Abstract
Introduction . Pulmonary hypertension (PH) definition was recently changed and led to a new subset of PH patients with mildly impaired pulmonary hemodynamics, characterized by a mean pulmonary artery pressure of 21–24 mmHg and with a pulmonary vascular resistance >2Wood Units. We evaluated the association of PH-targeted therapy and outcome in mild precapillary PH using the PVRI GoDeep meta-registry.
Methods . All patients with mild precapillary PH (mPAP 21–24 mmHg, PAWP ≤15 mmHg, PVR >2WU) diagnosed with PAH and CTEPH were enrolled. Patients were considered treated if PH-targeted therapy was initiated within 6 months of diagnostic right heart catheterization. Various statistical models, including in-depth sensitivity analyses, were used to examine the association between PH-targeted therapy and transplant-free survival.
Results . 132 patients with group 1 or group 4 mild PH were identified, of whom 34 patients received PH-targeted therapy. There were no differences in baseline hemodynamics between untreated and treated groups, while treated patients suffered more frequently from renal comorbidities and required long-term oxygen treatment more often. Most prescribed were phosphodiesterase-5-inhibitors. PH-targeted therapy was associated with significantly higher survival rates, compared to those without treatment. Cox-regression analysis revealed significantly reduced hazard ratios among treated patients in Cox-regression analyses adjusted for various confounders. Subgroup analyses in PAH (n=78) similarly indicated higher survival rates and reduced hazard ratios in treated patients.
Conclusion . PH-targeted therapy may be associated with improved survival in PAH and CTEPH patients with mild PH. To mitigate potential bias of the results due to the retrospective study design, randomized controlled trials are warranted.
Footnotes
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Conflict of interest: 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.
Conflict of interest: Dr. Hassoun reports personal fees from Merck Co., outside the submitted work.
Conflict of interest: Dr. Hassoun reports personal fees from Merck Co, outside the submitted work.
Conflict of interest: Dr. Wilkins reports personal fees from MorphogenIX, personal fees from Janssen, personal fees from Chiesi, personal fees from Aerami, grants from British Heart Foundation, grants from NIHR, personal fees from MSD, personal fees from Benevolent AI, personal fees from Tiakis Biotech, outside the submitted work; In addition, Dr. Wilkins has a patent Zip12 as a drug target issued. Dr. Howard reports personal fees and non-financial support from Janssen, personal fees from MSD, personal fees from Gossamer, personal fees from Altavant, outside the submitted work.
Conflict of interest: 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, Actelion, Pfizer, Merck, GSK, and Takeda, grants and personal fees from Novartis, Bayer HealthCare, and Encysive/Pfizer, and grants from Aires, the German Research Foundation, Excellence Cluster Cardiopulmonary Research, and the German Ministry for Education and Research outside the submitted work.
Conflict of interest: 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 fees from Pfizer and Bayer Pharma AG outside the submitted work.
Conflict of interest: 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. All other authors declare no conflicts of interest.
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- Received May 6, 2024.
- Accepted August 20, 2024.
- Copyright ©The authors 2024
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