Efficacy of a Simple Left Atrial Procedure for Chronic Atrial Fibrillation in Mitral Valve Operations

Background. We have devised a simple surgical procedure to be performed on the posterior wall of the left atrium for the treatment of chronic atrial fibrillation (AF) associated with mitral valve disease. The effectiveness of this procedure for serial mitral valve operations was then evaluated. We postulated that chronic AF associated with mitral valve disease could be attributable to a distended left atrium. The refractory period of the distended left atrium was significantly shorter in the left posterior atrial wall, especially at the base of the left atrial appendage and at the orifice of the left posterior pulmonary vein. We hypothesized that the left posterior atrial wall with its shorter fibrillatory cycle length would act as a driver for maintaining the AF, and therefore, surgical ablation of this critical area in the left atrium could terminate the chronic AF. Methods. The surgical patients were divided into two groups. In group 1 (control group), 15 patients with chronic AF were operated on by the mitral valve procedure only. In group 2, 36 patients underwent this procedure in combination with a concomitant mitral valve operation. The disappearance rate of the AF was estimated by electrocardiography, and atrial function was estimated by transthoracic and transesophageal echocardiography. Results. The chronic AF had been reduced significantly or eliminated at discharge in 4 of 15 patients (26.7%) in the group 1, versus 31 of 36 patients (86%) in group 2 (p < 0.05). In group 2, 29 of the 31 patients (94%) whose AF had disappeared recovered the atrial kick of their right atrium, and 21 patients (22/31; 71%) recovered the atrial kick of their left atrium. Conclusions. Surgical ablation of the posterior wall of the left atrium was effective in the treatment of chronic AF associated with mitral valve disease. This simple procedure could restore a sinus rhythm and also recovered atrial systolic function. We conclude that the left atrium may act as a driver for sustaining AF in mitral valve disease.