title: Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation.
abstract: OBJECTIVE
  This study aimed to separate proposed mechanisms for segmental ischemic mitral regurgitation (MR), including left ventricular (LV) dysfunction versus geometric distortion by LV dilation, using models of acute and chronic segmental ischemic LV dysfunction evaluated by three-dimensional (3D) echocardiography.
  
  
  BACKGROUND
  Dysfunction and dilation-both mechanisms with practical therapeutic implications-are difficult to separate in patients.
  
  
  METHODS
  In seven dogs with acute left circumflex (LCX) coronary ligation, LV expansion was initially restricted and then permitted to occur. In seven sheep with LCX branch ligation, LV expansion was also initially limited but became prominent with remodeling over eight weeks. Three-dimensional echo reconstruction quantified mitral apparatus geometry and MR volume.
  
  
  RESULTS
  In the acute model, despite LV dysfunction with ejection fraction = 23 +/- 8%, MR was initially trace with limited LV dilation, but it became moderate with subsequent prominent dilation. In the chronic model, MR was also initially trace, but it became moderate over eight weeks as the LV dilated and changed shape. In both models, the only independent predictor of MR volume was increased tethering distance from the papillary muscles (PMs) to the anterior annulus, especially medial and posterior shift of the ischemic medial PM, measured by 3D reconstruction (r2 = 0.75 and 0.86, respectively). Mitral regurgitation volume did not correlate with LV ejection fraction or dP/dt.
  
  
  CONCLUSIONS
  Segmental ischemic LV contractile dysfunction without dilation, even in the PM territory, fails to produce important MR. The development of MR relates strongly to changes in the 3D geometry of the mitral apparatus, with implications for approaches to restore a more favorable configuration.
authors.affiliation: Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Otsuji
authors.forename: M D
authors.initials: MD
authors.lastname: Handschumacher
authors.forename: N
authors.initials: N
authors.lastname: Liel-Cohen
authors.forename: H
authors.initials: H
authors.lastname: Tanabe
authors.forename: L
authors.initials: L
authors.lastname: Jiang
authors.forename: E
authors.initials: E
authors.lastname: Schwammenthal
authors.forename: J L
authors.initials: JL
authors.lastname: Guerrero
authors.forename: L A
authors.initials: LA
authors.lastname: Nicholls
authors.forename: G J
authors.initials: GJ
authors.lastname: Vlahakes
authors.forename: R A
authors.initials: RA
authors.lastname: Levine
mesh_terms: D000818:Animals; D002306:Cardiac Volume / Q000502:physiology; D003327:Coronary Disease / Q000000981:diagnostic imaging*; D004285:Dogs; D019560:Echocardiography, Three-Dimensional; D005260:Female; D008297:Male; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging*; D010210:Papillary Muscles / Q000000981:diagnostic imaging; D012756:Sheep; D013318:Stroke Volume / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging*