Increase of pulmonary vascular resistance in PAH is related to different mechanisms, including vasoconstriction, loss of distal arteries, proliferative and obstructive remodelling of the pulmonary vessel wall, microthrombosis, and inflammation. The latter mechanism gained attention as elevated concentrations of inflammatory markers such as interleukin (IL)-1, IL-6, IL-13, and tumour necrosis factor-alpha were detected in PAH patients plasmas and tissues7. Recently, C-reactive protein (CRP), representing the most established clinical marker of inflammation, was shown to be a prognostic factor in PAH patients8. To which extent inflammation is relevant for CTEPH pathogenesis is uncertain.