Differential biomarker expression in heart failure patients with and without mitral regurgitation: Insights from BIOSTAT-CHF
- PMID: 38141725
- DOI: 10.1016/j.ijcard.2023.131664
Differential biomarker expression in heart failure patients with and without mitral regurgitation: Insights from BIOSTAT-CHF
Abstract
Background: Mitral regurgitation (MR) frequently coexists with heart failure (HF).
Objectives: To better understand potential pathophysiological differences between patients with HF with or without moderate-severe MR, we compared differentially expressed circulating biomarkers between these two groups.
Methods: The Olink Proteomics® Multiplex Cardiovascular (CVD) -II, CVD-III, Immune Response and Oncology-II panels of 363 unique proteins from different pathophysiological domains were used to investigate the biomarker profiles of HF patients from index and validation cohorts of the BIOSTAT-CHF study stratified according to the presence of moderate-to-severe MR or no-mild MR.
Results: The index cohort included 888 patients (46%) with moderate-to-severe MR and 1029 (54%) with no-mild MR at baseline. The validation cohort included 522 patients (33%) with moderate-to-severe MR and 1076 (66%) with no-mild MR at baseline. Compared to patients with no-mild MR, those with moderate-to-severe MR had lower body mass index, higher comorbidity burden, signs and symptoms of more severe HF, lower systolic blood pressure, and larger left atrial and ventricular dimensions, in both cohorts. NT-proBNP, CA125, fibroblast growth factor 23 (FGF23) and growth hormone 1 (GH1) were up-regulated, whereas leptin (LEP) was down-regulated in patients with moderate-severe MR versus no-mild MR, in both index and validation cohorts.
Conclusion: Circulating biomarkers differently expressed in HF patients with moderate-severe MR versus no-mild MR were related to congestion, lipid and mineral metabolism and oxidative stress. These findings may be of value for the development of novel treatment targets in HF patients with MR.
Keywords: Biomarkers; Heart failure; Mitral regurgitation.
Copyright © 2023 Elsevier B.V. All rights reserved.
Conflict of interest statement
Conflict of interest M.A. received speaker fees from Abbott Vascular. M.P. received personal fees from Abbott Vascular, AstraZeneca, Boehringer Ingelheim, Novartis, Roche Diagnostics and Vifor Pharma. S.D.A reports grants and personal fees from Vifor and Abbott Vascular, and personal fees for consultancies, trial committee work and/or lectures from Actimed, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bioventrix, Brahms, Cardiac Dimensions, Cardior, Cordio, CVRx, Cytoki-netics, Edwards, Farraday Pharmaceuticals, GSK, HeartKinetics, ImpulseDynamics, Novartis, Occlutech, Pfizer, Repairon, Sensible Medical, Servier, Vectorious, and V-Wave; he also declares that he is named co-inventor of two patent applications regarding MR-proANP (DE102007010834 & DE102007022367), but he does not benefit personally from the related issued patents. G.S.F. reports speaker honoraria and/or committee membership in trials and/or registries sponsored by Amgen, Bayer, Novartis, Boehringer Ingelheim, Medtronic, Vifor, and Servier; and research grants from the European Union. A.A.V. received consultancy fees and/or research grants from Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Merck, Myokardia, Novartis, NovoNordisk, and Roche Diagnostics. M.M. received personal consulting honoraria from Abbott, Actelion, Amgen, Bayer, Edwards Therapeutics, Servier, Vifor Pharma, and Windtree Therapeutics for participation in advisory board meetings and executive committees of clinical trials. All other authors have nothing to disclose.
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