Association of soluble Flt-1 with heart failure and cardiac morphology: The MESA angiogenesis study.
heart failure
left ventricular mass, mortality
soluble Fms-like tyrosine kinase 1
Journal
The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation
ISSN: 1557-3117
Titre abrégé: J Heart Lung Transplant
Pays: United States
ID NLM: 9102703
Informations de publication
Date de publication:
05 2022
05 2022
Historique:
received:
20
08
2021
revised:
23
11
2021
accepted:
02
01
2022
pubmed:
22
2
2022
medline:
27
4
2022
entrez:
21
2
2022
Statut:
ppublish
Résumé
Soluble Fms-like tyrosine kinase 1 (sFlt-1) may inhibit angiogenesis. Higher levels of sFlt-1 are associated with worse prognosis in prevalent heart failure patients. The aim of this study was to better understand the role of sFlt-1 in heart failure pathogenesis by characterizing relationships between sFlt-1, cardiac morphology, and the composite outcome of incident heart failure or cardiovascular (CV) death in in a multiethnic cohort free of CV disease at baseline. sFlt-1 was measured in 1,381 participants in the Multi-Ethnic Study of Atherosclerosis Angiogenesis sub-study. Linear regression was used to estimate the association between sFlt-1 and cardiac morphology and Cox proportional hazard regression was used to estimate associations with incident heart failure or CV mortality. Over a median follow-up of 13.1 years, higher sFlt-1 levels were associated with incident heart failure or CV mortality independent from CV risk factors or NT-proBNP levels (HR 1.17, 95% CI 1.10-1.26, p < 0.001). Higher sFlt-1 levels were also associated with greater baseline left ventricular (LV) mass by cardiac MRI and increased loss of LV mass over the 10 years following the baseline exam (p-value 0.02 for each), but this association was no longer statistically significant after adjustment for baseline NT-proBNP (p = 0.11 and 0.10 respectively). Baseline sFlt-1 levels are associated with incident heart failure and cardiovascular mortality independent of traditional CV risk factors or NT-proBNP. An association was also found with cardiac mass but was no longer significant after adjustment for NT-proBNP.
Sections du résumé
BACKGROUND
Soluble Fms-like tyrosine kinase 1 (sFlt-1) may inhibit angiogenesis. Higher levels of sFlt-1 are associated with worse prognosis in prevalent heart failure patients. The aim of this study was to better understand the role of sFlt-1 in heart failure pathogenesis by characterizing relationships between sFlt-1, cardiac morphology, and the composite outcome of incident heart failure or cardiovascular (CV) death in in a multiethnic cohort free of CV disease at baseline.
METHODS
sFlt-1 was measured in 1,381 participants in the Multi-Ethnic Study of Atherosclerosis Angiogenesis sub-study. Linear regression was used to estimate the association between sFlt-1 and cardiac morphology and Cox proportional hazard regression was used to estimate associations with incident heart failure or CV mortality.
RESULTS
Over a median follow-up of 13.1 years, higher sFlt-1 levels were associated with incident heart failure or CV mortality independent from CV risk factors or NT-proBNP levels (HR 1.17, 95% CI 1.10-1.26, p < 0.001). Higher sFlt-1 levels were also associated with greater baseline left ventricular (LV) mass by cardiac MRI and increased loss of LV mass over the 10 years following the baseline exam (p-value 0.02 for each), but this association was no longer statistically significant after adjustment for baseline NT-proBNP (p = 0.11 and 0.10 respectively).
CONCLUSIONS
Baseline sFlt-1 levels are associated with incident heart failure and cardiovascular mortality independent of traditional CV risk factors or NT-proBNP. An association was also found with cardiac mass but was no longer significant after adjustment for NT-proBNP.
Identifiants
pubmed: 35184966
pii: S1053-2498(22)00005-5
doi: 10.1016/j.healun.2022.01.003
pmc: PMC9038636
mid: NIHMS1782058
pii:
doi:
Substances chimiques
Biomarkers
0
Peptide Fragments
0
Natriuretic Peptide, Brain
114471-18-0
FLT1 protein, human
EC 2.7.10.1
Vascular Endothelial Growth Factor Receptor-1
EC 2.7.10.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
619-625Subventions
Organisme : NHLBI NIH HHS
ID : N01HC95160
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95163
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95169
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95164
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95162
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95168
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95159
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95161
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95167
Pays : United States
Organisme : NHLBI NIH HHS
ID : N01HC95166
Pays : United States
Informations de copyright
Copyright © 2022 International Society for Heart and Lung Transplantation. Published by Elsevier Inc. All rights reserved.
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