Extract
Pulmonary hypertension (PH) induces right ventricular (RV) pressure overload. Initially, the right ventricle is able to adapt to the augmented afterload by increasing contractility to maintain cardiac output [1]. Consequently, RV function is preserved through adaptive RV hypertrophy, with minimal dilation and fibrosis. Nevertheless, due to maintained pressure overload, RV adaptation eventually fails, and patients die from right heart failure. RV adaptation is heterogeneous among PH patients and the transition from the adaptive to the maladaptive RV phenotype is not fully understood. Several pathological processes have been associated with the RV maladaptive phenotype in PH, including: a metabolic shift to glycolysis, mitochondrial dysfunction, inflammation, capillary rarefaction, sympathetic overstimulation, increased RV diastolic stiffness, and RV fibrosis [2–8]. These insights have been obtained using human tissue of end-stage disease or animal models. However, to fully recapitulate the transition from RV adaptation to maladaptation, longitudinal assessment of the pathological processes in patients is necessary. One way to obtain longitudinal pathophysiological insights is to identify a disease-related circulating biomarker.
Abstract
The search for new biomarkers for right ventricular maladaptation in pulmonary hypertension is exciting. At this moment we are missing some key information that hampers full-scale clinical implementation. https://bit.ly/37xbgwx
Footnotes
Support statement: This work was supported by Hartstichting (grants 2018T059, CVON-2018-29) and Nederlandse Organisatie voor Wetenschappelijk Onderzoek (grant 917.18.338).
Conflict of interest: J. van Wezenbeek has nothing to disclose.
Conflict of interest: M-J. Goumans has nothing to disclose.
Conflict of interest: F.S. de Man has nothing to disclose.
Conflict of interest: A. Llucià-Valldeperas has nothing to disclose.
- Received November 20, 2020.
- Accepted November 30, 2020.
- Copyright ©ERS 2021