auteurs

Sara Moura-Ferreira (S)

Department of Imaging and Pathology, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
Department of Radiology, University Hospitals Leuven, Leuven, Belgium.

Bert Vandenberk (B)

Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.
Department of Cardiovascular Diseases, University Hospitals Leuven, Leuven, Belgium.

Pier Giorgio Masci (PG)

School of Biomedical Engineering and Imaging Sciences, King's College London, St Thomas Hospital, London, UK.

Tom Dresselaers (T)

Department of Imaging and Pathology, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
Department of Radiology, University Hospitals Leuven, Leuven, Belgium.

Christophe Garweg (C)

Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.
Department of Cardiovascular Diseases, University Hospitals Leuven, Leuven, Belgium.

Rolf Symons (R)

Department of Imaging and Pathology, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
Department of Radiology, University Hospitals Leuven, Leuven, Belgium.

Rik Willems (R)

Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.
Department of Cardiovascular Diseases, University Hospitals Leuven, Leuven, Belgium.

Jan Bogaert (J)

Department of Imaging and Pathology, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
Department of Radiology, University Hospitals Leuven, Leuven, Belgium.

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