A possible reason why we did not detect an association between fibrinogen concentrations and parameters of disease severity in PAH patients might be due to the heterogeneity of the underlying pathologies associated with PAH, e.g. scleroderma or HIV. Due to the small number of patients within each subgroup we were unable to identify a statistical relation of this aspect. In addition, fibrinogen plasma concentrations are influenced by a plethora of lifestyle and demographic factors such as gender, age, body weight, physical activity, smoking or stress10. In order to minimize these influences, we matched our study population with regard to age, sex and body weight. Moreover, anticoagulatory therapy was not administered in a controlled fashion. However, since vitamin K-antagonists do not seem to influence fibrinogen plasma concentrations, we do not believe that this issue provided a relevant bias to our data1033. Actually, heparin (that was used routinely before RHC in our patients) even seems to decrease fibrinogen plasma concentrations34. On the contrary, due to the small sample size and lack of an independent evaluation/follow-up cohort, we cannot rule out an overestimation of fibrinogen's role as a predictor of impaired haemodynamics in CTEPH. Additional limitations of the study include its retrospective nature and a low mortality within our CTEPH population, which made a statistical correlation of fibrinogen to survival impossible. Also, other coagulatory parameters (e.g. D-dimers or prothrombin fragments) that might have helped to distinguish between a thromboembolic and inflammatory nature of increased fibrinogen plasma concentrations were not available for our analysis.