Details

Autor(en) / Beteiligte

• Levine, Robert A
• Hagége, Albert A
• Judge, Daniel P
• Padala, Muralidhar
• Dal-Bianco, Jacob P
• Aikawa, Elena
• Beaudoin, Jonathan
• Bischoff, Joyce
• Bouatia-Naji, Nabila
• Bruneval, Patrick
• Butcher, Jonathan T
• Carpentier, Alain
• Chaput, Miguel
• Chester, Adrian H
• Clusel, Catherine
• Delling, Francesca N
• Dietz, Harry C
• Dina, Christian
• Durst, Ronen
• Fernandez-Friera, Leticia
• Handschumacher, Mark D
• Jensen, Morten O
• Jeunemaitre, Xavier P
• Le Marec, Hervé
• Le Tourneau, Thierry
• Markwald, Roger R
• Mérot, Jean
• Messas, Emmanuel
• Milan, David P
• Neri, Tui
• Norris, Russell A
• Peal, David
• Perrocheau, Maelle
• Probst, Vincent
• Pucéat, Michael
• Rosenthal, Nadia
• Solis, Jorge
• Schott, Jean-Jacques
• Schwammenthal, Ehud
• Slaugenhaupt, Susan A
• Song, Jae-Kwan
• Yacoub, Magdi H

Titel

Mitral valve disease--morphology and mechanisms

Ist Teil von

• Nature reviews cardiology, 2015-12, Vol.12 (12), p.689

Ort / Verlag

England

Erscheinungsjahr

2015

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.