Proinflammatory Matrix Metalloproteinase-1 Associates With Mitral Valve Leaflet Disruption Following Percutaneous

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Livia S A Passos1, Dakota Becker-Greene1, Renato Braulio2

  • 1Center for Excellence in Vascular Biology, Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, United States.

Frontiers in Cardiovascular Medicine
|February 7, 2022
PubMed

Insights

Inflammatory cells and specific molecules like MMP-1 and IFN-γ contribute to mitral valve leaflet tearing during percutaneous mitral valvuloplasty. This remodeling increases the risk of severe mitral regurgitation after the procedure.

Area of Science:

  • Cardiovascular Research
  • Pathology
  • Molecular Biology

Background:

  • Mitral regurgitation (MR) is a significant complication of percutaneous mitral valvuloplasty (PMV), with severe cases often caused by unpredictable leaflet tearing.
  • Current echocardiographic analysis cannot fully predict leaflet tearing, highlighting a gap in understanding the underlying mechanisms.
  • Rheumatic mitral stenosis (MS) is a common indication for PMV, and understanding complications is crucial for patient outcomes.

Purpose of the Study:

  • To investigate the histological and molecular characteristics of mitral valve leaflets in patients experiencing severe MR due to leaflet tear after PMV.
  • To compare these findings with mitral valves from patients with severe MS undergoing elective surgery without PMV.
  • To elucidate the role of cellular and molecular alterations in leaflet tear susceptibility.

Main Methods:

  • Histological and molecular analysis of excised mitral valves from two patient groups: emergency surgery post-PMV (leaflet tear) and elective surgery for MS.
  • Comparison of valvular tissue characteristics, focusing on collagen remodeling and inflammatory markers.
  • In vitro assays using peripheral blood mononuclear cells to assess the impact of identified molecular factors, specifically IFN-γ on MMP-1 expression in monocytes.

Main Results:

  • Focal infiltration of inflammatory cells was observed in mitral valve leaflets associated with leaflet tear.
  • Elevated levels of Matrix Metalloproteinase-1 (MMP-1) and Interferon-gamma (IFN-γ) were found in these leaflets.
  • In vitro studies demonstrated that IFN-γ enhances MMP-1 expression in CD14+ cells (monocytes).

Conclusions:

  • Inflammatory cell infiltration and associated molecular factors (MMP-1, IFN-γ) contribute to abnormal collagen remodeling in mitral valve leaflets.
  • This irregular remodeling leads to leaflet thickening and architectural abnormalities, increasing susceptibility to tearing during PMV.
  • Targeting inflammatory pathways may offer a strategy to reduce leaflet tear complications and severe MR after PMV.
Keywords:
MMP-1collageninflammationpercutaneous mitral valvuloplastyrheumatic heart disease

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