Is increased myocardial triglyceride content associated with early changes in left ventricular function? A


Journal

Frontiers in endocrinology
ISSN: 1664-2392
Titre abrégé: Front Endocrinol (Lausanne)
Pays: Switzerland
ID NLM: 101555782

Informations de publication

Date de publication:
2023
Historique:
received: 07 03 2023
accepted: 06 06 2023
medline: 11 7 2023
pubmed: 10 7 2023
entrez: 10 7 2023
Statut: epublish

Résumé

Type 2 diabetes (T2D) and obesity induce left ventricular (LV) dysfunction. The underlying pathophysiological mechanisms remain unclear, but myocardial triglyceride content (MTGC) could be involved. This study aimed to determine which clinical and biological factors are associated with increased MTGC and to establish whether MTGC is associated with early changes in LV function. A retrospective study was conducted using five previous prospective cohorts, leading to 338 subjects studied, including 208 well-phenotyped healthy volunteers and 130 subjects living with T2D and/or obesity. All the subjects underwent proton magnetic resonance spectroscopy and feature tracking cardiac magnetic resonance imaging to measure myocardial strain. MTGC content increased with age, body mass index (BMI), waist circumference, T2D, obesity, hypertension, and dyslipidemia, but the only independent correlate found in multivariate analysis was BMI (p=0.01; R²=0.20). MTGC was correlated to LV diastolic dysfunction, notably with the global peak early diastolic circumferential strain rate (r=-0.17, p=0.003), the global peak late diastolic circumferential strain rate (r=0.40, p<0.0001) and global peak late diastolic longitudinal strain rate (r=0.24, p<0.0001). MTGC was also correlated to systolic dysfunction Predicting MTGC remains a challenge in routine clinical practice, as only BMI independently correlates with increased MTGC. MTGC may play a role in LV dysfunction but does not appear to be involved in the development of subclinical strain abnormalities.

Sections du résumé

Background
Type 2 diabetes (T2D) and obesity induce left ventricular (LV) dysfunction. The underlying pathophysiological mechanisms remain unclear, but myocardial triglyceride content (MTGC) could be involved.
Objectives
This study aimed to determine which clinical and biological factors are associated with increased MTGC and to establish whether MTGC is associated with early changes in LV function.
Methods
A retrospective study was conducted using five previous prospective cohorts, leading to 338 subjects studied, including 208 well-phenotyped healthy volunteers and 130 subjects living with T2D and/or obesity. All the subjects underwent proton magnetic resonance spectroscopy and feature tracking cardiac magnetic resonance imaging to measure myocardial strain.
Results
MTGC content increased with age, body mass index (BMI), waist circumference, T2D, obesity, hypertension, and dyslipidemia, but the only independent correlate found in multivariate analysis was BMI (p=0.01; R²=0.20). MTGC was correlated to LV diastolic dysfunction, notably with the global peak early diastolic circumferential strain rate (r=-0.17, p=0.003), the global peak late diastolic circumferential strain rate (r=0.40, p<0.0001) and global peak late diastolic longitudinal strain rate (r=0.24, p<0.0001). MTGC was also correlated to systolic dysfunction
Conclusions
Predicting MTGC remains a challenge in routine clinical practice, as only BMI independently correlates with increased MTGC. MTGC may play a role in LV dysfunction but does not appear to be involved in the development of subclinical strain abnormalities.

Identifiants

pubmed: 37424866
doi: 10.3389/fendo.2023.1181452
pmc: PMC10323751
doi:

Substances chimiques

Triglycerides 0

Banques de données

ClinicalTrials.gov
['NCT01284816', 'NCT02042664', 'NCT03118336']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1181452

Informations de copyright

Copyright © 2023 Soghomonian, Dutour, Kachenoura, Thuny, Lasbleiz, Ancel, Cristofari, Jouve, Simeoni, Kober, Bernard and Gaborit.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Astrid Soghomonian (A)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Marseille, France.

Anne Dutour (A)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Marseille, France.

Nadjia Kachenoura (N)

Sorbonne Université, INSERM, CNRS, Laboratoire d'Imagerie Biomédicale, Paris, France.

Franck Thuny (F)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Intensive Care Unit, Department of Cardiology, Assistance Publique-Hôpitaux de Marseille, Hôpital Nord, Aix-Marseille University, Marseille, France.

Adele Lasbleiz (A)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Marseille, France.

Patricia Ancel (P)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.

Robin Cristofari (R)

Department of Biology, University of Turku, Turku, Finland.

Elisabeth Jouve (E)

UPCET, Clinical Pharmacology, Assistance-Publique Hôpitaux de Marseille, Marseille, France.

Umberto Simeoni (U)

Division of Pediatrics & DOHaD Laboratory, CHUV University Hospital and University of Lausanne, Lausanne, Switzerland.

Frank Kober (F)

Aix-Marseille Université, CNRS, CRMBM, Marseille, France.

Monique Bernard (M)

Aix-Marseille Université, CNRS, CRMBM, Marseille, France.

Bénédicte Gaborit (B)

Aix-Marseille Université, INSERM, INRAE, C2VN, Marseille, France.
Department of Endocrinology, Metabolic Diseases and Nutrition, Pôle ENDO, APHM, Marseille, France.

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