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European Heart Journal Advance Access published online on March 17, 2008
European Heart Journal, doi:10.1093/eurheartj/ehn103
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Pulmonary vascular resistance and compliance stay inversely related during treatment of pulmonary hypertension

Jan-Willem Lankhaar1,2, Nico Westerhof2,3, Theo J.C. Faes1, C. Tji-Joong Gan2, Koen M. Marques4, Anco Boonstra2, Fred G. van den Berg5, Pieter E. Postmus2 and Anton Vonk-Noordegraaf2,*

1 Department of Physics and Medical Technology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
2 Department of Pulmonary Diseases, Institute for Cardiovascular Research, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands
3 Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
4 Department of Cardiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands
5 Department of Radiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands

Received 15 August 2007; revised 9 February 2008; accepted 16 February 2008.

* Corresponding author. Tel: +31 20 44 44 782, Fax: +31 20 44 44 328, Email: a.vonk{at}vumc.nl

Aims: Pulmonary arterial compliance (C) is increasingly being recognized as an important contributor to right ventricular afterload, but for monitoring of treatment of pulmonary hypertension (PH) most often still only pulmonary vascular resistance (R) is used. We aimed at testing the hypothesis that R and C are coupled during treatment of PH and that substantial changes in both R and C would result in more haemodynamic improvement than changes in R alone.

Methods and results: Data were analysed of two right-heart catheterizations of 52 patients with pulmonary arterial hypertension and 10 with chronic-thromboembolic PH. The product of R and C (= stroke volume over pulse pressure) did not change during therapy (P = 0.320), implying an inverse relationship. Changes in cardiac index correlated significantly (P < 0.001) with changes in R (R2 = 0.37), better with changes in C (R2 = 0.66), and best with changes in both (R2 = 0.74).

Conclusion: During therapy for PH, R and C remain inversely related. Therefore, changes in both R and C better explain changes in cardiac index than either of them alone. Not only resistance but also compliance plays a prominent role in PH especially in an early stage of the disease.

Key Words: Pulmonary arterial compliance • Pulmonary vascular resistance • Pulmonary pressure decay time • Right ventricular afterload


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