Liver stiffness is associated with right heart dysfunction, cardiohepatic syndrome, and prognosis in pulmonary hypertension.

BACKGROUND

Pulmonary hypertension (PH) can lead to congestive hepatopathy, known as cardiohepatic syndrome (CHS). Hepatic congestion is associated with increased liver stiffness, which can be quantified using shear wave elastography. We aimed to investigate whether hepatic shear wave elastography detects patients at risk in the early stages of PH.

METHODS

Sixty-three prospectively enrolled patients undergoing right heart catheterization (52 diagnosed with PH and 11 with invasive exclusion of PH) and 52 healthy volunteers underwent assessments including echocardiography and hepatic shear wave elastography. CHS was defined as increased levels of ≥ 2 of the following: gamma-glutamyl transferase, alkaline phosphatase, and bilirubin. Liver stiffness was defined as normal (≤ 5.0 kPa) or high (> 5.0 kPa).

RESULTS

Compared with normal liver stiffness, high liver stiffness was associated with impaired right ventricular (RV) and right atrial (RA) function (median [interquartile range] RV ejection fraction: 54 [49; 57]% vs. 45 [34; 51]%, p < 0.001; RA reservoir strain: 49 [41; 54]% vs. 33 [22; 41]%, p < 0.001), more severe tricuspid insufficiency (p < 0.001), and higher prevalence of hepatovenous backflow (2% vs 29%, p < 0.001) and CHS (2% vs. 10%, p = 0.038). In the patient subgroup with precapillary PH (n = 48), CHS and high liver stiffness were associated with increased European Society of Cardiology/European Respiratory Society 2022 risk scores (p = 0.003).

CONCLUSIONS

Shear wave liver elastography yields important information regarding right heart function and may complement risk assessment in patients with (suspected) PH.

Informations de copyright

Copyright © 2024. Published by Elsevier Inc.

Déclaration de conflit d'intérêts

Disclosure statement Dr. Rako, Ms. Yildiz, Mr. Weidemann, Mr. Zedler, Mr. Brito da Rocha, Dr. Kryvenko, and Mr. Schäfer report non-financial support from the University of Giessen during the conduct of the study. Dr. Yogeswaran reports non-financial support from the University of Giessen during the conduct of the study, and personal fees from MSD outside the submitted work. Dr. Kremer reports non-financial support from the University of Giessen during the conduct of the study, and speaking fees from Janssen outside the submitted work. Dr. Ghofrani reports grants from the German Research Foundation and non-financial support from the University of Giessen during the conduct of the study, and personal fees from Bayer, Janssen, Pfizer, Xeros, Liquidia, and Takeda, grants and personal fees from Gossamer, Bayer HealthCare, and MSD/Acceleron, and grants from Aires, the German Research Foundation, Excellence Cluster Cardiopulmonary Research, and the German Ministry for Education and Research outside the submitted work. Dr. Seeger reports grants from the German Research Foundation and non-financial support from the University of Giessen during the conduct of the study, and personal consulting fees from United Therapeutics, Tiakis Biotech AG, Liquidia, Pieris Pharmaceuticals, Abivax, Pfizer and Medspray BV outside the submitted work. Dr. Tello reports non-financial support from the University of Giessen during the conduct of the current study and speaker honoraria from Actelion and Bayer outside the submitted work. This work was supported by the Excellence Cluster Cardio-Pulmonary System (ECCPS) and the Collaborative Research Center (SFB) 1213 - Pulmonary Hypertension and Cor Pulmonale, grant number SFB1213/1, project B08 (German Research Foundation, Bonn, Germany). For the manuscript, editorial assistance was provided by Dr Claire Mulligan (Beacon Medical Communications, Ltd, Brighton, United Kingdom), funded by the University of Giessen.