Author + information
- Meerarani Purushothaman,
- Purushothaman K–Raman,
- David Adams,
- Federico Milla,
- Annapoorna Kini,
- Samin Sharma,
- Valentin Fuster and
- Pedro Moreno
Chordae rupture triggering severe mitral regurgitation is a life–threatening event requiring emergent surgery. Elastic fibrils within the chordae tendineae maintain the integrity and distensibility of the mitral leaflets. In Degenerative Mitral Valve Disease (DMVD), chordal rupture is more prevalent in Fibro Elastic Deficiency (FED) when compared to Barlow's Disease (BD). We tested the hypothesis that reduced elastin content and altered elastic fibril architecture may be more commonly seen in FED with chordal rupture when compared to BD without chordal rupture.
Twenty human posterior mitral valve leaflets were studied, 9 FED with rupture and 11–BD without rupture. Elastin protein density and architecture (elastic fibril fragmentation and disorganization), and valve morphology, were quantified using histochemistry and immunohistochemistry.
Elastin protein density was reduced and fragmentation/disorganization increased in FED (Table and Figure).
Mitral valve chordal rupture is associated with diminished elastin protein density and altered elastic architecture in fibro elastic deficiency in DMVD. Future development of pharmacological or molecular technology preserving elastin protein content and architecture may have the potential to reduce chordae rupture, reducing the need for emergent surgery in DMVD.
Poster Sessions, Expo North
Saturday, March 09, 2013, 10:00 a.m.–10:45 a.m.
Session Title: Evolving Concepts for the Optimal Management of Mitral Regurgitation from E–Clip to Robotics
Abstract Category: 32. Valvular Heart Disease: Therapy
Presentation Number: 1111–76
- 2013 American College of Cardiology Foundation