Inflammation, atrial fibrillation, and the potential role for colchicine therapy.

Bibin Varghese,Christopher Chew,David I Feldman,Garima Sharma,Eva Valilis,Roger S Blumenthal,Hugh Calkins

doi:10.1016/j.hroo.2021.03.011

Abstract

Increasing evidence suggests that the “NACHT-LRR and PYD domain-containing protein 3” (NLRP3) inflammasome plays an important role in atherosclerotic cardiovascular disease (ASCVD). Recent preclinical evidence has suggested that the NLRP3 inflammasome may play a prominent role in the pathogenesis of atrial fibrillation (AF). As such, the therapies that have shown efficacy in reducing ASCVD events may also prove beneficial in AF. In this article, we review the findings that implicate the NLRP3 inflammasome in the pathogenesis of AF, discuss existing evidence behind the use of anti-inflammatory agents for AF, and discuss the future role that colchicine and other anti-inflammatory agents may play in the prevention and treatment of AF.

Highlights

Atrial fibrillation (AF), the most common arrhythmia worldwide, affects 2%–3% of the population and is associated with significant morbidity and mortality.[1,2] AF is commonly preceded by structural remodeling of the atrial myocardium, which predisposes to impaired electrical conduction.[3]
We review the findings that implicate the NLRP3 inflammasome in the pathogenesis of AF, discuss existing evidence behind the use of anti-inflammatory agents for AF, and discuss the future role that colchicine and other anti-inflammatory agents may play in the prevention and treatment of AF
We review the findings from this study, discuss the evidence behind the use of antiinflammatory agents for AF, and discuss the future role that colchicine may play in the prevention and treatment of AF

Summary

Introduction

Atrial fibrillation (AF), the most common arrhythmia worldwide, affects 2%–3% of the population and is associated with significant morbidity and mortality.[1,2] AF is commonly preceded by structural remodeling of the atrial myocardium, which predisposes to impaired electrical conduction.[3]. Many nonmodifiable and modifiable risk factors, such as age, sex, ion channel mutations, hypertension, diabetes, obesity, and obstructive sleep apnea, have been linked to the progression of AF.[3] whether there is a common fundamental mechanism leading to clinical AF remains unknown.[8] Enhanced inflammatory signaling has been previously proposed as one potential link in the pathogenesis of AF.[9] The association between inflammation and AF was first noted over 20 years ago with the high incidence rate of postoperative AF (up to 50%) after cardiac surgery.[10] In studies of postoperative AF, elevated inflammatory markers such. NLRP3 is a type of inflammasome that has been noted in numerous cell types including immune

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