Physiological mechanisms behind respiratory variations in right atrial pressure in pulmonary hypertension.

Conductance catheterization Diastolic dysfunction End-diastolic elastance Exercise haemodynamics Prognosis Pulmonary hypertension Respiratory variation Retrospective analysis Right atrial pressure Right ventricular dysfunction

Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
31 May 2024
Historique:
received: 27 12 2023
accepted: 10 05 2024
medline: 1 6 2024
pubmed: 1 6 2024
entrez: 31 5 2024
Statut: epublish

Résumé

Impaired respiratory variation of right atrial pressure (RAP) in severe pulmonary hypertension (PH) suggests difficulty tolerating increased preload during inspiration. Our study explores whether this impairment links to specific factors: right ventricular (RV) diastolic function, elevated RV afterload, systolic RV function, or RV-pulmonary arterial (PA) coupling. We retrospectively evaluated respiratory RAP variation in all participants enrolled in the EXERTION study. Impaired respiratory variation was defined as end-expiratory RAP - end-inspiratory RAP ≤ 2 mm Hg. RV function and afterload were evaluated using conductance catheterization. Impaired diastolic RV function was defined as end-diastolic elastance (Eed) ≥ median (0.19 mm Hg/mL). Seventy-five patients were included; PH was diagnosed in 57 patients and invasively excluded in 18 patients. Of the 75 patients, 31 (41%) had impaired RAP variation, which was linked with impaired RV systolic function and RV-PA coupling and increased tricuspid regurgitation and Eed as compared to patients with preserved RAP variation. In backward regression, RAP variation associated only with Eed. RAP variation but not simple RAP identified impaired diastolic RV function (area under the receiver operating characteristic curve [95% confidence interval]: 0.712 [0.592, 0.832] and 0.496 [0.358, 0.634], respectively). During exercise, patients with impaired RAP variation experienced greater RV dilatation and reduced diastolic reserve and cardiac output/index compared with patients with preserved RAP variation. Preserved RAP variation was associated with a better prognosis than impaired RAP variation based on the 2022 European Society of Cardiology/European Respiratory Society risk score (chi-square P = 0.025) and survival free from clinical worsening (91% vs 71% at 1 year and 79% vs 50% at 2 years [log-rank P = 0.020]; hazard ratio: 0.397 [95% confidence interval: 0.178, 0.884]). Subgroup analyses in patients with group 1 and group 4 PH demonstrated consistent findings with those observed in the overall study cohort. Respiratory RAP variations reflect RV diastolic function, are independent of RV-PA coupling or tricuspid regurgitation, are associated with exercise-induced haemodynamic changes, and are prognostic in PH.Trial registration. NCT04663217.

Identifiants

pubmed: 38822042
doi: 10.1038/s41598-024-61825-6
pii: 10.1038/s41598-024-61825-6
doi:

Banques de données

ClinicalTrials.gov
['NCT04663217']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

12547

Subventions

Organisme : Collaborative Research Center (SFB) 1213 - Pulmonary Hypertension and Cor Pulmonale
ID : SFB1213/1, project B08 (German Research Foundation, Bonn, Germany)

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Athiththan Yogeswaran (A)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Bruno Brito da Rocha (BB)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Zvonimir A Rako (ZA)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Samuel J Kaufmann (SJ)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Simon Schäfer (S)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Nils Kremer (N)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Hossein Ardeschir Ghofrani (HA)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.
Department of Pneumology, Kerckhoff Heart, Rheuma and Thoracic Center, Bad Nauheim, Germany.
Department of Medicine, Imperial College London, London, UK.

Werner Seeger (W)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany.

Khodr Tello (K)

Department of Internal Medicine, Universities of Giessen and Marburg Lung Center (UGMLC), Institute for Lung Health (ILH), Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Giessen, Germany. Khodr.Tello@innere.med.uni-giessen.de.
Department of Internal Medicine, Justus-Liebig-University Giessen, Klinikstrasse 32, 35392, Giessen, Germany. Khodr.Tello@innere.med.uni-giessen.de.

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