• DOI:10.1152/AJPHEART.00336.2006
• Corpus ID: 3111832

Quantification of right ventricular afterload in patients with and without pulmonary hypertension.

@article{Lankhaar2006QuantificationOR,
  title={Quantification of right ventricular afterload in patients with and without pulmonary hypertension.},
  author={J. W. Lankhaar and Nico Westerhof and Theo J. C. Faes and Koen M.J. Marques and J. Tim Marcus and Pieter E Postmus and Anton Vonk-Noordegraaf},
  journal={American journal of physiology. Heart and circulatory physiology},
  year={2006},
  volume={291 4},
  pages={
          H1731-7
        }
}

• J. Lankhaar, N. Westerhof, +4 authors A. Vonk-Noordegraaf
• Published 1 October 2006
• Medicine, Biology
• American journal of physiology. Heart and circulatory physiology

Right ventricular (RV) afterload is commonly defined as pulmonary vascular resistance, but this does not reflect the afterload to pulsatile flow. The purpose of this study was to quantify RV afterload more completely in patients with and without pulmonary hypertension (PH) using a three-element windkessel model. The model consists of peripheral resistance (R), pulmonary arterial compliance (C), and characteristic impedance (Z). Using pulmonary artery pressure from right-heart catheterization and pulmonary artery flow from MRI velocity quantification, we estimated the windkessel parameters in patients with chronic thromboembolic PH (CTEPH; n = 10) and idiopathic pulmonary arterial hypertension (IPAH; n = 9). Patients suspected of PH but in whom PH was not found served as controls (NONPH; n = 10). R and Z were significantly lower and C significantly higher in the NONPH group than in both the CTEPH and IPAH groups (P < 0.001). R and Z were significantly lower in the CTEPH group than in the IPAH group (P < 0.05). The parameters R and C of all patients obeyed the relationship C = 0.75/R (R(2) = 0.77), equivalent to a similar RC time in all patients. Mean pulmonary artery pressure P and C fitted well to C = 69.7/P (i.e., similar pressure dependence in all patients). Our results show that differences in RV afterload among groups with different forms of PH can be quantified with a windkessel model. Furthermore, the data suggest that the RC time and the elastic properties of the large pulmonary arteries remain unchanged in PH.