Phenotype and Clinical Outcomes in Desmin-Related Arrhythmogenic Cardiomyopathy.

arrhythmogenic cardiomyopathy desmin desminopathy genetics

Journal

JACC. Clinical electrophysiology
ISSN: 2405-5018
Titre abrégé: JACC Clin Electrophysiol
Pays: United States
ID NLM: 101656995

Informations de publication

Date de publication:
23 Apr 2024
Historique:
received: 02 11 2023
revised: 22 02 2024
accepted: 27 02 2024
medline: 10 5 2024
pubmed: 10 5 2024
entrez: 10 5 2024
Statut: aheadofprint

Résumé

Desmin (DES) pathogenic variants cause a small proportion of arrhythmogenic cardiomyopathy (ACM). Outcomes data on DES-related ACM are scarce. This study sought to provide information on the clinical phenotype and outcomes of patients with ACM caused by pathogenic variants of the DES gene in a multicenter cohort. We collected phenotypic and outcomes data from 16 families with DES-related ACM from 10 European centers. We assessed in vitro DES aggregates. Major cardiac events were compared to historical controls with lamin A/C truncating variant (LMNA-tv) and filament C truncating variant (FLNC-tv) ACM. Of 82 patients (54% males, median age: 36 years), 11 experienced sudden cardiac death (SCD) (n = 7) or heart failure death (HFd)/heart transplantation (HTx) (n = 4) before clinical evaluation. Among 68 survivors, 59 (86%) presented signs of cardiomyopathy, with left ventricular (LV) dominant (50%) or biventricular (34%) disease. Mean LV ejection fraction was 51% ± 13%; 36 of 53 had late gadolinium enhancement (ring-like pattern in 49%). During a median of 6.73 years (Q1-Q3: 3.55-9.52 years), the composite endpoint (sustained ventricular tachycardia, aborted SCD, implantable cardioverter-defibrillator therapy, SCD, HFd, and HTx) was achieved in 15 additional patients with HFd/HTx (n = 5) and SCD/aborted SCD/implantable cardioverter-defibrillator therapy/sustained ventricular tachycardia (n = 10). Male sex (P = 0.004), nonsustained ventricular tachycardia (P = 0.017) and LV ejection fraction ≤50% (P = 0.012) were associated with the composite endpoint. Males with DES variants had similar outcomes to historical FLNC-tv and LMNA-tv controls. However, females showed better outcomes than those with LMNA-tv. In vitro experiments showed the characteristic finding of DES aggregates in 7 of 12 variants. DES ACM is associated with poor outcomes which can be predicted with potentially successful treatments, underscoring the importance of familial evaluation and genetic studies to identify at risk individuals.

Sections du résumé

BACKGROUND BACKGROUND
Desmin (DES) pathogenic variants cause a small proportion of arrhythmogenic cardiomyopathy (ACM). Outcomes data on DES-related ACM are scarce.
OBJECTIVES OBJECTIVE
This study sought to provide information on the clinical phenotype and outcomes of patients with ACM caused by pathogenic variants of the DES gene in a multicenter cohort.
METHODS METHODS
We collected phenotypic and outcomes data from 16 families with DES-related ACM from 10 European centers. We assessed in vitro DES aggregates. Major cardiac events were compared to historical controls with lamin A/C truncating variant (LMNA-tv) and filament C truncating variant (FLNC-tv) ACM.
RESULTS RESULTS
Of 82 patients (54% males, median age: 36 years), 11 experienced sudden cardiac death (SCD) (n = 7) or heart failure death (HFd)/heart transplantation (HTx) (n = 4) before clinical evaluation. Among 68 survivors, 59 (86%) presented signs of cardiomyopathy, with left ventricular (LV) dominant (50%) or biventricular (34%) disease. Mean LV ejection fraction was 51% ± 13%; 36 of 53 had late gadolinium enhancement (ring-like pattern in 49%). During a median of 6.73 years (Q1-Q3: 3.55-9.52 years), the composite endpoint (sustained ventricular tachycardia, aborted SCD, implantable cardioverter-defibrillator therapy, SCD, HFd, and HTx) was achieved in 15 additional patients with HFd/HTx (n = 5) and SCD/aborted SCD/implantable cardioverter-defibrillator therapy/sustained ventricular tachycardia (n = 10). Male sex (P = 0.004), nonsustained ventricular tachycardia (P = 0.017) and LV ejection fraction ≤50% (P = 0.012) were associated with the composite endpoint. Males with DES variants had similar outcomes to historical FLNC-tv and LMNA-tv controls. However, females showed better outcomes than those with LMNA-tv. In vitro experiments showed the characteristic finding of DES aggregates in 7 of 12 variants.
CONCLUSIONS CONCLUSIONS
DES ACM is associated with poor outcomes which can be predicted with potentially successful treatments, underscoring the importance of familial evaluation and genetic studies to identify at risk individuals.

