Progression of aortic stenosis after an acute myocardial infarction.
aortic valve stenosis
echocardiography
myocardial infarction
Journal
Open heart
ISSN: 2053-3624
Titre abrégé: Open Heart
Pays: England
ID NLM: 101631219
Informations de publication
Date de publication:
06 2022
06 2022
Historique:
received:
24
04
2022
accepted:
26
05
2022
entrez:
21
6
2022
pubmed:
22
6
2022
medline:
24
6
2022
Statut:
ppublish
Résumé
Myocardial infarction (MI) has been shown to induce fibrotic remodelling of the mitral and tricuspid valves. It is unknown whether MI also induces pathological remodelling of the aortic valve and alters aortic stenosis (AS) progression. We thus compared AS progression after an acute MI and in patients with/without history of MI, and assessed post-MI pathobiological changes within the aortic valve leaflets in a sheep model. Serial echocardiograms in human patients with AS were retrospectively analysed and compared between 3 groups: (1) acute MI at baseline (n=68), (2) prior history of MI (n=45) and (3) controls without MI (n=101). Annualised progression rates of AS severity were compared between these 3 groups. In addition, aortic valves were harvested from 15 sheep: (1) induced inferior MI (n=10) and (2) controls without MI (n=5), for biological and histological analyses. In humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVA The results of this study suggest that AS progression is accelerated following acute MI, which could be caused by increased collagen production and thickening of the aortic valve after the ischaemic event.
Sections du résumé
BACKGROUND
Myocardial infarction (MI) has been shown to induce fibrotic remodelling of the mitral and tricuspid valves. It is unknown whether MI also induces pathological remodelling of the aortic valve and alters aortic stenosis (AS) progression. We thus compared AS progression after an acute MI and in patients with/without history of MI, and assessed post-MI pathobiological changes within the aortic valve leaflets in a sheep model.
METHODS
Serial echocardiograms in human patients with AS were retrospectively analysed and compared between 3 groups: (1) acute MI at baseline (n=68), (2) prior history of MI (n=45) and (3) controls without MI (n=101). Annualised progression rates of AS severity were compared between these 3 groups. In addition, aortic valves were harvested from 15 sheep: (1) induced inferior MI (n=10) and (2) controls without MI (n=5), for biological and histological analyses.
RESULTS
In humans, the acute MI, previous MI and control groups had comparable baseline AS severity. Indexed aortic valve area (AVA
CONCLUSIONS
The results of this study suggest that AS progression is accelerated following acute MI, which could be caused by increased collagen production and thickening of the aortic valve after the ischaemic event.
Identifiants
pubmed: 35728891
pii: openhrt-2022-002046
doi: 10.1136/openhrt-2022-002046
pmc: PMC9214429
pii:
doi:
Substances chimiques
Collagen
9007-34-5
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
Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL136431
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141917
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL147095
Pays : United States
Organisme : CIHR
ID : 399323
Pays : Canada
Informations de copyright
© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: None declared.
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