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Am J Physiol Heart Circ Physiol (May 12, 2006). doi:10.1152/ajpheart.00336.2006
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Submitted on March 30, 2006
Accepted on May 8, 2006

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

Jan-Willem Lankhaar1*, Nicolaas Westerhof2, Theo J.C. Faes3, Koen M. J. Marques4, J. Tim Marcus3, Piet E. Postmus5, and Anton Vonk-Noordegraaf5

1 Physics and medical technology, VU University Medical Center, Amsterdam, Netherlands; Pulmonary Diseases, VU University Medical Center, Amsterdam, Netherlands
2 Physiology, VU University Medical Center, Amsterdam, Netherlands
3 Physics and medical technology, VU University Medical Center, Amsterdam, Netherlands
4 Cardiology, VU University Medical Center, Amsterdam, Netherlands
5 Pulmonary Diseases, VU University Medical Center, Amsterdam, Netherlands

* To whom correspondence should be addressed. E-mail: jw.lankhaar{at}vumc.nl.

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 flow from MRI velocity quantification, the windkessel parameters were estimated 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 group. R and Z were significantly lower in the CTEPH than in the IPAH group (p < 0.05). The parameters R and C of all patients obeyed the relationship C = 0.75/R (R2 = 0.77), equivalent with 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 between 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.




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