Identifiants

pubmed: 38727660
pii: S2405-500X(24)00177-4
doi: 10.1016/j.jacep.2024.02.031
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures Dr Bermudez-Jimenez has received grants from Instituto de Salud Carlos III (ISCIII) through the project JR21/00031 (cofounded by European Regional Development Fund). Dr Zorio has received grants from the Instituto de Salud Carlos III through the projects PI18/01582 and PI21/01282 (co-funded by European Regional Development Fund “A way to make Europe”). Dr Brodehl has received grants from the Medical Faculty of the Ruhr-University Bochum (FoRUM, F1074-2023) and the ‘Deutsche Herzstiftung e.V. (Frankfurt a.M., Germany); and is a shareholder with Tenaya Therapeutics. Dr Lopes has received grants from a Medical Research Council (MRC) Clinical Academic Research Partnership (CARP) award (MR/T005181/1). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Francisco J Bermudez-Jimenez (FJ)

Department of Cardiology, Virgen de las Nieves University Hospital, Granada, Spain; Instituto de Investigación Biosanitaria. ibs.GRANADA, Granada, Spain.

Alexandros Protonotarios (A)

Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, London, United Kingdom; Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London, United Kingdom.

Soledad García-Hernández (S)

Instituto de Investigación Biomédica de A Coruña (INIBIC, CIBERCV), A Coruña, Spain; Health in Code SL, Cardiología, A Coruña, Spain.

Ana Pérez Asensio (A)

Department of Cardiology, Puerta del Mar University Hospital, Cádiz, Spain; Biomedical Research and Innovation Institute of Cadiz (INiBICA), Cádiz, Spain.

Alessandra Rampazzo (A)

Departments of Biology and Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.

Esther Zorio (E)

Inherited Cardiac Diseases Unit, Cardiology Department at Hospital Universitario y Politécnico La Fe and Research Group on Inherited Heart Diseases, Sudden Death and Mechanisms of Disease (CaFaMuSMe), Barcelona, Spain; Instituto de Investigación Sanitaria La Fe, Valencia, Spain; Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.

Andreas Brodehl (A)

Erich and Hanna Klessmann Institute for Cardiovascular Research & Development, Heart and Diabetes Centre NRW, Ruhr-University Bochum, Bad Oeynhausen, Germany.

Miguel A Arias (MA)

Arrhythmia Unit, Hospital Universitario de Toledo, Toledo, Spain.

Rosa Macías-Ruiz (R)

Department of Cardiology, Virgen de las Nieves University Hospital, Granada, Spain; Instituto de Investigación Biosanitaria. ibs.GRANADA, Granada, Spain.

Juan Fernández-Armenta (J)

Department of Cardiology, Puerta del Mar University Hospital, Cádiz, Spain; Biomedical Research and Innovation Institute of Cadiz (INiBICA), Cádiz, Spain.

Paloma Remior Perez (P)

Centro de Investigación Biomédica en Red en Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain; Inherited Cardiac Disease Unit, Hospital Universitario Virgen Arrixaca, Murcia, Spain.

Carmen Muñoz-Esparza (C)

Inherited Cardiac Disease Unit, Hospital Universitario Virgen Arrixaca, Murcia, Spain.

Kalliopi Pilichou (K)

Departments of Biology and Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.

Barbara Bauce (B)

Departments of Biology and Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.

Jose L Merino (JL)

Viamed Santa Elena and La Paz University Hospitals, Idipaz, Madrid, Spain.

Carlos Moliner-Abós (C)

Cardiology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain; IIB-SantPau, CIBERCV, Universidad Autónoma de Barcelona, Barcelona, Spain.

Juan P Ochoa (JP)

Instituto de Investigación Biomédica de A Coruña (INIBIC, CIBERCV), A Coruña, Spain; Health in Code SL, Cardiología, A Coruña, Spain.

Roberto Barriales-Villa (R)

Instituto de Investigación Biomédica de A Coruña (INIBIC, CIBERCV), A Coruña, Spain; Department of Cardiology, Complexo Hospitalario Universitario A Coruña, Spain.

Pablo Garcia-Pavia (P)

Heart Failure and Inherited Cardiac Diseases Unit, Department of Cardiology, Hospital Universitario Puerta de Hierro, Madrid, Spain; Inherited Cardiac Disease Unit, Hospital Universitario Virgen Arrixaca, Murcia, Spain; Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.

Luis R Lopes (LR)

Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, London, United Kingdom; Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London, United Kingdom.

Petros Syrris (P)

Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London, United Kingdom.

Domenico Corrado (D)

Departments of Biology and Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.

Perry M Elliott (PM)

Inherited Cardiovascular Diseases Unit, St Bartholomew's Hospital, London, United Kingdom; Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London, United Kingdom.

William J McKenna (WJ)

Centre for Heart Muscle Disease, Institute of Cardiovascular Science, University College London, London, United Kingdom; Instituto de Investigación Biomédica de A Coruña (INIBIC, CIBERCV), A Coruña, Spain.

Juan Jimenez-Jaimez (J)

Department of Cardiology, Virgen de las Nieves University Hospital, Granada, Spain; Instituto de Investigación Biosanitaria. ibs.GRANADA, Granada, Spain. Electronic address: jimenez.jaimez@gmail.com.

Classifications MeSH