Abstract 18641: Relationship Between Effective Arterial Elastance and Specific Measures of Left Ventricular Afterload

Abstract

Background: Effective arterial elastance (E A ), the ratio of left ventricular (LV) end-systolic pressure and stroke volume, was proposed as a lumped parameter that incorporates pulsatile and resistive afterload and is increasingly being used in clinical studies. In conjunction with LV end-systolic elastance, it is used to assess combined “ventricular-arterial stiffening”. However, theoretical modeling studies indicate that E A is not prominently affected by arterial stiffness or pulsatile load. However, empirical data assessing the relationship between E A and specific measures of arterial load are not available. Methods: We used multiple linear regression to assess the relationship between E A and arterial load determined non-invasively from time-resolved central pressure-flow analyses performed at rest in a diverse clinical population of adults (n=133). We also investigated the sensitivity of E A to detect changes in pulsatile load induced by isometric handgrip exercise (n=72) and by the administration of 0.4 mg of sublingual nitroglycerin (n=30). Results: Measurements at rest demonstrated that Ea was essentially a function of SVR (standardized β=0.99; P <0.0001), and heart rate (standardized β=0.18; P <0.0001), without significant contributions from aortic characteristic impedance (standardized β=0.0001; P =0.98), total arterial compliance (standardized β=0.007; P =0.63) or reflection magnitude (β=0.02; P =0.20). Despite pronounced changes in indices of pulsatile load induced by isometric exercise and sublingual nitroglycerin, changes in E A were unrelated to changes in indices of pulsatile load in response to either intervention (all R 2 <0.02). However, changes in Ea were essentially a linear function of the change in the SVR*heart rate product (isometric exercise R=0.98; nitroglycerin R=0.97; both P <0.0001). Conclusions: Our empirical findings demonstrate, in agreement with modeling studies, that E A is essentially a function of resistive afterload and heart rate and is negligibly influenced by (and insensitive to) variations in pulsatile afterload. Its current interpretation as a lumped parameter of pulsatile and resistive afterload should thus be reassessed.