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Measurement of In-Vivo Pulmonary Vascular Impedance in Two Animal Models of Pulmonary Hypertension

[+] Author Affiliations
Kendall S. Hunter, Craig J. Lanning

The Children’s Hospital/UCHSC, Denver, CO

Joseph A. Albietz, Masahiko Oka, Karen A. Fagan, Kurt R. Stenmark

University of Colorado Health Sciences Center, Denver, CO

Robin Shandas

The Children’s Hospital/UCHSC, Denver, COUniversity of Colorado at Boulder, Boulder, CO

Paper No. SBC2007-175993, pp. 155-156; 2 pages
  • ASME 2007 Summer Bioengineering Conference
  • ASME 2007 Summer Bioengineering Conference
  • Keystone, Colorado, USA, June 20–24, 2007
  • Conference Sponsors: Bioengineering Division
  • ISBN: 0-7918-4798-5


Pulmonary vascular input impedance has been increasingly promoted as an important diagnostic for pulmonary arterial hypertension (PAH) [1,2]. The gold-standard clinical diagnostic for the disease, pulmonary vascular resistance (PVR), quantifies only the mean resistance to flow but ignores the impact of vascular stiffness and flow pulsatility, which in PAH can represent up to 40% of the total load presented to the right ventricle. PVR has also been found to be only a moderate predictor of PAH outcomes [3]. The first of these deficiencies is not present in impedance; clinical studies have found the sum of its 1st and 2nd harmonic moduli to have good correlation (r2 = 0.812) with global pulmonary vascular stiffness (PVS) [2], a hemodynamically-measured quantifier of vascular stiffness. Additionally, the 0th harmonic modulus of impedance has excellent correlation to PVR (r2 = 0.974); thus, it also quantifies the resistive load. Moreover, because PVS has recently been found as a valuable determinant of mortality in PAH [4], we believe that impedance, as a combined measure of PVR and PVS, might be an excellent predictor of disease outcomes.



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