Thorac Cardiovasc Surg 2007; 55 - MP_7
DOI: 10.1055/s-2007-967301

Outcome after primary repair of atrioventricular septal defects with regard to anatomy and timing of repair

D Rassoulian 1, J Sachweh 1, A Tiete 1, R Kozlik-Feldmann 2, U Römer 2, B Reichart 1, S Daebritz 1
  • 1Ludwig-Maximilians-Universität München, Klinikum Grosshadern, Herzchirurgische Klinik, München, Germany
  • 2Ludwig-Maximilians-Universität München, Klinikum Grosshadern, Kinderkardiologische Klinik, München, Germany

Repair of atrioventricular septal defects (AVSD) remains a challenging procedure due to the complex three-dimensional malformation and variable anatomy. Timing of repair is discussed controversially because of the delicate AV-valve tissue in young infants.

Methods: We retrospectively analyzed 59 patients with repair of AVSD since 1999. Malformations in 26 patients were complete AVSD, 7 had complex AVSD (with tetralogy of Fallot/others) and 26 had partial AVSD (transitional 19%, ASD I 81%). Median age was 4.3, 11.0, and 23 months, respectively (p=0.000); 11 were <4 months of age. Trisomy 21 was present in 54% (complete AVSD 85%, complex 14%, partial 35%, p=0.000). Preoperative mitral regurgitation (MR) > grade 2 was present in 15%, 14% and 27% (p=0.536), respectively. The mitral cleft was completely closed in all but 10 patients for anatomical reasons (6 single papillary muscle).

Results: There was no operative mortality. Two patients (1 heterotaxy) died 0.9 and 4.8 years after surgery (primary pulmonary hypertension, unknown). Three patients (5%) had MR > grade 2 at discharge. Median follow-up was 2.3 years (0.01–4.8years). All but 1 survivors are in NYHA class I/II. One patient in each group was reoperated for MR, 4 have MR>grade2. Late development of moderate/severe MR or reoperation was not related to anatomic subgroups (p=0.603), trisomy (p=1.000), incomplete cleft closure (p=0.130), or age at repair (p=0.220).

Conclusions: Survival of primary AVSD repair is very good in all anatomical subgroups and at any age. Development of late mitral regurgitation is independent of the complexity of the AVSD, presence of trisomy 21, incomplete cleft closure, or age at repair.