title: Role of inadequate adaptive left ventricular hypertrophy in the genesis of mitral regurgitation in patients with severe aortic stenosis: implications for its prevention.
abstract: OBJECTIVE
  Mitral regurgitation (MR) is frequent in patients with severe calcific aortic stenosis (AS). This complicates not only the clinical course of AS, but also its surgical management. The aim of the present study was to investigate the mechanism of genesis of MR in patients with severe AS.
  
  
  METHODS
  The echocardiographic database was searched for subjects with severe AS defined as a calculated (continuity equation) aortic valve area < 0.7 cm2. Patients with previous valve surgery were excluded; thus, the study group comprised 123 patients.
  
  
  RESULTS
  Among 123 patients (mean age 75 +/- 10 years) with severe AS, 54 (44%) had no MR, 37 (30%) had mild MR, 20 (16%) had moderate MR, and 12 (10%) had severe MR. Hence, moderate or severe MR was present in approximately 25% of patients. Patients with moderate or severe MR had a larger left ventricular (LV) end-diastolic diameter (5.1 +/- 1.0 versus 4.8 +/- 0.8 cm; p = 0.08), larger LV end-systolic diameter (3.8 +/- 1.2 versus 3.1 +/- 0.8 cm; p = 0.001), lower LV ejection fraction (40 +/- 16 versus 58 +/- 18%; p = 0.0001), higher degree of aortic regurgitation (p = 0.002), larger left atrial diameter (4.7 +/- 0.9 versus 4.1 +/- 0.6 cm; p = 0.001), lower LV free wall thickness (1.1 +/- 0.2 versus 1.3 +/- 0.4 cm; p = 0.05), and lower combined wall thickness (2.4 +/- 0.3 versus 2.7 +/- 0.5 cm; p = 0.02) and relative wall thickness (0.5 +/- 0.1 versus 0.6 +/- 0.1 cm; p = 0.02). Both groups had similar degrees of AS and mitral annular calcification.
  
  
  CONCLUSIONS
  MR in severe AS is associated with a larger LV size and lesser wall thickness, and this may result from failure of adequate adaptive LV hypertrophy necessitated by the pressure overload imposed by AS. This might have important clinical implications in terms of timing of aortic valve replacement before the left ventricle begins to dilate, and also in the choice of pharmacologic therapy that may modulate the adaptive response of the left ventricle.
authors.affiliation: Loma Linda University Loma Linda, CA 92354, USA.
authors.forename: Sanjeev
authors.initials: S
authors.lastname: Palta
authors.forename: Kanwaljit S
authors.initials: KS
authors.lastname: Gill
authors.forename: Ramdas G
authors.initials: RG
authors.lastname: Pai
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001021:Aortic Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D001022:Aortic Valve Insufficiency / Q000235:genetics / Q000517:prevention & control; D001024:Aortic Valve Stenosis / Q000235:genetics* / Q000517:prevention & control; D004452:Echocardiography; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics / Q000517:prevention & control; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000235:genetics* / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000000981:diagnostic imaging / Q000503:physiopathology; D008944:Mitral Valve Insufficiency / Q000235:genetics* / Q000517:prevention & control; D012189:Retrospective Studies; D012720:Severity of Illness Index; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology