Late left ventricular dysfunction after anatomic repair of congenitally corrected transposition of the great arteries
Victor Bautista-Hernandez1, Patrick O Myers2, Frank Cecchin3
1Department of Cardiac Surgery, Children's Hospital Boston, Harvard Medical School, Boston, Mass; Department of Pediatric Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Mass.
Insights
Late left ventricular dysfunction after congenital heart repair is common, especially in older patients needing pacemakers. Early repair and cardiac resynchronization therapy may prevent this complication.
Area of Science:
- Cardiology
- Pediatric Cardiac Surgery
- Congenital Heart Disease
Background:
- Anatomic repair of congenitally corrected transposition of the great arteries (ccTGA) shows early success.
- Late left ventricular dysfunction remains a significant concern after ccTGA repair.
- Understanding risk factors and preventive strategies is crucial.
Purpose of the Study:
- To identify factors contributing to late left ventricular dysfunction post-ccTGA repair.
- To evaluate the impact of cardiac resynchronization therapy (CRT) as primary or secondary pacing.
- To assess the efficacy of CRT in preventing or improving left ventricular function.
Main Methods:
- Retrospective review of 106 patients with ccTGA undergoing anatomic repair (1992-2012).
- Analysis of preoperative variables, surgical procedures, and postoperative outcomes.
- Assessment of pacemaker implantation and cardiac resynchronization therapy (CRT) use.
Main Results:
- 12% of patients developed moderate to severe left ventricular dysfunction.
- Older age at repair (>10 years), higher weight (>20 kg), pacemaker use, and neo-aortic regurgitation were associated with dysfunction.
- CRT, particularly as an upgrade, improved left ventricular function in most patients; primary CRT precluded dysfunction.
Conclusions:
- Late left ventricular dysfunction is a notable risk after ccTGA repair, particularly in older patients and those requiring pacemakers.
- Early anatomic repair combined with CRT for indicated patients may prevent the onset of left ventricular dysfunction.
- CRT appears to be a promising strategy for preserving or improving cardiac function post-ccTGA repair.
Objective:
Early results for anatomic repair of congenitally corrected transposition of the great arteries (ccTGA) are excellent. However, the development of left ventricular dysfunction late after repair remains a concern. 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, 1.2 years; range, 2 months to 43 years) with ccTGA had anatomic repair. A retrospective review of preoperative variables, surgical procedures, and postoperative outcomes was performed.
Results:
In-hospital deaths occurred in 5.7% (n = 6), and there were 3 postdischarge deaths during a mean follow-up period of 5.2 years (range, 7 days to 18.2 years). Twelve patients (12%) developed moderate or severe left ventricular dysfunction. Thirty-eight patients (38%) were being paced at latest follow-up evaluation. 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 left ventricular dysfunction were age at repair older than 10 years, weight greater than 20 kg, pacemaker implantation, and severe neo-aortic regurgitation. Eight of 9 patients undergoing secondary cardiac resynchronization therapy (upgrade) improved left ventricular function. None of the 8 patients undergoing primary resynchronization developed left ventricular dysfunction.
Conclusions:
Late left ventricular dysfunction after anatomic repair of ccTGA is not uncommon, occurring most often in older patients and in those requiring pacing. Early anatomic repair and cardiac resynchronization therapy in patients requiring a pacemaker could preclude the development of left ventricular dysfunction.
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