Inflammation in the genesis and perpetuation of atrial fibrillation

Abstract

The prevalence and persistence of atrial fibrillation (AF) and the relative inefficacy of the currently available pharmacotherapy requires development of new treatment strategies. Recent findings have suggested a mechanistic link between inflammatory processes and the development of AF. Epidemiological studies have shown an association between C-reactive protein and both the presence of AF and the risk of developing future AF. In case-control studies, C-reactive protein is significantly elevated in AF patients and is associated with successful cardioversion. Moreover, C-reactive protein elevation is more pronounced in patients with persistent AF than in those with paroxysmal AF. Furthermore, treatment with glucocorticoids, statins, angiotensin converting enzyme inhibitors, and angiotensin II receptor blockers seems to reduce recurrence of AF. Part of this anti-arrhythmic effect may be through anti-inflammatory activity. This article reviews what is known about inflammation in genesis and perpetuation of AF, the putative underlying mechanisms, and possible therapeutic implications for the inhibition of inflammation as an evolving treatment modality for AF.

Role of mineralocorticoid receptor on atrial structural remodeling and inducibility of atrial fibrillation in hypertensive rats

“…Recent studies indicate a mechanistic link between the inflammatory processes and the development of AF. 31,32 Frustaci et al first demonstrated a high prevalence of inflammatory infiltrates, myocyte necrosis and fibrosis in atrial biopsies from patients with lone AF, but not in atrial biopsies from control patients. 33 Other papers have reported that an increase in high-sensitivity C-reactive protein levels is an independent risk factor for future AF among patients with sinus rhythm.…”

Association Between Serum C‐reactive Protein Elevation and Atrial Fibrillation After First Anterior Myocardial Infarction

“…26 Inflammatory changes have been observed in atrial tissues obtained from patients with isolated persistent AF. 27 Serum CRP level has been found to be significantly higher in patients with paroxysmal and chronic AF than in normal controls.…”

“…29 Atrial damage may trigger a lowgrade inflammatory response and be part of a structural remodeling with increased persistence of AF. 26 Dernellis et al showed that complements increase the CRP-related incidence of AF in apparently healthy subjects with normal sinus rhythm. 30 Also in this study, no significant relation was found between a high CRP level and AF in the absence of elevated complement components.…”

Targeting the renin–angiotensin–aldosterone system in atrial fibrillation: from pathophysiology to clinical trials

“…26,27 Furthermore, Cardin et al 25 were able to demonstrate increased atrial expression of angiotensin II is linked with increased atrial cell death and leukocyte infiltration, again supporting a potential link between the RAAS, inflammation and AF.…”

“…10 The RAAS, inflammation and AF There is accumulating evidence (from genetic studies, quantification of established inflammatory markers and histological sampling) pointing to an important association between inflammation and AF. 26 While a detailed synopsis of this putative link is beyond the scope of this commentary, there is evidence to date in support of a role for RAAS activation as an important factor in this association.…”