Abstract 16101: Cardiac Resynchronization Therapy after Anatomic Repair for Congenitally Corrected Transposition of the Great Arteries
OBJECTIVE: Early results for anatomic repair of congenitally corrected transposition of the great arteries (ccTGA) are excellent. However, development of left ventricular dysfunction late after repair remains a concern. Ventricular pacing and prolonged QRS have been shown to be risk factors for left ventricular dysfunction. In this study we sought to determine factors leading to late left ventricular dysfunction and the impact of cardiac resynchronization as a primary and secondary (upgrade) mode of pacing.
METHODS: From 1992 to 2012, 106 patients (median age at surgery, 14 months; range, 2 months to 43 years) with ccTGA had anatomic repair. A retrospective review of pre-operative variables, surgical procedure, and post-operative outcomes was performed. Sixty-two patients had an arterial switch, 42 patients a Rastelli procedure, and 2 had an aortic translocation.
RESULTS: Early mortality was 5.7% (n = 6), and there were 3 late deaths during a median follow-up 32 months (range, 7 days to 7.2 years). The early deaths were excluded from further analysis. Twelve patients (12%) developed moderate or severe LV dysfunction. Thirty-eight patients (38%) were pacing at latest follow-up. Seventeen patients had resynchronization therapy, 9 as an upgrade from a prior dual chamber system (8.5%) and 8 as a primary pacemaker (7.5%). Factors associated with LV dysfunction were age at repair > 10 years (P < 0.001), weight > 20 kg (P < 0.001), and pacemaker implantation (P < 0.001). Eight of nine patients undergoing secondary CRT (upgrade) improved LV function. None of the 8 patients undergoing primary CRT developed LV dysfunction.
CONCLUSIONS: Late left ventricular dysfunction after anatomic repair of ccTGA is not uncommon, with higher incidence in older patients and in those requiring pacing. Early repair and primary CRT in patients requiring a pacemaker could be of value to preclude the development of LV dysfunction.
- © 2012 by American Heart Association, Inc.