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Original Research: Pulmonary Vascular Disease |

The Right Ventricle Explains Sex Differences in Survival in Idiopathic Pulmonary Arterial HypertensionSex Differences in Pulmonary Arterial Hypertension

Wouter Jacobs, MD; Mariëlle C. van de Veerdonk, MD; Pia Trip, MD; Frances de Man, PhD; Martijn W. Heymans, PhD; Johannes T. Marcus, PhD; Steven M. Kawut, MD, FCCP; Harm-Jan Bogaard, MD, PhD; Anco Boonstra, MD, PhD; Anton Vonk Noordegraaf, MD, PhD, FCCP
Author and Funding Information

From the Department of Pulmonology (Drs Jacobs, van de Veerdonk, Trip, de Man, Bogaard, and Boonstra and Prof Vonk Noordegraaf), the Department of Epidemiology and Biostatistics (Dr Heymans), and the Department of Physics and Medical Technology (Dr Marcus), VU University Medical Centre, Amsterdam, The Netherlands; the Department of Pulmonology (Dr Jacobs), Martini Hospital, Groningen, The Netherlands; and the Department of Medicine (Dr Kawut), Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.

Correspondence to: Anton Vonk Noordegraaf, MD, PhD, FCCP, VU University Medical Centre, Department of Pulmonary Medicine, PO Box 7057, 1007MB Amsterdam, The Netherlands; e-mail: a.vonk@vumc.nl


For editorial comment see page 1184

Funding/Support: Prof Vonk Noordegraaf was financially supported by De Nederlandse Organisatie voor Wetenschappelijk Onderzoek, Vidi Grant [Grant 91.796.306]. Dr Kawut was supported by the National Institutes of Health [Grant K24HL103844].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(6):1230-1236. doi:10.1378/chest.13-1291
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Background:  Male sex is an independent predictor of worse survival in pulmonary arterial hypertension (PAH). This finding might be explained by more severe pulmonary vascular disease, worse right ventricular (RV) function, or different response to therapy. The aim of this study was to investigate the underlying cause of sex differences in survival in patients treated for PAH.

Methods:  This was a retrospective cohort study of 101 patients with PAH (82 idiopathic, 15 heritable, four anorexigen associated) who were diagnosed at VU University Medical Centre between February 1999 and January 2011 and underwent right-sided heart catheterization and cardiac MRI to assess RV function. Change in pulmonary vascular resistance (PVR) was taken as a measure of treatment response in the pulmonary vasculature, whereas change in RV ejection fraction (RVEF) was used to assess RV response to therapy.

Results:  PVR and RVEF were comparable between men and women at baseline; however, male patients had a worse transplant-free survival compared with female patients (P = .002). Although male and female patients showed a similar reduction in PVR after 1 year, RVEF improved in female patients, whereas it deteriorated in male patients. In a mediator analysis, after correcting for confounders, 39.0% of the difference in transplant-free survival between men and women was mediated through changes in RVEF after initiating PAH medical therapies.

Conclusions:  This study suggests that differences in RVEF response with initiation of medical therapy in idiopathic PAH explain a significant portion of the worse survival seen in men.

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