Presence of contractile impairment appears crucial for structural remodeling in idiopathic left bundle-branch block.


Journal

Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance
ISSN: 1532-429X
Titre abrégé: J Cardiovasc Magn Reson
Pays: England
ID NLM: 9815616

Informations de publication

Date de publication:
01 04 2021
Historique:
received: 26 07 2020
accepted: 08 02 2021
entrez: 1 4 2021
pubmed: 2 4 2021
medline: 17 8 2021
Statut: epublish

Résumé

To differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB). We hypothesize, that functional asynchrony with septal flash volume effects alone might not entirely explain the degree of functional impairment. Hence, we suggest the presence of a superimposed contractile cardiomyopathy. In this retrospective study, 53 patients with idiopathic LBBB were identified and matched to controls with and without cardiovascular risk factors. Cardiovascular magnetic resonance (CMR) was used to evaluate cardiac function, volumes and myocardial fibrosis using native T1 mapping and late gadolinium enhancement (LGE). Septal flash volume was assessed by CMR volumetric measurements and allowed to stratify patients with systolic dysfunction solely due to isolated ventricular asynchrony or superimposed contractile impairment. Reduced systolic LV-function, increased LV-volumes and septal myocardial fibrosis were found in patients with idiopathic LBBB compared to healthy controls. LV-volumes increased and systolic LV-function declined with prolonged QRS duration. Fibrosis was typically located at the right ventricular insertion points. Subgroups with superimposed contractile impairment appeared with pronounced LV dilation and increased fibrotic remodeling compared to individuals with isolated ventricular asynchrony. The presence of superimposed contractile impairment in idiopathic LBBB is crucial to identify patients with enhanced structural remodeling. This finding suggests an underlying cardiomyopathy. Future studies are needed to assess a possible prognostic impact of this entity and the development of heart failure. This study was retrospectively registered.

Sections du résumé

BACKGROUND
To differentiate effects of ventricular asynchrony from an underlying hypocontractile cardiomyopathy this study aimed to enhance the understanding of functional impairment and structural remodeling in idiopathic left bundle-branch block (LBBB). We hypothesize, that functional asynchrony with septal flash volume effects alone might not entirely explain the degree of functional impairment. Hence, we suggest the presence of a superimposed contractile cardiomyopathy.
METHODS
In this retrospective study, 53 patients with idiopathic LBBB were identified and matched to controls with and without cardiovascular risk factors. Cardiovascular magnetic resonance (CMR) was used to evaluate cardiac function, volumes and myocardial fibrosis using native T1 mapping and late gadolinium enhancement (LGE). Septal flash volume was assessed by CMR volumetric measurements and allowed to stratify patients with systolic dysfunction solely due to isolated ventricular asynchrony or superimposed contractile impairment.
RESULTS
Reduced systolic LV-function, increased LV-volumes and septal myocardial fibrosis were found in patients with idiopathic LBBB compared to healthy controls. LV-volumes increased and systolic LV-function declined with prolonged QRS duration. Fibrosis was typically located at the right ventricular insertion points. Subgroups with superimposed contractile impairment appeared with pronounced LV dilation and increased fibrotic remodeling compared to individuals with isolated ventricular asynchrony.
CONCLUSIONS
The presence of superimposed contractile impairment in idiopathic LBBB is crucial to identify patients with enhanced structural remodeling. This finding suggests an underlying cardiomyopathy. Future studies are needed to assess a possible prognostic impact of this entity and the development of heart failure.
TRIAL REGISTRATION
This study was retrospectively registered.

Identifiants

pubmed: 33789682
doi: 10.1186/s12968-021-00731-6
pii: 10.1186/s12968-021-00731-6
pmc: PMC8015193
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

39

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Auteurs

Janek Salatzki (J)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany. janek.salatzki@med.uni-heidelberg.de.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany. janek.salatzki@med.uni-heidelberg.de.

Theresa Fischer (T)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.

Johannes Riffel (J)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Florian André (F)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Kristóf Hirschberg (K)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
Semmelweis University Heart and Vascular Center, Budapest, Hungary.

Andreas Ochs (A)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Hauke Hund (H)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.

Matthias Müller-Hennessen (M)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Evangelos Giannitsis (E)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Matthias G Friedrich (MG)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.
Division of Cardiology, Departments of Medicine and Diagnostic Radiology, Mc-Gill University Health Centre, Montreal, Canada.

Eberhard Scholz (E)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Norbert Frey (N)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Hugo A Katus (HA)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

Marco Ochs (M)

Department of Cardiology, Angiology and Pneumology, Heidelberg University Hospital, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany.
DZHK (German Centre for Cardiovascular Research), Partner site Heidelberg, Heidelberg, Germany.

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