Effect of Effective Arterial Elastance on Left Ventricular Systolic Function in Severe Valvular Aortic Stenosis

pp 278-285

Abstract

Background
Left ventricular dysfunction in valvular aortic stenosis (AS) is related to an elevated afterload. This increase may be related to a reduction in aortic valve area (AVA), to changes in ventricular geometry and to the characteristics of the arterial vessels. Effective arterial elastance (Ea) is an index of arterial vascular load which incorporates the characteristic arterial impedance, arterial resistance and arterial compliance.

Objective
To assess the effect of Ea on left ventricular systolic function in severe valvular AS.

Material and Methods
We prospectively studied 54 patients with severe AS; transvalvular gradient, AVA, valvular resistance and energy loss index were assessed. Ea was estimated as the end-systolic pressure/stroke volume ratio. Carotid blood pressure waveform was calibrated against blood pressure measured by conventional cuff sphygmomanometry to calculate end-systolic pressure. We estimated global afterload by the “valvulo-arterial impedance” (Zva) formulated as follows: (systolic arterial pressure + mean net pressure gradient)/stroke-volume index. Zva considers the effect of AS and Ea. Patients were divided in three groups: G1, AS with
heart failure (NYHA III-IV) (n = 13), G2, symptomatic AS without heart failure (n = 13), and G3, asymptomatic AS (n =28).

Results
Ejection fraction (EF) (%) was lower in G1 (33±15) compared to G2 (42±16) and to G3 (65±14); p<0.01. Ea (mm Hg/ml) and Zva (mm Hg/ml/m2) were greater in G1 (2.46±0.8 and 6.5±2.2, respectively) than in G2 and G3 (1.83±0.52 and 1.73±0.47; p<0.01, and 4.8±1.0 y 4.7±1.5; p < 0.01, respectively). When univariate analysis was performed, Zva correlated with Ea (r=0.88; p<0.0001) and EF (r=-0.41; p<0.01). In multivariate analysis Ea and Zva were independent predictors for EF.

Conclusions
In severe AS, the increase of the vascular component of the afterload, assessed by the Ea, contributes to a reduction in systolic function.