# Pro- and Anti-Inflammatory Cytokines’ Implication in Right Heart Disease, Arrhythmogenesis, and Atrial Fibrillation

## TL;DR

This review explores how inflammation and fibrosis in right heart disease contribute to atrial fibrillation and suggests targeting cytokines for better treatment.

## Contribution

The paper reviews recent evidence on inflammation's role in right heart disease and proposes cytokine targeting for atrial fibrillation management.

## Key findings

- Inflammation and fibrosis are key in arrhythmogenesis in right heart disease.
- Current anti-inflammatory drugs do not irreversibly cure atrial fibrillation.
- Targeting inflammatory cytokines may improve future AF management in RHD.

## Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia responsible for increased risk of a stroke and sudden death. Right heart disease (RHD), characterized by myocardial dysfunction and structural alteration affecting the right ventricle and the right atrium, is recognized as an important risk factor for AF. Inflammation and cardiac fibrosis emerge as arrhythmogenic pathophysiological events commonly occurring in most diseases responsible for cardiac arrhythmias and AF. However, no commercially available anti-inflammatory drugs were shown to irreversibly cure AF. Hence, more investigations are required to identify the key inflammatory and fibrosis agents involved in arrhythmogenesis. In this review, we explore (i) the recent evidence of myocardial, and especially atrial, inflammation in RHD, and (ii) the relevance of targeting inflammatory and anti-inflammatory cytokines in future strategies, combined with current AF management, in RHD.