Profile of serum microRNAs in heart failure with reduced and preserved ejection fraction: Correlation with myocardial remodeling.

Background and Aims: Cardiomyocyte hypertrophy and interstitial fibrosis are key components of myocardial remodeling in Heart Failure (HF) with preserved (HFpEF) or reduced ejection fraction (HFrEF). MicroRNAs (miRNAs) are non-coding, evolutionarily conserved RNA molecules that may offer novel insights into myocardial remodeling. This study aimed to characterize miRNA expression in HFpEF (LVEF  ≥  45%) and HFrEF (LVEF < 45%) and its association with myocardial remodeling.
Methods: Prospectively enrolled symptomatic HF patients (HFpEF:n = 36; HFrEF:n = 31) and controls (n = 23) underwent cardiac magnetic resonance imaging with T1-mapping and circulating miRNA expression (OpenArray system).
Results: 13 of 188 miRNAs were differentially expressed between HF groups (11 downregulated in HFpEF). Myocardial extracellular volume (ECV) was increased in both HF groups (HFpEF 30 ± 5%; HFrEF 30 ± 3%; controls 26 ± 2%, p < 0.001). miR-128a-3p, linked to cardiac hypertrophy, fibrosis, and dysfunction, correlated positively with ECV in HFpEF (r = 0.60, p = 0.01) and negatively in HFrEF (r =  - 0.51, p = 0.04). miR-423-5p overexpression, previously associated HF mortality, was inversely associated with LVEF (r =  - 0.29, p = 0.04) and intracellular water lifetime ( τ _ic ) (r =  - 0.45, p < 0.05) in both HF groups, and with NT-proBNP in HFpEF (r =  - 0.63, p < 0.01).
Conclusions: miRNA expression profiles differed between HF phenotypes. The differential expression and association of miR-128a-3p with ECV may reflect the distinct vascular, interstitial, and cellular etiologies of HF phenotypes.
Competing Interests: The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Otavio R Coelho-Filho reports financial support was provided by State of Sao Paulo Research Foundation. Otavio R Coelho-Filho reports was provided by. Otavio R Coelho-Filho reports a relationship with 10.13039/100004325AstraZeneca Pharmaceuticals LP that includes: funding grants and speaking and lecture fees. Otavio R Coelho-Filho reports a relationship with 10.13039/100002429Amgen Inc that includes: funding grants. Otavio R Coelho-Filho reports a relationship with 10.13039/100004319Pfizer Inc that includes: funding grants and speaking and lecture fees. Otavio R Coelho-Filho reports a relationship with 10.13039/100004336Novartis AG that includes: speaking and lecture fees. Otavio R Coelho-Filho reports a relationship with 10.13039/100004326Bayer AG that includes: speaking and lecture fees. Otavio R Coelho-Filho reports a relationship with 10.13039/100001003Boehringer Ingelheim Ltd that includes: speaking and lecture fees. Otavio R Coelho-Filho reports a relationship with 10.13039/100007723Takeda Pharmaceutical Company Limited that includes: funding grants and speaking and lecture fees. Tomas G Neilan reports a relationship with H3 Biomedicine Inc that includes: funding grants. Tomas G Neilan reports a relationship with 10.13039/100002429Amgen Inc that includes: funding grants. Tomas G Neilan reports a relationship with 10.13039/100006483AbbVie Inc that includes: funding grants. Tomas G Neilan reports a relationship with 10.13039/100004325AstraZeneca that includes: funding grants. T.G.N. has received support from 10.13039/100004325AstraZeneca, Bristol Myer Squibb, 10.13039/100006483AbbVie, 10.13039/100002429Amgen, and H3 Biomedicine. O.R.C.F. has received research grants and/or speaking honoraria from 10.13039/100002429Amgen, 10.13039/100004325AstraZeneca, 10.13039/100004326Bayer, 10.13039/100001003Boehringer Ingelheim, 10.13039/100004336Novartis, 10.13039/100007723Takeda, and 10.13039/100004319Pfizer. The remaining authors declare no conflict of interest.
(© 2024 The Authors.)