title: Dynamic change of mitral apparatus as potential cause of left ventricular outflow tract obstruction in hypertrophic cardiomyopathy.
abstract: OBJECTIVE
  the geometry of the mitral apparatus changes dynamically throughout systole and diastole. We investigated how geometric dynamics of the mitral apparatus could affect the haemodynamics of the outflow tract in patients with hypertrophic cardiomyopathy presenting with systolic anterior motion (HCM(SAM)) using three-dimensional (3D) echocardiography.
  
  
  RESULTS
  we obtained transthoracic volumetric images in 21 patients with HCM(SAM) with differing trans-left ventricular (LV) outflow tract pressure gradient (PG(LVOT)) and in 23 controls. Original software was used to crop the 3D data into 18 radial planes; the mitral annulus, leaflets, coaptation point, protruding septum, and papillary muscles (PMs) tips were traced in each plane. The data were then reconstructed for 3D distance measurements and volumetric assessment. Shorter coaptation-septal distance (12 ± 4 vs. 21 ± 3 mm, P < 0.001), shorter inter-PM distance (13 ± 5 vs. 18 ± 4 mm, P = 0.02), and larger mitral tenting volume/body surface area (TVindex) (2.1 ± 1 vs. 0.5 ± 0.3 mL/m(2), P < 0.001) were associated with HCM(SAM) vs. control. PG(LVOT) increased with TVindex (r = 0.51, P = 0.01), and decreased with coaptation-septal distance(r = -0.83, P < 0.001) and the inter-PM distance (r = -0.69, P < 0.001) at mid-systole but not at mid-diastole (all P> 0.05). In addition, the coaptation-septal distance, TVindex, and inter-PM distance correlated each other (all P < 0.05). After adjustment for measures of mitral geometric change, the coaptation-septal distance was closely associated with PG(LVOT) (β = -0.73, P < 0.001).
  
  
  CONCLUSIONS
  these findings suggest that dynamic geometric changes by interaction of PMs, mitral tenting, and the coaptation point at mid-systole may be important contributors to outflow obstruction in HCM(SAM).
authors.affiliation: Cardiology Division, Yonsei Cardiovascular Center and Cardiovascular Research Institute, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, South Korea.
authors.forename: Hye Jin
authors.initials: HJ
authors.lastname: Hwang
authors.forename: Eui-Young
authors.initials: EY
authors.lastname: Choi
authors.forename: Jun
authors.initials: J
authors.lastname: Kwan
authors.forename: Sung Ai
authors.initials: SA
authors.lastname: Kim
authors.forename: Chi Young
authors.initials: CY
authors.lastname: Shim
authors.forename: Jong-Won
authors.initials: JW
authors.lastname: Ha
authors.forename: Se-Joong
authors.initials: SJ
authors.lastname: Rim
authors.forename: Namsik
authors.initials: N
authors.lastname: Chung
authors.forename: Sung Soon
authors.initials: SS
authors.lastname: Kim
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology; D019560:Echocardiography, Three-Dimensional; D005260:Female; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D012984:Software; D018709:Statistics, Nonparametric; D013599:Systole / Q000502:physiology; D014694:Ventricular Outflow Obstruction / Q000000981:diagnostic imaging* / Q000503:physiopathology*