title: Reduced left ventricular compliance in human mitral stenosis. Role of reversible internal constraint.
abstract: BACKGROUND
  The mechanisms of depressed left ventricular (LV) pump performance in human mitral stenosis (MS) remain poorly understood, because reduced filling alone affects many hemodynamic measurements. Therefore, pressure-volume relations were examined in nine subjects with MS and compared with eight age-matched normal controls.
  
  
  RESULTS
  Data were obtained by conductance catheter/micromanometer technique with transient inferior vena cava occlusion used to alter load and generate pressure-volume relations. In a subset of patients (n = 5), data were obtained both acutely and at 3 months (n = 4) after balloon valvuloplasty. MS patients had reduced cardiac output (3.3 +/- 0.9 versus 5.6 +/- 1.7 l/min) and end-diastolic volume (68.0 +/- 6.9 versus 115 +/- 31 ml) versus controls (p less than 0.001), with a mean transvalvular gradient of 14 +/- 6 mm Hg and estimated valve area of 0.6 +/- 0.2 cm2. Systolic function as assessed by the end-systolic pressure-volume relation was virtually the same in MS and control subjects. In contrast, end-diastolic pressure-volume relations in MS were consistently shifted leftward and had an increased slope (lower compliance) at matched pressure ranges (6.5 +/- 3.0 versus 2.2 +/- 0.53 ml/mm Hg at a mean diastolic pressure of 8 mm Hg, p less than 0.001). This change was not a result of reduced LV filling or probably of increased right heart loading. Valvuloplasty acutely returned chamber compliance to near normal, a change that was sustained at 3-month follow-up. Systolic function was little altered at this time.
  
  
  CONCLUSIONS
  These data indicate an impairment of diastolic function in human MS that can be acutely reversed by balloon valvuloplasty. Lowered LV compliance probably results from a functional restriction caused by ventricular attachment to a thickened and immobile valve apparatus.
authors.affiliation: Department of Internal Medicine, Johns Hopkins Medical Institutions, Baltimore, Md.
authors.forename: C P
authors.initials: CP
authors.lastname: Liu
authors.forename: C T
authors.initials: CT
authors.lastname: Ting
authors.forename: T M
authors.initials: TM
authors.lastname: Yang
authors.forename: J W
authors.initials: JW
authors.lastname: Chen
authors.forename: M S
authors.initials: MS
authors.lastname: Chang
authors.forename: W L
authors.initials: WL
authors.lastname: Maughan
authors.forename: W
authors.initials: W
authors.lastname: Lawrence
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D006328:Cardiac Catheterization; D002302:Cardiac Output / Q000502:physiology; D002404:Catheterization; D006801:Humans; D008365:Manometry / Q000379:methods; D008875:Middle Aged; D008946:Mitral Valve Stenosis / Q000503:physiopathology* / Q000628:therapy; D009200:Myocardial Contraction / Q000502:physiology*; D012214:Rheumatic Heart Disease / Q000503:physiopathology / Q000628:therapy; D013318:Stroke Volume / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*