title: Surgical treatment of ischemic mitral regurgitation might not influence ventricular remodeling.
abstract: OBJECTIVE
  Surgical treatment for ischemic mitral regurgitation has become more aggressive. However, no clinical study has demonstrated that surgical correction of chronic ischemic mitral regurgitation improves survival. We used 4 well-developed ovine models of postinfarction left ventricular remodeling to test the hypothesis that ischemic mitral regurgitation does not significantly contribute to postinfarction left ventricular remodeling.
  
  
  METHODS
  Infarction of 21% to 24% of the left ventricular mass was induced by means of coronary ligation in 77 sheep. Infarctions varied only by anatomic location in the left ventricle: anteroapical, n = 26; anterobasal, n = 16; laterobasal, n = 9; and posterobasal, n = 20. Six additional sheep had ring annuloplasty before posterobasal infarction. End-systolic and end-diastolic left ventricular volume, end-systolic muscle-to-cavity area ratio, left ventricular sphericity, ejection fraction, and degree of ischemic mitral regurgitation, as determined by means of quantitative echocardiography, were assessed before infarction and at 2, 5, and 8 weeks after infarction.
  
  
  RESULTS
  All infarcts resulted in significant postinfarction remodeling and decreased ejection fraction. Anteroapical infarcts lead to left ventricular aneurysms. Only posterobasal infarcts caused severe and progressive ischemic mitral regurgitation. Remodeling because of posterobasal infarcts was not more severe than that caused by infarcts at other locations. Furthermore, prophylactic annuloplasty prevented the development of mitral regurgitation after posterobasal infarction but had no effect on remodeling.
  
  
  CONCLUSIONS
  The extent of postinfarction remodeling is determined on the basis of infarct size and location. The development of ischemic mitral regurgitation might not contribute significantly to adverse remodeling. Ischemic mitral regurgitation is likely a manifestation rather than an important impetus for postinfarction remodeling.
authors.affiliation: Harrison Department of Surgical Research, University of Pennsylvania School of Medicine, Philadelphia, USA.
authors.forename: Yoshiharu
authors.initials: Y
authors.lastname: Enomoto
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Gorman
authors.forename: Sina L
authors.initials: SL
authors.lastname: Moainie
authors.forename: T Sloane
authors.initials: TS
authors.lastname: Guy
authors.forename: Benjamin M
authors.initials: BM
authors.lastname: Jackson
authors.forename: Landi M
authors.initials: LM
authors.lastname: Parish
authors.forename: Theodore
authors.initials: T
authors.lastname: Plappert
authors.forename: Ahmad
authors.initials: A
authors.lastname: Zeeshan
authors.forename: Martin G
authors.initials: MG
authors.lastname: St John-Sutton
authors.forename: Robert C
authors.initials: RC
authors.lastname: Gorman
mesh_terms: D000818:Animals; D002908:Chronic Disease; D004195:Disease Models, Animal; D008297:Male; D008944:Mitral Valve Insufficiency / Q000503:physiopathology* / Q000601:surgery*; D012756:Sheep; D013318:Stroke Volume; D020257:Ventricular Remodeling