Edward Buratto1, Adrienne Lui2, Thomas Hu3, Phillip S Naimo1, Yaroslav Ivanov3, Yves d'Udekem4, Christian P Brizard4, Igor E Konstantinov5. 1. Department of Cardiac Surgery, Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research Group, Murdoch Children's Research Institute, Melbourne, Australia. 2. Department of Paediatrics, University of Melbourne, Melbourne, Australia. 3. Department of Cardiac Surgery, Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia. 4. Department of Cardiac Surgery, Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research Group, Murdoch Children's Research Institute, Melbourne, Australia; Melbourne Children's Centre for Cardiovascular Genomics and Regenerative Medicine, Melbourne, Australia. 5. Department of Cardiac Surgery, Royal Children's Hospital, Melbourne, Australia; Department of Paediatrics, University of Melbourne, Melbourne, Australia; Heart Research Group, Murdoch Children's Research Institute, Melbourne, Australia; Melbourne Children's Centre for Cardiovascular Genomics and Regenerative Medicine, Melbourne, Australia. Electronic address: igor.konstantinov@rch.org.au.
Abstract
BACKGROUND: Repair of complete atrioventricular septal defect (cAVSD) is achieved with low mortality. However, there is a high rate of reoperation on the left atrioventricular valve (LAVV), which is often attributed to nonclosure of the cleft. Although nonclosure of the cleft has been reported to be a risk factor for reoperation, no randomized controlled or propensity-matched trials have ever been performed. We investigated the effect of cleft closure on outcomes after cAVSD repair. METHODS: We reviewed 455 patients who underwent cAVSD repair between 1990 and 2019. To determine the effect of cleft closure, propensity score matching was performed on risk factors for reoperation after cAVSD repair. RESULTS: Median age was 3.6 months (mean, 9.6 ± 20.4 months), median weight was 4.3 kg (mean, 4.7 ± 4.3 kg) and 41.9% (191 of 455) were male. Early mortality was 2.9% (13 of 455), and survival was 89.8% ± 1.9% at 20 years. Early reoperation was a risk factor for mortality (P = .004). Freedom from reoperation was 72.5% ± 4.0% at 20 years. Freedom from LAVV reoperation was 74.1% ± 4.0% at 20 years. Preoperative severe LAVV regurgitation (P < .001) and early postoperative moderate or greater LAVV regurgitation (P = .007) were risk factors for reoperation, while trisomy 21 (P = .03) and recent era of surgery (P = .02) were protective. Propensity score matching yielded 106 pairs. There were no differences in long-term survival (P = .71) or reoperation (P = .26) between the 2 groups. CONCLUSIONS: Repair of cAVSD can be achieved with low mortality and good long-term survival, although the reoperation rate remains high. Similar freedom from reoperation can be achieved with or without closure of the LAVV cleft.
BACKGROUND: Repair of complete atrioventricular septal defect (cAVSD) is achieved with low mortality. However, there is a high rate of reoperation on the left atrioventricular valve (LAVV), which is often attributed to nonclosure of the cleft. Although nonclosure of the cleft has been reported to be a risk factor for reoperation, no randomized controlled or propensity-matched trials have ever been performed. We investigated the effect of cleft closure on outcomes after cAVSD repair. METHODS: We reviewed 455 patients who underwent cAVSD repair between 1990 and 2019. To determine the effect of cleft closure, propensity score matching was performed on risk factors for reoperation after cAVSD repair. RESULTS: Median age was 3.6 months (mean, 9.6 ± 20.4 months), median weight was 4.3 kg (mean, 4.7 ± 4.3 kg) and 41.9% (191 of 455) were male. Early mortality was 2.9% (13 of 455), and survival was 89.8% ± 1.9% at 20 years. Early reoperation was a risk factor for mortality (P = .004). Freedom from reoperation was 72.5% ± 4.0% at 20 years. Freedom from LAVV reoperation was 74.1% ± 4.0% at 20 years. Preoperative severe LAVV regurgitation (P < .001) and early postoperative moderate or greater LAVV regurgitation (P = .007) were risk factors for reoperation, while trisomy 21 (P = .03) and recent era of surgery (P = .02) were protective. Propensity score matching yielded 106 pairs. There were no differences in long-term survival (P = .71) or reoperation (P = .26) between the 2 groups. CONCLUSIONS: Repair of cAVSD can be achieved with low mortality and good long-term survival, although the reoperation rate remains high. Similar freedom from reoperation can be achieved with or without closure of the LAVV cleft.