Atrial fibrillation (AF) is the most common cardiac arrhythmia and the treatment options include medical treatment and catheter-based or surgical interventions. AF is a major cause of stroke, and its prevalence is increasing. The surgical treatment of AF has been revolutionized over the past 2 decades through surgical innovation and improvements in endoscopic imaging, ablation technology and surgical instrumentation. The Cox-maze (CM) procedure, which was developed by James Cox and introduced clinically in 1987, is a procedure in which multiple incisions are created in both the left and the right atria to eliminate AF while allowing the sinus impulse to reach the atrioventricular node. This procedure became the gold standard for the surgical treatment of AF. Its latest iteration is termed the CM IV and was introduced in 2002. The CM IV replaced the previous cut-and-sew method (CM III) by replacing most of the incisions with a combination of bipolar radiofrequency and cryoablation. The use of ablation technologies, made the CM IV technically easier, faster and more amenable to minimally invasive approaches. The aims of this article are to review the indications and preoperative planning for the CM IV, to describe the operative technique and to review the literature including comparisons of the CM IV with the previous cut-and-sew method. Finally, this review explores future directions for the surgical treatment of patients with AF.

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Objective: The purpose of this study was to determine the effects of chronic left atrial volume overload on atrial anatomy, hemodynamics, and electrophysiology using a titratable left ventriculoatrial shunt in a canine model. Methods: Canines (n = 16) underwent implantation of a shunt between the left ventricle and the left atrium. Sham animals (n = 8) underwent a median sternotomy without a shunt. Atrial activation times and effective refractory periods were determined using 250-bipolar epicardial electrodes. Biatrial pressures, systemic pressures, left atrial and left ventricle diameters and volumes, atrial fibrillation inducibility, and durations were recorded at the initial and at 6-month terminal study. Results: Baseline shunt fraction was 46% ± 8%. The left atrial pressure increased from 9.7 ± 3.5 mm Hg to 13.8 ± 4 mm Hg (P<.001). At the terminal study, the left atrial diameter increased from a baseline of 2.9 ± 0.05 cm to 4.1 ± 0.6 cm (P<.001) and left ventricular ejection fraction decreased from 64% ± 1.5% to 54% ± 2.7% (P <.001). Induced atrial fibrillation duration (median, range) was 95 seconds (0–7200) compared with 0 seconds (0–40) in the sham group (P = .02). The total activation time was longer in the shunt group compared with the sham group (72 ± 11 ms vs 62 ± 3 ms, P = .003). The right atrial and not left atrial effective refractory periods were shorter in the shunt compared with the sham group (right atrial effective refractory period: 156 ± 11 ms vs 141 ± 11 ms, P = .005; left atrial effective refractory period: 142 ± 23 ms vs 133 ± 11 ms, P = .35). Conclusions: This canine model of mitral regurgitation reproduced the mechanical and electrical remodeling seen in clinical mitral regurgitation. Left atrial size increased, with a corresponding decrease in left ventricle systolic function, and an increased atrial activation times, lower effective refractory periods, and increased atrial fibrillation inducibility. This model provides a means to understand the remodeling by which mitral regurgitation causes atrial fibrillation.