Left ventricular relaxation in patients with left ventricular hypertrophy secondary to aortic valve disease

Abstract

We studied 58 patients with aortic valve disease (AVD). Twenty-three patients had aortic stenosis (AS), 17 aortic insufficiency (AI) and 18 combined lesion (AS + AI). In these 58 patients and in 10 control subjects, left ventricular (LV) high-fidelity pressure and single-beam echocardiographic measurements were carried out simultaneously. Relaxation was assessed from peak negative dP/dt (index of left-heart relaxation) and peak negative dS/dt (index of myocardial relaxation, S = meridional wall stress). Peak negative dP/dt was 1793, 1645 and 1373 mm Hg/sec in AS, AS + AI and AI, respectively, and did not differ from the value in control subjects (1589 mm Hg/sec). LV peak systolic pressure was higher in AS (212 mm Hg, p < 0.01), AS + AI (190 mm Hg, p < 0.01) and AI (144 mm Hg, p < 0.02) than in control subjects (116 mm Hg). In contrast, peak negative dS/dt was increased in AS (1415.103 dyn/cm2/sec, p < 0.01), in AS + AI (1467.103 dyn/cm2/sec), p < 0.01 and in AI (1355.10 3 dyn/cm 2/sec, p < 0.02) compared with control subjects, (900.103 dyn/cm 2/sec. LV S(peak) was 131.103 dyn/cm2 in controls and was increased (p < 0.01) in all three groups with AVD (261, 257 and 212.103 dyn/cm2, respectively). Linear regression analysis between peak negative dS/dt and S(peak) yielded significant correlations in controls (r = 0.84), in 27 patients with AVD and normal LV systolic function (r = 0.79) and 31 patients with AVD and depressed LV systolic function (r = 0.79). Slopes and intercepts of these three regressions did not differ significantly. In 33 patients with AVD (12 AS, 11 AS + AI, 10 AI) in whom the early relaxation phase (A2 to mitral valve opening) could be determined from combined echophono measurements the time constant of LV pressure decay (T) was calculated from the regression plot of negative dP/dt vs LV pressure. T, which was also considered an index of chamber relaxation, was increased in AS (67 msec, p < 0.01), in AS + AI (68 msec, p < 0.01) and in AI (56 msec, p < 0.05) compared with control subjects (41 msec). T was similar in 20 patients with depressed and 13 with normal LV systolic function. T did not correlate with S(peak) but did correlate with LV angiographic mass (p < 0.01, r = 0.40). We conclude that in LV hypertrophy secondary to AVD, the speed of left-heart relaxation is impaired, but the peak rate of myocardial relaxation is unaltered. Abnormalities of LV systolic function have no direct bearing on relaxation, and the extent of LV hypertrophy appears to be a determinant of left-heart relaxation.