Tenting volume: three-dimensional assessment of geometric perturbations in functional mitral regurgitation and implications for surgical repair.
OBJECTIVE
Functional mitral regurgitation (FMR) often complicates dilated cardiomyopathy (DCM), and portends a poor prognosis. Debate over the optimal treatment continues, underscoring the present incomplete understanding of the patho-anatomic mechanisms of this disease. Studies of mitral tenting volume and tenting area, and echocardiographic measures of abnormal apical systolic leaflet geometry have linked mitral leaflet deformation with subvalvular left ventricular (LV) remodeling in chronic ischemic MR. The relative contributions of annular versus subvalvular remodeling in FMR due to DCM are less clear. Here, the validity of 3-D measurement of mitral deformation, tenting volume, as a correlate of MR in DCM, was tested. The ability of annular and subvalvular remodeling to predict mitral deformation was then determined.


METHODS
Eight sheep underwent placement of radiopaque markers on the mitral annulus and leaflets. Global LV, annular and subvalvular geometry, as well as mitral tenting height, area and volume were calculated before (Control) and after the development of pacing-induced cardiomyopathy and MR (DCM). Multivariable regression determined which measure of mitral deformation was the best predictor of MR. Regression analysis was also used to find geometric predictors of mitral tenting volume.


RESULTS
In a multivariable analysis, mitral tenting volume was the only independent predictor of severity of MR (r(2) = 0.79, standard error of estimate (SEE) = 0.58). Increased tenting volume correlated best with increased mitral annular septal-lateral diameter (r(2) = 0.67, SEE = 0.72).


CONCLUSIONS
The 3-D tenting volume correlates best with severity of FMR. Mitral deformation (increased tenting volume) observed in DCM is predicted by annular dilation, but not by subvalvular LV remodeling. These data support the use of an undersized annuloplasty in DCM complicated by FMR, and may guide the rational design of new therapies for this vexing disease.
Tibayan
Frederick A
FA
Department of Cardiothoracic Surgery, Falk Cardiovascular Research Center, Stanford University School of Medicine, Stanford, California 94305-5247, USA.
Wilson
Ariane
A
Lai
David T M
DT
Timek
Tomasz A
TA
Dagum
Paul
P
Rodriguez
Filiberto
F
Zasio
Mary K
MK
Liang
David
D
Daughters
George T
GT
Ingels
Neil B
NB
Miller
D Craig
DC
D000818:Animals; D002304:Cardiac Pacing, Artificial; D002311:Cardiomyopathy, Dilated / Q000150:complications*; D004195:Disease Models, Animal; D004452:Echocardiography; D004567:Electrodes, Implanted; D005471:Fluoroscopy; D006321:Heart / Q000000981:diagnostic imaging* / Q000503:physiopathology; D021621:Imaging, Three-Dimensional; D008943:Mitral Valve / Q000000981:diagnostic imaging* / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging* / Q000209:etiology; D008955:Models, Cardiovascular; D012756:Sheep; D014741:Video Recording