Recurrent depression predicts high leptin concentrations in patients with coronary artery disease over an 18-months follow-up period: Findings from the prospective multicenter randomized controlled SPIRR-CAD Trial.
Coronary artery disease
Hyperleptinemic state
NT-proBNP
Negative mood regulation
Plasma leptin level
Recurrent depressed mood
Journal
Journal of affective disorders
ISSN: 1573-2517
Titre abrégé: J Affect Disord
Pays: Netherlands
ID NLM: 7906073
Informations de publication
Date de publication:
23 Sep 2024
23 Sep 2024
Historique:
received:
18
03
2024
revised:
16
09
2024
accepted:
21
09
2024
medline:
26
9
2024
pubmed:
26
9
2024
entrez:
25
9
2024
Statut:
aheadofprint
Résumé
Leptin, an adipokine suspected to play a role in coronary artery disease (CAD), may also be associated with deteriorated mental health. We investigated the prospective impact of recurrent depressed mood (RDM) on heightened plasma leptin levels in CAD patients. Derived from the randomized SPIRR-CAD trial, plasma leptin were measured by the Human Leptin DuoSet ELISA at baseline in 539 patients (including 115 (21.3 %) women and 424 (78.7 %) men) and in 373 participants after 18-months follow up (T At baseline, highest leptin level (3rd tertile) was associated with type 2 diabetes (p = 0.009), heart failure symptoms (NYHA III) (p < 0.001), female sex and BMI ≥30 (p < 0.001) but not with age and depression. At study endpoint (T3), RDM was associated with a substantially increased risk of experiencing the highest plasma leptin level (OR 2.92 (95 % CI 1.27-6.75)) followed by increased NT-proBNP (the most prominent indicator of CHF) with an OR of 2.73 (1.22-6.11) - both after adjustment for concurrent factors including weight gain (diff BMI T Findings are limited to people of Caucasian ancestry which prevents being generalized to other ethnicities. Although relying upon a prospective design, reverse causality cannot be excluded but is unlikely. In CAD patients, RDM is a significant predictor of heightened leptin -a finding opening room for a new pathway of the psychobiological underpinning of depression on CAD risk.
Sections du résumé
BACKGROUND
BACKGROUND
Leptin, an adipokine suspected to play a role in coronary artery disease (CAD), may also be associated with deteriorated mental health. We investigated the prospective impact of recurrent depressed mood (RDM) on heightened plasma leptin levels in CAD patients.
METHODS
METHODS
Derived from the randomized SPIRR-CAD trial, plasma leptin were measured by the Human Leptin DuoSet ELISA at baseline in 539 patients (including 115 (21.3 %) women and 424 (78.7 %) men) and in 373 participants after 18-months follow up (T
RESULTS
RESULTS
At baseline, highest leptin level (3rd tertile) was associated with type 2 diabetes (p = 0.009), heart failure symptoms (NYHA III) (p < 0.001), female sex and BMI ≥30 (p < 0.001) but not with age and depression. At study endpoint (T3), RDM was associated with a substantially increased risk of experiencing the highest plasma leptin level (OR 2.92 (95 % CI 1.27-6.75)) followed by increased NT-proBNP (the most prominent indicator of CHF) with an OR of 2.73 (1.22-6.11) - both after adjustment for concurrent factors including weight gain (diff BMI T
LIMITATIONS
CONCLUSIONS
Findings are limited to people of Caucasian ancestry which prevents being generalized to other ethnicities. Although relying upon a prospective design, reverse causality cannot be excluded but is unlikely.
CONCLUSIONS
CONCLUSIONS
In CAD patients, RDM is a significant predictor of heightened leptin -a finding opening room for a new pathway of the psychobiological underpinning of depression on CAD risk.
Identifiants
pubmed: 39321975
pii: S0165-0327(24)01635-5
doi: 10.1016/j.jad.2024.09.146
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
Copyright © 2024. Published by Elsevier B.V.
Déclaration de conflit d'intérêts
Declaration of competing interest All the authors declare no conflicts of interest. All authors certify that they have no affiliations with or involvement in any organization or entity with any financial interest or non-financial interest in the subject matter or materials discussed in this manuscript. Christoph Herrmann-Lingen receives royalties from Hans Huber Publishers (Berne, Switzerland) for the German HADS version and for lecture honoraria from Pfizer and Novatis. Karl-Heinz Ladwig received lecture honoraria from Amgen, AstraZeneca, Bayer Vital and for advisory board activities for Idorsia (Switzerland). Furthermore, all authors have no competing interests to declare that are relevant to the content of this article.