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Nat Rev Cardiol. 2015 Dec;12(12):689-710. doi: 10.1038/nrcardio.2015.161. Epub 2015 Oct 20.

Mitral valve disease--morphology and mechanisms.

Author information

1
Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Yawkey 5E, Boston, MA 02114, USA.
2
Hôpital Européen Georges Pompidou, Université René Descartes, UMR 970, Paris, France.
3
Johns Hopkins University, Baltimore, MD, USA.
4
Emory University School of Medicine, Atlanta, GA, USA.
5
Massachusetts General Hospital, Cardiac Ultrasound Laboratory, Harvard Medical School, Boston, MA, USA.
6
Brigham and Women's Hospital, Boston, MA, USA.
7
Laval Hospital, Quebec City, Canada.
8
Boston Children's Hospital, Boston, MA, USA.
9
Cornell University, Ithaca, NY, USA.
10
University of Montreal, Montreal, Canada.
11
Imperial College London, London, UK.
12
INSERM-Transfert, Paris, France.
13
Beth Israel Deaconess Medical Centre, Harvard Medical School, Boston, MA, USA.
14
University of Nantes, Thoracic Institute, INSERM UMR 1097, CNRS UMR 6291, Nantes, France.
15
Hadassah-Hebrew University Medical Centre, Jerusalem, Israel.
16
Hospital Universitario HM Monteprincipe and the Centro Nacional de Investigaciones Cardiovasculares, Carlos III (CNIC), Madrid, Spain.
17
University of Aarhus, Aarhus, Denmark.
18
Medical University of South Carolina, Charleston, SC, USA.
19
Cardiovascular Research Center, Harvard Medical School, Boston, MA, USA.
20
Aix-Marseille University, INSERM UMR 910, Marseille, France.
21
European Molecular Biology Laboratory, Monterotondo, Italy.
22
Tel Aviv University, Tel Aviv, Israel.
23
Center for Human Genetic Research, MGH Research Institute, Harvard Medical School, Boston, MA, USA.
24
Asan Medical Centre, Seoul, South Korea.

Abstract

Mitral valve disease is a frequent cause of heart failure and death. Emerging evidence indicates that the mitral valve is not a passive structure, but--even in adult life--remains dynamic and accessible for treatment. This concept motivates efforts to reduce the clinical progression of mitral valve disease through early detection and modification of underlying mechanisms. Discoveries of genetic mutations causing mitral valve elongation and prolapse have revealed that growth factor signalling and cell migration pathways are regulated by structural molecules in ways that can be modified to limit progression from developmental defects to valve degeneration with clinical complications. Mitral valve enlargement can determine left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and might be stimulated by potentially modifiable biological valvular-ventricular interactions. Mitral valve plasticity also allows adaptive growth in response to ventricular remodelling. However, adverse cellular and mechanobiological processes create relative leaflet deficiency in the ischaemic setting, leading to mitral regurgitation with increased heart failure and mortality. Our approach, which bridges clinicians and basic scientists, enables the correlation of observed disease with cellular and molecular mechanisms, leading to the discovery of new opportunities for improving the natural history of mitral valve disease.

PMID:
26483167
PMCID:
PMC4804623
DOI:
10.1038/nrcardio.2015.161
[Indexed for MEDLINE]
Free PMC Article

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