Objectives: This study sought to determine the incidence of incomplete ligation of the left atrial appendage (LAA) during mitral valve surgery.
Background: Ligation of the LAA to prevent future thromboembolic events is commonly performed during mitral surgery. However, success in completely excluding the appendage from the circulation has never been systematically assessed.
Methods: Using transesophageal Doppler echocardiography, we studied 50 patients who underwent mitral valve surgery and ligation of the LAA. Thirty patients were studied immediately postoperative, and 20 patients were studied 6 days to 13 years after surgery. Incomplete ligation was detected by demonstrating a color jet traversing the separation between the left atrial body and appendage.
Results: Transesophageal echocardiography detected incomplete LAA ligation in 18 of 50 (36%) patients. The incidence of incomplete ligation was not significantly different between patients studied immediately postoperative and patients studied at various times after surgery. Type of mitral surgery (repair vs. replacement), operative approach (sternotomy vs. port access), left atrial size or degree of mitral regurgitation did not significantly correlate with the incidence of incomplete appendage ligation. However, the power to detect a significant difference in left atrial size was only 64%. Spontaneous echo contrast or thrombus was identified within appendages in 9 of 18 (50%) patients with incomplete ligation, while 4 of these 18 (22%) patients had thromboembolic events.
Conclusions: Surgical LAA ligation is frequently incomplete. The similar incidence of incomplete ligation detected immediately postoperative and at various times thereafter suggest that this results from an intraoperative phenomenon rather than from gradual dehiscence of sutures over years. The incidence of incomplete left atrial ligation was unrelated to type of surgery, surgical approach, left atrial size or degree of mitral regurgitation. Residual communication between the incompletely ligated appendage and the left atrial body may produce a milieu of stagnant blood flow within the appendage and be a potential mechanism for embolic events.