Pathophysiology of the right ventricle and of the pulmonary circulation in pulmonary hypertension: an update.
Journal
The European respiratory journal
ISSN: 1399-3003
Titre abrégé: Eur Respir J
Pays: England
ID NLM: 8803460
Informations de publication
Date de publication:
01 2019
01 2019
Historique:
received:
05
10
2018
accepted:
09
10
2018
pubmed:
14
12
2018
medline:
2
10
2020
entrez:
15
12
2018
Statut:
epublish
Résumé
The function of the right ventricle determines the fate of patients with pulmonary hypertension. Since right heart failure is the consequence of increased afterload, a full physiological description of the cardiopulmonary unit consisting of both the right ventricle and pulmonary vascular system is required to interpret clinical data correctly. Here, we provide such a description of the unit and its components, including the functional interactions between the right ventricle and its load. This physiological description is used to provide a framework for the interpretation of right heart catheterisation data as well as imaging data of the right ventricle obtained by echocardiography or magnetic resonance imaging. Finally, an update is provided on the latest insights in the pathobiology of right ventricular failure, including key pathways of molecular adaptation of the pressure overloaded right ventricle. Based on these outcomes, future directions for research are proposed.
Identifiants
pubmed: 30545976
pii: 13993003.01900-2018
doi: 10.1183/13993003.01900-2018
pmc: PMC6351344
pii:
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL119201
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL129990
Pays : United States
Informations de copyright
Copyright ©ERS 2019.
Déclaration de conflit d'intérêts
Conflict of interest: A. Vonk Noordegraaf reports grants and speaker fees from Actelion, MSD and GSK, outside the submitted work. Conflict of interest: K.M. Chin reports personal fees for consulting work on clinical trials from Actelion, grants (paid to institution) from Ironwood and Sonivie, personal fees for consulting work for a clinical registry from University of California San Diego, and research grants from the NIH, outside the submitted work. Conflict of interest: F. Haddad has nothing to disclose. Conflict of interest: P.M. Hassoun has nothing to disclose. Conflict of interest: A.R. Hemnes reports personal fees from Actelion, Bayer, Complexa and United Therapeutics, and grants from the CMREF and NIH, outside the submitted work; and in addition has a patent issued: Annamometer (oral mechanism for detection of end-tidal CO2; not referenced in this work). Conflict of interest: S.R. Hopkins is funded by the NIH via research grants to study the pulmonary circulation. Conflict of interest: S.M. Kawut reports non-financial travel support from the ATS and Pulmonary Hypertension Association, grants from Actelion, United Therapeutics, Gilead, Lung Biotech, Bayer and Mallinkrodt, and grants and non-financial support from the CMREF, outside the submitted work and paid to his university; and has served in an advisory capacity (for grant review and other purposes) for United Therapeutics, Akros Pharmaceuticals, GSK and Complexa, Inc., without financial support or in-kind benefits. Conflict of interest: D. Langleben reports grants, personal fees and non-financial support from Actelion and Bayer, personal fees from United Therapeutics and Merck, and grants from Northern Therapeutics, outside the submitted work. Conflict of interest: J. Lumens has nothing to disclose. Conflict of interest: R. Naeije has nothing to disclose.
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