Associations of Circulating Vascular Cell Adhesion Molecule-1 and Intercellular Adhesion Molecule-1 With Long-Term Cardiac Function.

atrial fibrillation cellular adhesion molecule heart failure interstitial fibrosis left atrial strain myocardial scar

Journal

Journal of the American Heart Association
ISSN: 2047-9980
Titre abrégé: J Am Heart Assoc
Pays: England
ID NLM: 101580524

Informations de publication

Date de publication:
18 Mar 2024
Historique:
medline: 18 3 2024
pubmed: 18 3 2024
entrez: 18 3 2024
Statut: aheadofprint

Résumé

Although VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1) have been associated with incident heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF), the associations of VCAM-1 and ICAM-1 with sensitive measures of cardiac structure/function are unclear. The objective of this study is to evaluate associations between VCAM-1, ICAM-1, and measures of cardiac structure and function as potential pathways through which cellular adhesion molecules promote HFpEF and AF risk. In MESA (Multi-Ethnic Study of Atherosclerosis), we evaluated the associations of circulating VCAM-1 and ICAM-1 at examination 2 (2002-2004) with measures of cardiac structure/function on cardiac magnetic resonance imaging at examination 5 (2010-2011) after multivariable adjustment. Mediation analysis of left atrial (LA) strain on the association between VCAM-1 or ICAM-1 and AF or HFpEF was also performed. Overall, 2304 individuals (63±10 years; 47% men) with VCAM-1 or ICAM-1, cardiac magnetic resonance imaging, and covariate data were included in analysis. Higher VCAM-1 and ICAM-1 were associated with lower LA peak longitudinal strain and worse global circumferential left ventricular strain but were not associated with left ventricular myocardial scar or interstitial fibrosis. Lower LA peak longitudinal strain mediated 8% (95% CI, 2-30) of the relationship between VCAM-1 and HFpEF and 9% (95% CI, 2-21) of the relationship between VCAM-1 and AF. Higher VCAM-1 and ICAM-1 were associated with lower LA function and left ventricular systolic function but were not associated with myocardial scar or interstitial fibrosis. VCAM-1 and ICAM-1 may promote HFpEF and AF risk through impaired LA reservoir function.

Sections du résumé

BACKGROUND BACKGROUND
Although VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1) have been associated with incident heart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF), the associations of VCAM-1 and ICAM-1 with sensitive measures of cardiac structure/function are unclear. The objective of this study is to evaluate associations between VCAM-1, ICAM-1, and measures of cardiac structure and function as potential pathways through which cellular adhesion molecules promote HFpEF and AF risk.
METHODS AND RESULTS RESULTS
In MESA (Multi-Ethnic Study of Atherosclerosis), we evaluated the associations of circulating VCAM-1 and ICAM-1 at examination 2 (2002-2004) with measures of cardiac structure/function on cardiac magnetic resonance imaging at examination 5 (2010-2011) after multivariable adjustment. Mediation analysis of left atrial (LA) strain on the association between VCAM-1 or ICAM-1 and AF or HFpEF was also performed. Overall, 2304 individuals (63±10 years; 47% men) with VCAM-1 or ICAM-1, cardiac magnetic resonance imaging, and covariate data were included in analysis. Higher VCAM-1 and ICAM-1 were associated with lower LA peak longitudinal strain and worse global circumferential left ventricular strain but were not associated with left ventricular myocardial scar or interstitial fibrosis. Lower LA peak longitudinal strain mediated 8% (95% CI, 2-30) of the relationship between VCAM-1 and HFpEF and 9% (95% CI, 2-21) of the relationship between VCAM-1 and AF.
CONCLUSIONS CONCLUSIONS
Higher VCAM-1 and ICAM-1 were associated with lower LA function and left ventricular systolic function but were not associated with myocardial scar or interstitial fibrosis. VCAM-1 and ICAM-1 may promote HFpEF and AF risk through impaired LA reservoir function.

Identifiants

pubmed: 38497480
doi: 10.1161/JAHA.123.032213
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e032213

Auteurs

Daniel T Mathew (DT)

Northwestern University Feinberg School of Medicine Chicago IL.

Graham Peigh (G)

Division of Cardiology, Department of Medicine Northwestern University Feinberg School of Medicine Chicago IL.

Joao A C Lima (JAC)

Division of Cardiology, Department of Medicine Johns Hopkins University Baltimore MD.

Suzette J Bielinski (SJ)

Department of Quantitative Health Sciences Mayo Clinic Rochester MN.

Nicholas B Larson (NB)

Department of Quantitative Health Sciences Mayo Clinic Rochester MN.

Matthew A Allison (MA)

Division of Preventive Medicine, Department of Family Medicine University of California La Jolla CA.

Sanjiv J Shah (SJ)

Division of Cardiology, Department of Medicine Northwestern University Feinberg School of Medicine Chicago IL.
Department of Preventive Medicine Northwestern University Feinberg School of Medicine Chicago IL.

Ravi B Patel (RB)

Division of Cardiology, Department of Medicine Northwestern University Feinberg School of Medicine Chicago IL.
Department of Preventive Medicine Northwestern University Feinberg School of Medicine Chicago IL.

Classifications MeSH