Cardioversion for Atrial Fibrillation: Does Inflammation Matter?

Abstract

m t A s s e p p t I p t n The long-term maintenance of sinus rhythm after cardioersion for atrial fibrillation (AF) has long been acknowledged s problematic. Even after initial successful restoration of sinus hythm, some 53% patients will return to AF over the followng months, whereas only approximately 25% remain in sinus hythm at 5 years.1,2 This is despite an aggressive rhythm ontrol strategy, using serial attempts at cardioversion and oncomitant antiarrhythmic drug prescription. More recently, he advent of catheter-based (and surgical-based) technologies as offered the potential of a cure for AF, with some promising esults,3 but even after these procedures, recurrence, often symptomatic, is common, further highlighting the difficulties ncountered in maintaining sinus rhythm.4,5 What contributes to the poor results of cardioversion and ong-term maintenance of sinus rhythm? Structural and lectrical remodeling within the atria may perpetuate AF— hat is, “AF begets AF”—admittedly in an experimental oat model.6 These remodeling changes include progressive eft atrial dilatation and increasing atrial fibrosis,7 the loss of ate adaptation, and the prolongation of atrial conductivity.8 alcium may also accumulate within atrial myocytes, hereby shortening the atrial refractory period, and hence, romoting the propagation of multiple wavelet reentry ciruits.7 The net result is that the biophysical properties of trial tissue are altered at microscopic and macroscopic evels in AF,9 thereby serving to perpetuate the arrhythmia. Does inflammation have a role in this, contributing to the erpetuation and maintenance of AF? Although the precise timulus for the initiation of these atrial changes remains oorly understood, an increasing body of evidence suggests hat inflammation may be central to this pathogenic proess.10 The histology of atrial biopsies taken from patients ith AF has demonstrated evidence of inflammatory infilrates and oxidative damage within the atrial tissue.11,12 Of ourse, these changes may clearly be a consequence of the arious underlying co-morbidities that commonly associate ith AF (e.g., ischemic heart disease, hypertension, diabees mellitus). However, this observation holds true even for hose with lone AF, thereby raising the possibility that nflammation may still play some role in the initiation of F, at least in this patient group.12 Systemic indexes of inflammation are also reported in F.10 For example, C-reactive protein (CRP) is a circulating cute-phase reactant and is considered the prototypic downtream marker of inflammation.13,14 CRP is synthesized by he liver in response primarily to interleukin-6 (IL-6) but also o interleukin-1. Many markers of inflammation exist, but