Abstract 18641: Relationship Between Effective Arterial Elastance and Specific Measures of Left Ventricular Afterload
Background: Effective arterial elastance (EA), 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 EA is not prominently affected by arterial stiffness or pulsatile load. However, empirical data assessing the relationship between EA and specific measures of arterial load are not available.
Methods: We used multiple linear regression to assess the relationship between EA 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 EA 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 EA were unrelated to changes in indices of pulsatile load in response to either intervention (all R2<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 EA 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.
- © 2013 by American Heart Association, Inc.