|| Checking for direct PDF access through Ovid
Effort intolerance, measured objectively by reduced peak oxygen consumption (VO2), has been considered as an important prognosticator in degenerative mitral regurgitation (MR). However, its mechanism is unknown.In 25 asymptomatic/minimally symptomatic patients with grade III+ or greater degenerative MR undergoing semisupine invasive exercise testing, Doppler estimates and invasive measurement of systolic (SPAP) and mean pulmonary artery pressure (MPAP) and cardiac output (CO) were simultaneously obtained. Echocardiographic estimates of SPAP, MPAP, and CO correlated well with invasive measurement at peak exercise (bias, SPAP, −0.7±7.4 mm Hg; MPAP, 1.2±6.3 mm Hg; CO, 0.2±2.5 L/min). Heart rate reserve (β, 3.997; 95% CI, 2.704–5.290 per 41.5% increase; P<0.001), MPAP/CO slope (β, −3.846; 95% CI, −5.926 to −1.766 per 4.85 mm Hg/L per minute increase; P=0.001), and tricuspid annular plane systolic excursion/SPAP slope (β, 4.094; 95% CI, 2.252–5.936 per 0.22 mm/mm Hg increase; P=0.003) were associated with peak VO2 even after adjustment for increase in MR vena contracta during exercise and peak SPAP. The MPAP/CO slope of 4.13 had a sensitivity and a specificity for predicting effort intolerance (%predicted peak VO2 <70%) of 57% and 91%, respectively, whereas the tricuspid annular plane systolic excursion/SPAP slope of 0.25 had a respective sensitivity and specificity of 86% and 82%.The agreement between echocardiographic and invasive measures of pulmonary artery pressures and CO during exercise is acceptable. In patients with degenerative MR, effort intolerance is predominantly because of chronotropic incompetence, abnormal pulmonary vascular reserve, and limited right ventricular contractile reserve and not simply because of exercise-induced MR or pulmonary hypertension.