Relationship of contractile state to ejection performance in patients with chronic aortic valve disease.

Abstract

To assess the relative contributions of afterload mismatch and impaired contractility to pump dysfunction in patients with chronic aortic valve disease, simultaneous left ventricular cineangiography and micromanometry were performed in 56 patients: 21 with severe aortic stenosis, 16 with severe aortic regurtitation, and 19 normal control subjects. Left ventricular mass was increased in patients with aortic stenosis and aortic regurgitation (172 + 52 and 224 ± 63 g/m2, respectively, vs 89 + 16 for control subjects; p < .05) as were end-diastolic volume (101 ± 39 and 167 ± 44 vs 77 + 16 ml/m2; p < .05) and end-systolic volume (50 + 40 and 84 ± 43 vs 24 7 ml/m2; p < .05). Although ejection fraction was depressed in both abnormal groups (0.56 ± 0.18 for patients with aortic stenosis and 0.53 + 0.13 for those with aortic regurgitation vs 0.69 0.05 for control subjects; p < .05), the decrease in ejection fraction was disproportionate to the mild degree of afterload mismatch (end ejection stress 129 + 17 in patients with aortic stenosis and 154 ± 58 in those with aortic regurgitation vs 117 46 kdyn/cm2 in control subjects; p = NS) with 10 of 21 patients with aortic stenosis and 12 of 16 patients with aortic regurgitation falling below the 95% prediction limit of the linear inverse relationship between ejection fraction and end-systolic stress for controls (EF = 0.78 -0.00074.ESS). The maximum stress:volume index ratio, which is an index of inotropic state that is independent of preload but sensitive to afterload, was also depressed in patients with aortic stenosis and aortic regurgitation (3.8 ± 1.4 and 2.5 ± 0.9 vs 5.0 1.3 kdyn/cm5/m2 for control subjects; p < .05), and first-order partial correlation demonstrated that this decrease was inversely related to left ventricular mass index. Thus, although afterload mismatch may adversely affect ventricular performance in patients with aortic valve disease, extensive hypertrophy and contractile dysfunction appear to be the major determinants of pump dysfunction. Circulation 73, No. 1, 47-53, 1986. AFTERLOAD MISMATCH has been recognized as a cause of impaired pump performance in patients with chronic aortic valve disease.'-5 However, separating the effect of myocardial contractile dysfunction from that of afterload mismatch on pump performance has been difficult because of the lack of a load-independent index of contractile function.Recently, the relationship between end-systolic stress and either ejection fraction or end-systolic volume has been used to estimate myocardial contractile

Left ventricular mass: impact on left ventricular contractile function and its reversibility in patients undergoing aortic valve replacement

“…An association between the development of hypertrophy and contractile dysfunction was reported by Wisenbaugh et al [11], and our findings confirm those results and also suggest that contractile dysfunction develops at similar degrees of hypertrophy, regardless of the type of aortic valve lesion. In the present study, the AS and AR subgroups within the same contractile group had equivalent amounts of hypertrophy (increased LV mass index), though they showed distinctly different hemodynamic characteristics and geometric patterns of hypertrophy.…”

The relationship of afterload to ejection performance in chronic mitral regurgitation.

“…The absence of such a displacement suggests that these ventricles may have been operating with diminished contractility and were using preload reserve to merely maintain a normal level of performance.32 In contrast, patients with mitral regurgitation and a reduced ejection fraction were downwardly displaced. The precise response of the normal ventricle to a sustained increase in afterload remains to be elucidated34' 35 41; however, group 3 patients clearly fell below the confidence interval defined by the control group. In the setting of normal muscle fiber stretch and elevated end-diastolic pressure and stress, the depression of * References 2, 4, 9, 21, 30, 34, 35, 40, 41.…”

Relation of left ventricular filling dynamics to alterations in load and compliance in patients with and without pressure-overload hypertrophy.

“…We previously have shown the intraobserver and interobserver variability of our volume measurements to be approximately 5%. 13 To make the volume-time waveform analysis as objective as possible, the data were fit to 9-llth-order polynomial equations with a Marquardt curve-fitting program. Differentiation of this equation at each frame with respect to time (dV/dT) yields instantaneous flow rate.…”