TY - JOUR
T1 - Differential biomarker expression in heart failure patients with and without mitral regurgitation
T2 - Insights from BIOSTAT-CHF
AU - Adamo, Marianna
AU - Pagnesi, Matteo
AU - Di Pasquale, Mattia
AU - Ravera, Alice
AU - Dickstein, Kenneth
AU - Ng, Leong L
AU - Anker, Stefan D
AU - Cleland, John G
AU - Filippatos, Gerasimos S
AU - Lang, Chim C
AU - Ponikowski, Piotr
AU - Samani, Nilesh J
AU - Zannad, Faiez
AU - van Veldhuisen, Dirk J
AU - Lipsic, Erik
AU - Voors, Adriaan
AU - Metra, Marco
N1 - Publisher Copyright:
© 2023 Elsevier B.V.
PY - 2024/3/15
Y1 - 2024/3/15
N2 - 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.
AB - 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.
KW - Biomarkers
KW - Heart failure
KW - Mitral regurgitation
U2 - 10.1016/j.ijcard.2023.131664
DO - 10.1016/j.ijcard.2023.131664
M3 - Article
C2 - 38141725
SN - 0167-5273
VL - 399
JO - International Journal of Cardiology
JF - International Journal of Cardiology
M1 - 131664
ER -