title: Excessive vasoconstriction in rheumatic mitral stenosis with modestly reduced ejection fraction.
abstract: OBJECTIVE
  The primary hypothesis examined was that underfilling due to inflow obstruction accounts for modestly depressed ejection performance in mitral stenosis. Having found little evidence to support this hypothesis, we sought to determine other factors that might differentiate patients with different levels of ejection performance.
  
  
  METHODS
  Ventricular load and performance were compared in two groups of patients before and immediately after successful balloon valvuloplasty that was not complicated by mitral regurgitation: those in whom prevalvuloplasty ejection fraction was > or = 0.55 (group I, n = 10) and those in whom it was < 0.55 (group II, n = 11).
  
  
  RESULTS
  Before valvuloplasty, mitral valve area was less in group II (0.65 cm2) than in group I (0.84 cm2, p = 0.02), but end-diastolic pressure (12 vs. 12 mm Hg in group I), end-diastolic wall stress (46 vs. 44 kdynes/cm2 in group I) and end-diastolic volume (152 vs. 150 ml in group I) were not less in group II, nor were these variables significantly reduced compared with those of a normal control group. In group II, end-systolic volume was larger (77 vs. 55 ml in group I, p = 0.001) and cardiac output was less (3.1 vs. 3.6 liters/min in group I, p = 0.03), possibly owing to higher systemic vascular resistance (2,438 vs. 1,921 dynes.s.cm-5 in group I, p = 0.05) and end-systolic wall stress (273 vs. 226 kdynes/cm2 in group I, p = 0.06), although mean arterial pressure in the two groups was similar (91 vs. 84 mm Hg in group I, p = 0.22). Group II patients also had higher values for pulmonary vascular resistance (712 vs. 269 dynes.s.cm-5 in group I, p = 0.03) and mean pulmonary artery pressure (47 vs. 29 mm Hg in group I, p = 0.02) despite similar values for mean left atrial pressure (20 vs. 18 mm Hg in group I, p = 0.35). After valvuloplasty, mitral valve area increased by 2.5- and 3-fold, respectively, in group I (to 2.1 cm2) and group II (to 2.0 cm2). Modest increases in left ventricular end-diastolic pressure, end-diastolic stress and end-diastolic volume (+9%) after valvuloplasty were statistically significant only for group II. End-systolic wall stress did not decline in either group II (281 kdynes/cm2) or group I (230 kdynes/cm2), and ejection fraction failed to increase significantly (0.49 to 0.51 for group II and 0.62 to 0.61 for group I) after valvuloplasty. Contractile performance estimated with a preload-corrected ejection fraction-afterload relation was within or near normal limits in all 19 patients in whom it was assessed.
  
  
  CONCLUSIONS
  Excessive vasoconstriction may account for the higher afterload, lower ejection performance and lower cardiac output observed in a subset of patients with mitral stenosis because contractile dysfunction could not be detected and left ventricular filling--which was not subnormal despite severe inflow obstruction--improved only modestly after valvuloplasty.
authors.affiliation: Baragwanath Hospital, Johannesburg, South Africa.
authors.forename: T
authors.initials: T
authors.lastname: Wisenbaugh
authors.forename: R
authors.initials: R
authors.lastname: Essop
authors.forename: S
authors.initials: S
authors.lastname: Middlemost
authors.forename: J
authors.initials: J
authors.lastname: Skoularigis
authors.forename: P
authors.initials: P
authors.lastname: Sareli
mesh_terms: D000293:Adolescent; D000328:Adult; D000704:Analysis of Variance; D006328:Cardiac Catheterization; D002404:Catheterization / Q000706:statistics & numerical data; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008943:Mitral Valve; D008944:Mitral Valve Insufficiency / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D008946:Mitral Valve Stenosis / Q000453:epidemiology / Q000503:physiopathology* / Q000628:therapy; D012214:Rheumatic Heart Disease / Q000453:epidemiology / Q000503:physiopathology* / Q000628:therapy; D013318:Stroke Volume; D014661:Vasoconstriction