Background. Transposition of the great arteries (TGA) is a complex congenital heart disease that requires early diagnosis as well as advanced surgical repair and postoperative support. This study sought to investigate the impact of surgical timing on early postoperative morbidity.Methods. This study reviewed all patients with TGA repaired at a single institution (Skåne University Hospital, Lund, Sweden) by arterial switch operation (ASO) between June 2001 and June 2017. Major postoperative morbidity (MPM) and death within 30 days after ASOs were documented. Patients with double-outlet right ventricle, chromosomal abnormalities, and noncardiac diseases were excluded. MPM was defined as the presence of at least 1 of the following: delayed sternum closure, reoperation, prolonged mechanical ventilation, noninvasive ventilation after extubation, peritoneal dialysis, extracorporeal membrane oxygenation, and readmission.Results. A total of 241 patients were included, with medians for birth weight, gestational week, and age at surgery of 3.5 kg, 39 weeks, and 5 days, respectively. MPM was encountered in 32.3% of patients. Prematurity (P [ .001) and need for aortic arch repair at the time of ASO (P [ .04) were associated with a significant increase in MPM. Non-A coronary anatomy, associated ventricular septal defect requiring surgical closure, and fetal diagnosis of TGA had no significant impact on MPM (P [ .35, .08, and .21, respectively). There was no significant difference in MPM among the surgical groups (P [ .49).Conclusions. Early complications after ASO do occur and are mostly associated with prematurity and the need for aortic arch repair. Timing of surgical repair does not seem to influence the rate of these complications.

In transposition of the great arteries (TGA), certain coronary patterns have been associated with major adverse events early after the arterial switch operation (ASO). We sought to determine the impact of preoperative echocardiographic (ECHO) diagnosis on the intra­ and postoperative morbidity. All patients with TGA born between June 2001 and June 2017 and who underwent ASO were reviewed. Data on presumed coronary anatomy (CA) preoperatively were obtained from the preoperative ECHO report. Intraoperative CA was categorized according to Yacoub classification. Major postoperative morbidity included at least one of the following: delayed sternal closure (DSC), prolonged (> 72 h) mechanical ventilation, reintubation, peritoneal dialysis (PD), ECMO, reoperation, and readmission within 30 days after surgery. 240 patients with median age of 5 days (range 1–614) and mean weight at surgery was 3.6 kg (1.8–8.4) were included. Preoperative ECHO assessment of CA was available in 228 patients. Intraoperatively, 181 patients (75%) were found to have type A, 25 patients had type B or C or intramural (B–C–IM; 10%), and 34 patients had type D or E (D–E; 14%). Patients with types B, C, and intramural coronary (B–C–IM) had increased risk for delayed sternum closure (9/25 vs. 20/181 in type A and 8/34 in type D–E; p = 0.04), peritoneal dialysis (4/25 vs. 8/181 and 1/34; p = 0.04), and ECMO (2/25 vs. 1/131 and 1/34; p = 0.02). Within the B–C–IM group, preoperative ECHO raised suspicion of type A in 13 patients (i.e., incorrect diagnosis, ID; 52%), whereas non-A CA was suspected in 12 patients (i.e., correct diagnosis, CD; 48%). With the exception of reoperation, which was seen only in the ID subgroup (4/12 vs. 0/10 in the CD subgroup; p = 0.04), the intraoperative (cardiopulmonary bypass time and cross-clamp time) and postoperative morbidity indices were comparable in both ID and CD subgroups (p > 0.1). Although there is a significant risk for early postoperative morbidity in TGA patients with single, interarterial, and intramural CA, there seems to be relatively limited influence of preoperative ECHO assessment of coronary anatomy on this morbidity burden.

Introduction: RV failure is a significant complication in patients with congenital heart disease with right-sided obstructive lesions, and PH. Effective medical treatment for decompensated RV remains to be elucidated. While ARBs are known to reduce mortality in patients with left side heart failure by inhibiting cardiac remodeling, their effects for RV failure are unknown. Pressure overload stress induces a robust autophagic response and hypertrophic changes in cardiomyocytes. However, previous studies showed conflicting results with regards to whether induction of autophagy was adaptive or maladaptive in overloaded ventricle. Method: RV failure model rats were surgically generated by pulmonary artery banding using SD rats. Those rats were treated with oral telmisartan (T group: 5 mg/kg/day n 5 24) or water as control (n 5 12) for 4 weeks. RV-PV loops were examined using a micro catheter. For histological analysis of cardiac muscles remodeling, Masson's trichrome staining and electron microscopy were performed to obtain the view of morphological changes of cardiomyocytes. The level of LC3A/B, and p62 were measured by Western blotting. Results: Median survival time for the T group was significantly longer than the control rats. There were significant increases in RV cardiac output (p , 0.01), RV EDP, end-systolic elastance, and end-diastolic elastance (p , 0.05) derived from RV PV loop in the T group. RV/LV 1 S was decreased significantly in the T group (p , 0.01). Quantitative analysis for autophagy showed significant reduction of the number of autophagosome in the T group. Both LC3A/B and p62 expressions were reduced in the T group compared with control. The rate of fibrosis in RV was significantly lower in the T group (p , 0.01) as well as mRNA expression of Pro-collagen 3, CTGF, and periostin. Conclusions: In PA banded rats, telmisartan had effects to improve RV cardiac output and to decrease mortality without reduction of RV pressure by inhibiting cardiac fibrosis, autophagy and RV hypertrophy. Decreased expressions of LC3A/B and p62 indicated that the reduction of autophagy was induced by mitochondria dysfunction. These results suggest that telmisartan prohibit overload-dependent RV failure and fibrosis by blocking mitochondrial dysfunction and telmisartan may be an effective treatment option for RV failure.