Senning With Aortic Translocation and Anatomic Repair for Congenitally Corrected Transposition.

BACKGROUND: Anatomic repair for congenitally corrected transposition of the great arteries with ventricular septal defect (VSD) and pulmonic stenosis has been accomplished with atrial switch and Rastelli. Aortic translocation offers a direct left ventricular outflow without an extraanatomic right ventricular-to-pulmonary conduit, which may lead to decreased reoperations. We reviewed our entire experience performing Senning with aortic translocation (SAT). METHODS: From 2007 to 2017, 8 patients (mean age, 14.1 months; size, 8.86 kg) underwent SAT. Associated anomalies included situs inversus (n = 2), dextrocardia (n = 6), multiple muscular VSDs (n = 2), abnormal or straddling atrioventricular valve chords (n = 5), and branch pulmonary artery stenosis (n = 3). Four of 8 had previous systemic arterial shunts. Mean cardiopulmonary bypass was 487 minutes, and mean cardiac ischemic time was 307 minutes. Additional procedures included repair of branch pulmonary artery stenoses and closure of multiple muscular VSDs. RESULTS: There was no hospital death. One patient was supported with extracorporeal membrane oxygenation because of junctional tachycardia on postoperative day 5. One patient required pacemaker placement for first-degree heart block. Median hospital length of stay was 31 days. Mean length of follow-up was 52 months. All patients remain well with mild or no aortic regurgitation. The first patient underwent a repeat surgical operation for pulmonary venous baffle obstruction 2 years after SAT. CONCLUSIONS: Despite the technical complexity, patient outcomes have been satisfactory. We believe SAT provides a superior anatomic repair in these complex defects. Longer-term follow-up is needed regarding late intervention.

Effect of General Anesthesia on Cardiac Magnetic Resonance-Derived Cardiac Function in Repaired Tetralogy of Fallot.

Cardiac magnetic resonance imaging (CMR)-derived ejection fraction (EF) predicts adverse outcomes in repaired tetralogy of Fallot (rTOF) and drives timing of pulmonary valve replacement. Certain patient populations require sedation for successful CMR image acquisition. General anesthesia (GA) has been shown to depress EF and heart rate (HR) in animal models, however, its effect on congenital heart disease is unknown. A retrospective review was conducted of all CMR patients referred with rTOF between January 2011 and May 2019. The cohort was separated into GA and non-GA groups. Propensity score matching (PSM) adjusted for selection bias. A kernel matching algorithm was used to match subjects and the differences in mean treatment effect on the treated were computed for left ventricular (LV) and right ventricular (RV) EF, HR, and cardiac index (CI). 143 patients met criteria, 37 patients under GA (mean age 15 years, range 2-45, 59% male), and 106 patients without GA (mean age 21 years, range 10-53, 50% male). Unmatched analysis showed significant depression of LV EF (50 vs. 57%, p < 0.001) and RV EF (42 vs. 48%, p < 0.001) in the GA group compared to the non-GA group. There was no significant difference in HR or CI. After matching and PSM adjustment, the GA group had a significant decrease in LV EF (49 vs. 56%, p < 0.001), RV EF (41 vs. 48%, p < 0.001), CI (2728 vs. 3701 ml/min/m2, p < 0.001), and HR (72 vs. 79 bpm, p = 0.04). General anesthesia with sevoflurane results in depressed CMR-derived EF.

Percutaneous closure of a complex posttraumatic muscular ventricular septal defect.

We report the percutaneous closure of a complex traumatic ventricular septal defect resulting from a stab wound to the anterior chest. The patient presented with heart failure 3 months after the initial trauma. Evaluation revealed a new large ventricular septal defect with diminished cardiac function. Closure was accomplished with a combination of an Amplatzer muscular ventricular septal defect occluder and two Amplatzer vascular plugs.

Endovascular stent placement for right ventricle to pulmonary artery conduit stenosis in the Norwood with Sano modification.

OBJECTIVE: Conduit obstruction is increasingly recognized as a complication of the Sano modified Norwood procedure. We report our experience with stent placement to ameliorate conduit stenoses and prevent premature surgical intervention. DESIGN: Records for all patients having undergone a Sano modified Norwood between September 2003 and December 2006 were reviewed. All patients with Sano conduit obstruction requiring stent placement were included. Sites of obstruction, method of stenting, pre- and poststent oxygen saturations, reinterventions, age at next surgery, and complications were collected and reviewed. RESULTS: Forty-one patients underwent a Sano modified Norwood procedure, and 9 patients had stents deployed for conduit stenoses. The patients presented a median of 52 days following Norwood palliation. Twelve stents were successfully placed in 9 patients. In 8 patients, saturations improved from a median of 67.5% to 81% after stent placement (P = .0005). Arterial saturations were unavailable in 1 patient requiring extracorporeal membrane oxygenation. No patients required reintervention after stent placement. The median age at their next surgery was 144 days. Seven patients underwent a successful bidirectional Glenn, 1 patient underwent a modified Blalock-Taussig shunt, and 1 expired. Complications included hypotension during stent deployment and 1 episode of transient complete heart block. CONCLUSIONS: Transcatheter treatment of Sano conduit obstruction can be performed safely and results in immediate improvement in oxygenation, thereby allowing substantial delay of the cavo-pulmonary shunt.

Combined endothelial nitric oxide synthase upregulation and caveolin-1 downregulation decrease leukocyte adhesion in pial venules of ovariectomized female rats.

BACKGROUND AND PURPOSE: We recently found that chronic estrogen depletion enhances leukocyte adhesion in pial venules in the female rat, while estrogen repletion decreases it. Estrogen-associated repression of inflammation may be due to upregulation of the endothelial isoform of nitric oxide synthase (eNOS) and concomitant downregulation of the endogenous inhibitor of eNOS, caveolin-1 (CAV-1). In this study we examined the effects of estrogen-independent eNOS upregulation (via simvastatin) and/or CAV-1 downregulation (antisense) on pial venular leukocyte adhesion in ovariectomized (OVX) rats. METHODS: Intact and OVX rats were prepared with closed cranial windows. Adherent rhodamine 6G-labeled leukocytes were viewed by intravital microscopy. To demonstrate the importance of pial venular eNOS in the resistance to leukocyte adhesion, intact female rats were treated with a nonselective (N(G)-nitro-L-arginine) or a neuronal NOS-selective (7-nitroindazole) inhibitor. In OVX females, leukocyte adhesion was compared in the following groups: (1) untreated; (2) treated with simvastatin; (3) treated with simvastatin plus CAV-1 antisense; (4) treated with simvastatin plus CAV-1 missense; (5) treated with CAV-1 antisense; and (6) treated with CAV-1 missense. RESULTS: In intact females, pial venular leukocyte adhesion was increased when total NOS activity, but not neuronal NOS activity alone, was blocked. In OVX rats, basal leukocyte adhesion, measured as the percentage of venular area occupied by adherent leukocytes, was attenuated (by approximately equal 60%) only in the presence of combined simvastatin plus CAV-1 antisense treatment. CONCLUSIONS: Present findings demonstrate that eNOS-derived NO plays an important role in limiting cerebral venular leukocyte adhesion in female rats. These data also suggest that simvastatin-induced upregulation of eNOS expression in OVX rats will not restore eNOS function, as measured by decreased leukocyte adhesion, unless CAV-1 levels are reduced as well.