TY - JOUR
T1 - Mechanistic insights into functional mitral regurgitation
AU - Levine, Robert A.
AU - Hung, Judy
AU - Otsuji, Yutaka
AU - Messas, Emmanuel
AU - Liel-Cohen, Noah
AU - Nathan, Nadia
AU - Handschumacher, Mark D.
AU - Guerrero, J. Luis
AU - He, Shengqiu
AU - Yoganathan, Ajit P.
AU - Vlahakes, Gus J.
PY - 2002/12/1
Y1 - 2002/12/1
N2 - Effective valve repair in patients with mitral regurgitation (MR) demands an understanding of its mechanism. In patients with ischemic heart disease and functional MR, which doubles late mortality, normal leaflets are apically displaced. This reflects an altered balance of forces acting on the leaflets: increased tethering forces restricting closure, resulting from an altered geometry of leaflet attachments, and decreased ventricular forces acting to close the leaflets. Extensive evidence confirms a central and predominant role of tethering as the final common pathway inducing functional MR; left ventricular (LV) pressure dynamically modulates the orifice area. Because ischemic MR is a disease of the entire mitral complex, including the remodeling LV, reducing annular size alone is often ineffective. Undersizing rings attempts to compensate for tethering; new and potentially more effective strategies directly address tethering by infarct plication, papillary muscle repositioning with a localized patch, or basal chordal cutting to increase coaptational surface area without prolapse. A comprehensive understanding of the valve in its ventricular context, therefore, provides new opportunities for successful valve repair in patients.
AB - Effective valve repair in patients with mitral regurgitation (MR) demands an understanding of its mechanism. In patients with ischemic heart disease and functional MR, which doubles late mortality, normal leaflets are apically displaced. This reflects an altered balance of forces acting on the leaflets: increased tethering forces restricting closure, resulting from an altered geometry of leaflet attachments, and decreased ventricular forces acting to close the leaflets. Extensive evidence confirms a central and predominant role of tethering as the final common pathway inducing functional MR; left ventricular (LV) pressure dynamically modulates the orifice area. Because ischemic MR is a disease of the entire mitral complex, including the remodeling LV, reducing annular size alone is often ineffective. Undersizing rings attempts to compensate for tethering; new and potentially more effective strategies directly address tethering by infarct plication, papillary muscle repositioning with a localized patch, or basal chordal cutting to increase coaptational surface area without prolapse. A comprehensive understanding of the valve in its ventricular context, therefore, provides new opportunities for successful valve repair in patients.
UR - http://www.scopus.com/inward/record.url?scp=0036517399&partnerID=8YFLogxK
U2 - 10.1007/s11886-002-0024-6
DO - 10.1007/s11886-002-0024-6
M3 - Article
AN - SCOPUS:0036517399
VL - 4
SP - 125
EP - 129
JO - Current Cardiology Reports
JF - Current Cardiology Reports
SN - 1523-3782
IS - 2
ER -