Atrial fibrillation (AF) is associated with substantial morbidity, mortality, and economic burden and confers a lifetime risk of up to 25%. Current medical management involves thromboembolism prevention, rate, and rhythm control. An increased understanding of AF pathophysiology has led to enhanced pharmacological and medical therapies; however this is often limited by toxicity, variable symptom control, and inability to modulate the atrial substrate. Surgical AF ablation has been available since the original description of the Cox Maze procedure, either as a standalone or concomitant intervention. Advances in novel energy delivery systems have allowed the development of less technically demanding procedures potentially eliminating the need for median sternotomy and cardiopulmonary bypass. Variations in the definition, duration, and reporting of AF have produced methodological limitations impacting on the validity of interstudy comparisons. Standardization of these parameters may, in future, allow us to further evaluate clinical endpoints and establish the efficacy of these techniques. 1. Introduction Atrial fibrillation (AF) is associated with significant morbidity and mortality in both medical and surgical patients. Results from the Framingham Heart study found AF to be associated with an overall lifetime risk of 1 in 4 adults aged 40–95 years or 1 in 6 of those without previous myocardial infarction or congestive cardiac failure [1]. Coronary artery bypass grafting alone has been associated with an incidence of AF reaching 30% in multicentre observational studies [2, 3] and may be significantly higher following valvular surgery [4]. More importantly, postoperative AF has been found to triple the risk of death from cardiac causes and quadruple the risk of stroke and other disabling embolic events [2]. The original “corridor” procedure for the treatment of AF was described by Guiraudon in 1985, but for a number of reasons was soon superseded by the “Maze” procedure as described by Cox et al. in 1991 [5, 6]. His work outlined a series of “cut and sew” lesions which aimed to direct electrical impulses in one direction through the atrium, disrupting the macro reentrant circuits which allow the development and propagation of AF. This procedure, whilst effective, was not without its complications, and the resultant inability to mount a tachycardic response to exercise and left atrial dysfunction led to two further adaptations of this procedure culminating in the Cox Maze III lesion set [5]. These modifications resulted in an improvement in the rates of
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