Pulmonary hypertension (PH) is a common complication of left heart disease (LHD), as the result of a “passive” increase of left atrial pressure (LAP), leading to isolated post-capillary PH 1–3. Several haemodynamic parameters have been proposed to identify a more severe phenotype of PH-LHD, for which the increase in pulmonary artery pressure cannot be accounted for by the increase in LAP, and described as combined post-capillary PH with a pre-capillary component, or CpcPH 1–3. The latter haemodynamic phenotype may potentially expose patients to a higher risk of right ventricular failure and a poorer outcome 4, 5. However, since the last World Symposium in 2013, how to define the pre-capillary component in PH-LHD has been a matter of debate, as pathophysiological arguments have been suggested to potentially contrast with clinical and prognostic evidences 1.