Abstract 16054: Ventricular-Arterial Coupling Biphasically Correlates to Ventricular Diastolic Chamber Stiffness in Children–Association With Aldosterone Activation

Abstract

Introduction: Left ventricular–arterial coupling (LVAC), the ratio of end–systolic to effective arterial elastance (Ees/Ea), determines end–systolic pressure and stroke volume in a given preload. LV diastolic chamber stiffness (LV–K) is an important diastolic property to affect LV filling. However, the relationship between Ees/Ea and LV–K in children remains unestablished. Aldosterone (ALD) accelerates LV and arterial stiffening. Hypothesis: This study was undertaken to test the hypothesis that Ees/Ea may affect LV–K through ALD regulation in children. Methods: During catheterizations for children with biventricular circulation (N=75, median 2.5 years), blood samples for ALD were collected, and LV pressure and area relationships (PAR) were recorded using high-fidelity pressure–guidewire and echocardiographic AQ method during steady state and transient IVC occlusion. LV–K was obtained by dividing the pressure difference between LV minimal and end-diastolic pressure (EDP) by stroke volume. ALD levels were transformed into common logarithm. Results: Ees/Ea biphasically correlated to LV–K, which was approximated by downward convex parabola with a minimum at 0.9 of Ees/Ea (R=0.61, P<0.0001). Ees/Ea also bipahsically correlated to log ALD, which was approximated by downward convex parabola with a minimum at 0.8 of Ees/Ea (R=0.45, P<0.005). Moreover, LV–K linearly correlated to log ALD (R=0.38, P<0.005). There was no significant relationship between LV–K and relative wall thickness. Conclusions: To our knowledge, this is the first study to demonstrate that Ees/Ea bipahsically correlated to LV–K and ALD. Dilated LV with low Ees/Ea accompanies elevated filling pressure and shows restrictive physiology with higher LV–K. On the other hand, when Ees/Ea is higher than normal range, this study indicates that there should be an increased LV diastolic stiffness which is not always associated with wall hypertrophy. Because LVAC abnormality may induce LV stiffening associated with ALD activation, chronic inhibition therapy of renin–angiotensin system to keep Ees/Ea within appropriate range may inhibit LV stiffening directly and through LVAC & LV–K interaction.