Increases in mitral leaflet radii of curvature with chronic ischemic mitral regurgitation.
OBJECTIVE
Leaflet curvature is a primary determinant of leaflet stress, but no quantitative in-vivo leaflet curvature data exist. Chronic ischemic mitral regurgitation (CIMR) is associated with remodeling of the valvular-ventricular complex. It was hypothesized that leaflet radii of curvature (ROC) would change with such remodeling.


METHODS
Twelve sheep had placement of radiopaque markers on the anterior (APM) and posterior (PPM) papillary muscles, mitral annulus, and anterior (AL) and posterior leaflet (PL) midlines. After 8 +/- 2 days, videofluoroscopy provided baseline 3-D marker data prior to creating inferior myocardial infarction (MI) by snare occlusion of the obtuse marginal coronary arteries. After 7 +/- 1 weeks, the animals were re-studied; 3-D marker coordinates were used to determine end-systolic leaflet ROC, leaflet length, annular septal-lateral diameter, and the distance of each papillary muscle to the mid-septal annulus and each commissure.


RESULTS
Before and after CIMR, the AL had compound curvature, and CIMR increased ROC of both curves (proximal ROC 1.27 +/- 0.59 to 1.38 +/- 0.60 cm (p <0.05); distal ROC 1.41 +/- 0.61 to 2.60 +/- 1.52 cm (p < 0.05)). The PL ROC also increased with CIMR (from 2.01 +/- 1.40 to 3.46 +/- 3.93) (p <0.05). Multiple regression analysis determined that annular septal-lateral diameter (proximal AL and distal AL), distance from the APM to anterior commissure (distal AL), and PPM to mid-septal annulus (PL) were independent predictors of leaflet ROC.


CONCLUSIONS
CIMR increased ROC of both the AL and PL. Leaflet extension may be a compensatory mechanism to minimize the regurgitant orifice, but the attendant increase in ROC will tend to augment leaflet stress. Annular and subvalvular geometry both affect leaflet curvature, and should be considered during mitral repair. These novel quantitative in-vivo data are now available for modification of finite element models, and for comparison to finite element model output.
Department of Cardiovascular and Thoracic Surgery, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
Frederick A
FA
Tibayan
Filiberto
F
Rodriguez
Frank
F
Langer
Mary K
MK
Zasio
Lynn
L
Bailey
David
D
Liang
George T
GT
Daughters
Matts
M
Karlsson
Neil B
NB
Ingels
D Craig
DC
Miller
D000818:Animals; D001837:Body Weights and Measures; D002908:Chronic Disease; D005471:Fluoroscopy / Q000379:methods; D006801:Humans; D008943:Mitral Valve / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*; D023421:Models, Animal; D009203:Myocardial Infarction / Q000150:complications*; D012756:Sheep; D020257:Ventricular Remodeling / Q000502:physiology; D014741:Video Recording