# Prognostic impact of mitochondrial dynamics-related miRNA levels during the treatment of acute heart failure in the hospital

## TL;DR

This study shows that low levels of a specific miRNA during hospital treatment for acute heart failure are linked to worse long-term outcomes.

## Contribution

The study identifies miR-140-3p as a potential prognostic biomarker for adverse outcomes in acute heart failure patients.

## Key findings

- miR-140-3p levels significantly decreased on days 3 and 14 compared to day 1 in AHF patients.
- Low miR-140-3p levels were associated with higher mortality and more heart failure events within 1000 days.
- Decreased miRNA levels during treatment were independently linked to adverse outcomes.

## Abstract

Mitochondrial dynamics-related RNAs during hospitalization for acute heart failure (AHF) were rarely evaluated in various points. In total, 234 patients who visited the emergency room for AHF were retrospectively evaluated. Blood samples were collected within 15 min of admission (day 1), after 48–72 h, and between days 7 and 21. Low miR-140-3p during hospitalization was defined as the level being categorized as Q1 more than once (on days 1, 3 and/or 14), and normal-140-3p during hospitalization as the level never being categorized as Q1. The median miR-140-3p levels were significantly decreased on days 3 and 14 (2.53 [1.06–6.42] and 3.65 [1.41–9.05], respectively) in comparison to the value on day 1 (6.71 [2.66–14.0]). Kaplan–Meier curves indicated that all-cause mortality within 1000 days was significantly higher in the low-miR-140-3p group than in the other-miR-140-3p group on days 1 and 14. Moreover, the survival rate was significantly lower and the rate of HF events was significantly higher in the low-miR-140-3p group than in the normal-miR-140-3p group. The miRNA levels of patients further decreased during treatment for AHF. Low levels of mitochondrial fission-related miRNAs during AHF treatment were independently associated with an increased risk of long-term adverse outcomes.