Extract
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 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, where pathophysiological arguments have been suggested to potentially contrast with clinical and prognostic evidences [1].
Footnotes
This manuscript has recently been accepted for publication in the European Respiratory Journal. It is published here in its accepted form prior to copyediting and typesetting by our production team. After these production processes are complete and the authors have approved the resulting proofs, the article will move to the latest issue of the ERJ online. Please open or download the PDF to view this article.
Conflict of interest: Dr. Dewachter has nothing to disclose.
Conflict of interest: Dr. Soranna has nothing to disclose.
Conflict of interest: Sandy Carolino D'Araujo
Conflict of interest: Dr. Khaldi has nothing to disclose.
Conflict of interest: Dr. Zambon has nothing to disclose.
Conflict of interest: Dr. Parati has nothing to disclose.
Conflict of interest: Dr. Bondue has nothing to disclose.
Conflict of interest: Dr. Vachiéry reports grants from Actelion, outside the submitted work.
Conflict of interest: Dr. Carolino D'Araujo has nothing to disclose.
Conflict of interest: Dr. Caravita reports grants from Actelion, outside the submitted work.
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