Author + information
- Received March 3, 1992
- Revision received April 27, 1992
- Accepted May 29, 1992
- Published online November 15, 1992.
- Thomas Wisenbaugh, MD, FACC∗,
- Rafique Essop, MD,
- Shirley Middlemost, MD,
- John Skoularigis, MD and
- Pinhas Sareli, MD, FACC
- ↵∗Address for correspondence: Thomas Wisenbaugh, MD, Cardiology Department, Baragwanath Hospital, P.O. Bertsham 2013, Johannesburg, South Africa.
Objectives. 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 ≥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/cm2in 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−5in group I, p = 0.05) and end-systolic wall stress (273 vs. 226 kdynes/cm2in 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−5in 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, respeditely, in group I (to 2.1 cm2and 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 tower 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.
☆ This study was presented in part at the 40th Scientific Session of American College of Cardiology, Atlanta, Georgia, March 1991.
- Received March 3, 1992.
- Revision received April 27, 1992.
- Accepted May 29, 1992.