Extract
For nearly all forms of group 1 pulmonary hypertension (pulmonary arterial hypertension; PAH), incident and prevalent patients are more likely to be female [1, 2]. The skew toward the female sex has long prompted an interest in the sex hormones as contributors to disease pathogenesis, with a particular interest in oestrogens. In 2010, Tofovic [3] employed the term “oestrogen paradox” based upon a perceived discrepancy: while PAH is a female-prevalent disease in humans, many (but not all) animal models demonstrate a protective effect of being female. However, over time, the intent of the “oestrogen paradox” has been modified to incorporate a growing body of human data concerning sex and PAH. In particular, the female predominance in PAH incidence is lower than the female predominance among prevalent cases; and, females appear to tolerate right ventricular (RV) stress and live longer than older males, if not all males [4–9]. While comprehensive data to determine why females may tolerate a hypertensive pulmonary vasculature better than males is lacking, growing information suggests that either baseline RV performance, and/or ability to adapt to stress with or without PAH therapy, may favour the female heart [10–14].
Abstract
Baird and colleagues contribute further evidence that the justification for sex-associated investigations in pulmonary arterial hypertension extend beyond oestrogen signalling. Evaluation of the entire steroid hormone milieu is crucial. http://ow.ly/7wbz30kp5VQ
Footnotes
Conflict of interest: None declared.
Support statement: Funding was provided by NIH R01 HL 134802 (E.D. Austin). Funding information for this article has been deposited with the Crossref Funder Registry.
- Received June 6, 2018.
- Accepted June 6, 2018.
- Copyright ©ERS 2018