title: Effective arterial elastance as index of arterial vascular load in humans.
abstract: BACKGROUND
  This study tested whether the simple ratio of ventricular end-systolic pressure to stroke volume, known as the effective arterial elastance (Ea), provides a valid measure of arterial load in humans with normal and aged hypertensive vasculatures.
  
  
  RESULTS
  Ventricular pressure-volume and invasive aortic pressure and flow were simultaneously determined in 10 subjects (four young normotensive and six older hypertensive). Measurements were obtained at rest, during mechanically reduced preload, and after pharmacological interventions. Two measures of arterial load were compared: One was derived from aortic input impedance and arterial compliance data using an algebraic expression based on a three-element Windkessel model of the arterial system [Ea(Z)], and the other was more simply measured as the ratio of ventricular end-systolic pressure to stroke volume [Ea(PV)]. Although derived from completely different data sources and despite the simplifying assumptions of Ea(PV), both Ea(Z) and Ea(PV) were virtually identical over a broad range of altered conditions: Ea(PV) = 0.97.Ea(Z) + 0.17; n = 33, r2 = 0.98, SEE = 0.09, p less than 0.0001. Whereas Ea(PV) also correlated with mean arterial resistance, it exceeded resistance by as much as 25% in older hypertensive subjects (because of reduced compliance and wave reflections), which better indexed the arterial load effects on the ventricle. Simple methods to estimate Ea (PV) from routine arterial pressures were tested and validated.
  
  
  CONCLUSIONS
  Ea(PV) provides a convenient, useful method to assess arterial load and its impact on the human ventricle. These results highlight effects of increased pulsatile load caused by aging or hypertension on the pressure-volume loop and indicate that this load and its effects on cardiac performance are often underestimated by mean arterial resistance but are better accounted for by Ea.
authors.affiliation: Department of Internal Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21205.
authors.forename: R P
authors.initials: RP
authors.lastname: Kelly
authors.forename: C T
authors.initials: CT
authors.lastname: Ting
authors.forename: T M
authors.initials: TM
authors.lastname: Yang
authors.forename: C P
authors.initials: CP
authors.lastname: Liu
authors.forename: W L
authors.initials: WL
authors.lastname: Maughan
authors.forename: M S
authors.initials: MS
authors.lastname: Chang
authors.forename: D A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000328:Adult; D001011:Aorta / Q000502:physiology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008955:Models, Cardiovascular; D008962:Models, Theoretical; D009200:Myocardial Contraction / Q000502:physiology; D011673:Pulsatile Flow / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology*; D014655:Vascular Resistance / Q000502:physiology*; D016276:Ventricular Function / Q000502:physiology