# Anticoagulation Therapies and microRNAs in Heart Failure

## TL;DR

This paper explores how microRNAs influence the effectiveness of anticoagulant drugs in heart failure patients, suggesting they could help personalize treatments.

## Contribution

The paper identifies specific microRNAs linked to resistance and variability in anticoagulant therapies for heart failure.

## Key findings

- MicroRNAs like miR-223 and miR-26a are associated with resistance to Clopidogrel in heart failure patients.
- Digoxin upregulates miR-132, which is involved in cardiac hypertrophy and heart failure.
- MicroRNAs show potential as predictive biomarkers to improve anticoagulant therapy personalization.

## Abstract

Heart Failure (HF) remains a major cause of mortality despite the advances in pharmacological treatment. Anticoagulation therapies, including Clopidogrel, Aspirin, Warfarin, and novel oral anticoagulants (NOACs) such as Apixaban, Rivaroxaban, Edoxaban, and Dabigatran, are frequently administered to HF patients to prevent thromboembolism and adverse, life-threatening outcomes (e.g., stroke and myocardial infarction). In these settings, drug resistance and variability in responsivity to therapeutic approaches are challenging issues. Recent studies suggest that non-coding RNAs, particularly microRNAs (miRs) may play a modulatory role in HF therapy context, affecting drug efficacy. Specific miRs have been associated with resistance to Clopidogrel (e.g., miR-223 and miR-26a), Aspirin (e.g., miR-19b-1-5p and miR-92a) and Warfarin (e.g., miR-133 and miR-137). Moreover, Digoxin, a cardiac glycoside acting also over bleeding risk, upregulates miR-132, which is involved in HF-associated cardiac alteration and hypertrophy. Evidence linking miR expression to NOAC pharmacodynamics, cardiac remodeling and regulation of the coagulation is growing. These findings highlight the need of deeply harnessing the potential of miRs as predictive biomarkers or therapeutic targets in HF. Improving the knowledge on the relationship between miR and anticoagulant drugs in HF patients will contribute to personalization of the anticoagulant therapies, aimed at enhancing patient responsivity and minimizing adverse effects, ultimately improving patient life quality.