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Cited by 210Atrial Fibrillation Management and OutcomesCardiac Fibrosis and RemodelingProtease and Inhibitor Mechanisms

Matrix metalloproteinases and atrial remodeling in patients with mitral valve disease and atrial fibrillation

ANNE, W, WILLEMS, R, ROSKAMS, T, SERGEANT, P, HERIJGERS, P, HOLEMANS, P, ECTOR, H, HEIDBUCHEL, H·2005·Cardiovascular Research
DOI 10.1016/j.cardiores.2005.04.016
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Abstract

BACKGROUND: Atrial fibrillation (AF) is associated with extracellular matrix remodeling involving atrial fibrosis and atrial dilatation. Angiotensin II mediated pathways and matrix metalloproteinases (MMPs) have been implicated in these processes. Our aim was to study atrial structural remodeling and the expression of the angiotensin receptor subtypes and MMPs and their inhibitors (TIMPs) in patients with mitral valve disease with and without AF. METHODS AND RESULTS: Biopsies from right and left atrial appendages (RA and LA) were taken from patients undergoing CABG (n=9, all in sinus rhythm (SR)) or mitral valve surgery (MVS; n=19; 9 with permanent AF and 10 in SR). Patients with MVS and AF had significantly larger atria (versus MVS and SR: p=0.02; versus CABG: p<0.01). The MVS patients had significantly more fibrosis than the control CABG group. Fibrosis was increased in both the AF and SR MVS groups in the LA, but only in the MVS-AF group in the RA. These AF patients had significantly more tricuspid regurgitation than SR patients. MMP-1 was down-regulated in LA of MVS patients (p=0.02) independent of the underlying rhythm (SR or AF; p=0.95). In RA biopsies, MMP-1 was down-regulated only in the MVS and AF group. MMP-9 was down-regulated in the MVS patients compared to CABG both in the RA and LA, and without a difference between the SR and AF groups. Protein expression of AT-1, AT-2, MMP-2, TIMP-1, -2 and -4, TNF-alpha, and TNF-alpha-converting enzyme did not differ significantly between the 3 groups. CONCLUSIONS: Concordant changes between MMP-expression and fibrosis during mitral valve disease, both in LA and RA, suggest involvement of MMPs in structural atrial remodeling. AF itself did not contribute to altered fibrosis or MMP-expression in the LA. The association between AF and RA changes may be precipitated by greater hemodynamic load due to tricuspid regurgitation in these patients.

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Authors
ANNE, W., WILLEMS, R., ROSKAMS, T., SERGEANT, P., HERIJGERS, P., HOLEMANS, P., ECTOR, H., & HEIDBUCHEL, H.
Affiliations
Universitair Ziekenhuis Leuven (BE)
ORCID
Venue
Cardiovascular Research
Publisher
Oxford University Press (OUP)
Published
2005-09-01
Volume
67
Issue
4
Pages
655-666
ISSN
0008-6363 (ISSN-L)
DOI
10.1016/j.cardiores.2005.04.016
OpenAlex
W2059376978
Cited by
210
References
36
Citations by year
2026: 5 · 2025: 3 · 2024: 11 · 2023: 7 · 2022: 12 · 2021: 7 · 2020: 15 · 2019: 9 · 2018: 10 · 2017: 12 · 2016: 15 · 2015: 16 · 2014: 14 · 2013: 20 · 2012: 7
FWCI
3.42
Type
journal article
Language
en
Open access
closed
Locations
  • Cardiovascular Research (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Atrial Fibrillation Management and Outcomes
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
Keywords
matrix metalloproteinases, atrial remodeling, atrial fibrillation, mitral valve disease, atrial fibrosis, angiotensin II receptor, angiotensin-converting enzyme, tissue inhibitors of metalloproteinases, MMP-1, MMP-9, tricuspid regurgitation, atrial appendage, atrial dilatation, TNF-α
MeSH terms
Tissue Inhibitor of Metalloproteinase-4, Aged, Atrial Fibrillation, Female, Fibrosis, Humans, Immunohistochemistry, Male, Mitral Valve Insufficiency, Tumor Necrosis Factor-alpha, Blotting, Western, Case-Control Studies, Statistics, Nonparametric, Tissue Inhibitor of Metalloproteinases, Tissue Inhibitor of Metalloproteinase-1, Tissue Inhibitor of Metalloproteinase-2, Atrial Appendage, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Matrix Metalloproteinase 1, Matrix Metalloproteinases, Myocytes, Cardiac, Receptor, Angiotensin, Type 2, Receptor, Angiotensin, Type 1, Cell Size

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