title: Left ventricular shape is the primary determinant of functional mitral regurgitation in heart failure.
abstract: OBJECTIVE
  The aim of this study was to examine the temporal association between the onset of functional mitral regurgitation and the development of changes in left ventricular shape, chamber enlargement, mitral anulus dilation and regional wall motion abnormalities during the course of evolving heart failure.
  
  
  BACKGROUND
  Despite extensive characterization, the exact etiology of functional mitral regurgitation in patients with chronic heart failure remains unknown.
  
  
  METHODS
  Heart failure was produced in seven dogs by multiple sequential intracoronary microembolizations. Serial changes in left ventricular chamber volume and shape were evaluated from ventriculograms. Changes in mitral anulus diameter and ventricular regional wall motion abnormalities were evaluated echocardiographically. The presence and severity of mitral regurgitation were determined with Doppler color flow mapping. Measurements were obtained at baseline and then biweekly until mitral regurgitation was first observed.
  
  
  RESULTS
  No dog had mitral regurgitation at baseline but all developed mild to moderate regurgitation 12 +/- 1 weeks after the first embolization. The onset of mitral regurgitation was not associated with an increase in left ventricular end-diastolic volume relative to baseline (58 +/- 3 vs. 62 +/- 3 ml), mitral anulus diameter (2.4 +/- 0.1 vs. 2.4 +/- 0.1 cm) or wall motion abnormalities of left ventricular wall segments overlying the papillary muscles. In contrast, the onset of mitral regurgitation was accompanied by significant changes in global left ventricular shape evidenced by increased end-systolic chamber sphericity index (0.22 +/- 0.02 vs. 0.30 +/- 0.01) (p < 0.01) and decreased end-systolic major axis/minor axis ratio (1.71 +/- 0.05 vs. 1.43 +/- 0.04) (p < 0.001).
  
  
  CONCLUSIONS
  These data indicate that transformation of left ventricular shape (increased chamber sphericity) is the most likely substrate for the development of functional mitral regurgitation.
authors.affiliation: Henry Ford Heart and Vascular Institute, Division of Cardiovascular Medicine, Detroit, Michigan.
authors.forename: T
authors.initials: T
authors.lastname: Kono
authors.forename: H N
authors.initials: HN
authors.lastname: Sabbah
authors.forename: H
authors.initials: H
authors.lastname: Rosman
authors.forename: M
authors.initials: M
authors.lastname: Alam
authors.forename: S
authors.initials: S
authors.lastname: Jafri
authors.forename: S
authors.initials: S
authors.lastname: Goldstein
mesh_terms: D000792:Angiography; D000818:Animals; D006328:Cardiac Catheterization; D003971:Diastole; D004195:Disease Models, Animal; D004285:Dogs; D015150:Echocardiography, Doppler; D005069:Evaluation Studies as Topic; D006333:Heart Failure / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000175:diagnosis / Q000209:etiology / Q000473:pathology*; D012720:Severity of Illness Index; D013318:Stroke Volume; D013599:Systole; D013997:Time Factors