Sutureless Repair of Extracardiac Univentricular Total Anomalous Pulmonary Venous Connection.

BACKGROUND: This study aimed to evaluate the results of sutureless repair of extracardiac total anomalous pulmonary venous connection (TAPVC) with a functional single ventricle at a single institution, including changes in the anastomotic site over time. METHODS: The database contained 98 patients with single-ventricle anatomy who underwent extracardiac TAPVC repair from 1996 to 2022. The median age and body weight at surgery were 59 days and 3.8 kg, respectively. Eighty-seven patients had heterotaxy syndrome, and 42 had preoperatively obstructed TAPVC. Primary sutureless repair was performed in 18 patients, 13 of whom were neonates. The cross-sectional area of the anastomotic site of the atrium and pericardium was divided by the body surface area, and the changes in this value over time were assessed. The median follow-up was 5.2 years (range, 0-19.4 years). RESULTS: Operative mortality and late mortality occurred in 2 (2.0%) and 38 (38.8%) patients, respectively. The actuarial survival rate at 5 years postoperatively was 56.2%. Multivariate analysis identified preoperatively obstructed TAPVC as a risk factor for mortality. Recurrent pulmonary venous stenosis (PVS) developed in 25 patients, thus giving a 5-year rate of freedom from PVS of 64.9%. Multivariate analysis revealed that sutureless repair significantly decreased the incidence of recurrent PVS. The cross-sectional anastomotic area tended to grow in accordance with the patients' growth. CONCLUSIONS: Sutureless repair of extracardiac TAPVC with univentricular anatomy achieved acceptable results. The anastomotic site tended to grow over time and contributed to a decline in the rate of recurrent PVS.

Necrostatin-1 Attenuates Delayed Paraplegia after Transient Spinal Cord Ischemia in Rabbits by Inhibiting the Upregulation of Receptor-Interacting Protein Kinase 1 and 3.

BACKGROUND: Delayed-onset paraplegia is a disastrous complication after thoracoabdominal aortic open surgery and thoracic endovascular aortic repair. Studies have revealed that transient spinal cord ischemia caused by temporary occlusion of the aorta induces delayed motor neuron death owing to apoptosis and necroptosis. Recently, necrostatin-1 (Nec-1), a necroptosis inhibitor, has been reported to reduce cerebral and myocardial infarction in rats or pigs. In this study, we investigated the efficacy of Nec-1 in delayed paraplegia after transient spinal cord ischemia in rabbits and assessed the expression of necroptosis- and apoptosis-related proteins in motor neurons. METHODS: This study used rabbit transient spinal cord ischemia models using a balloon catheter. They were divided into a vehicle-treated group (n = 24), Nec-1-treated group (n = 24), and sham-controls (n = 6). In the Nec-1-treated group, 1 mg/kg of Nec-1 was intravascularly administered immediately before ischemia induction. Neurological function was assessed using the modified Tarlov score, and the spinal cord was removed 8 hr and 1, 2, and 7 days after reperfusion. Morphological changes were examined using hematoxylin and eosin staining. The expression levels of necroptosis-related proteins (receptor-interacting protein kinase [RIP] 1 and 3) and apoptosis-related proteins (Bax and caspase-8) were assessed using western blotting and histochemical analysis. We also performed double-fluorescence immunohistochemical studies of RIP1, RIP3, Bax, and caspase-8. RESULTS: Neurological function significantly improved in the Nec-1-treated group compared with that in the vehicle-treated group 7 days after reperfusion (median 3 and 0, P = 0.025). Motor neurons observed 7 days after reperfusion were significantly decreased in both groups compared with the sham group (vehicle-treated, P < 0.001; Nec-1-treated, P < 0.001). However, significantly more motor neurons survived in the Nec-1-treated group than in the vehicle-treated group (P < 0.001). Western blot analysis revealed RIP1, RIP3, Bax, and caspase-8 upregulation 8 hr after reperfusion in the vehicle-treated group (RIP1, P = 0.001; RIP3, P = 0.045; Bax, P = 0.042; caspase-8, P = 0.047). In the Nec-1-treated group, the upregulation of RIP1 and RIP3 was not observed at any time point, whereas that of Bax and caspase-8 was observed 8 hr after reperfusion (Bax, P = 0.029; caspase-8, P = 0.021). Immunohistochemical study revealed the immunoreactivity of these proteins in motor neurons. Double-fluorescence immunohistochemistry revealed the induction of RIP1 and RIP3, and that of Bax and caspase-8, in the same motor neurons. CONCLUSIONS: These data suggest that Nec-1 reduces delayed motor neuron death and attenuates delayed paraplegia after transient spinal cord ischemia in rabbits by selectively inhibiting necroptosis of motor neurons with minimal effect on their apoptosis.

Surgical results of total anomalous pulmonary venous connection repair in 256 patients.

OBJECTIVES: This study was performed to analyse the surgical results of total anomalous pulmonary venous connection (TAPVC) repair at a single institution and to identify trends and variables associated with mortality and morbidity, particularly predictors of recurrent pulmonary venous obstruction (PVO). METHODS: Our surgical database contained 256 patients with biventricular anatomy who underwent surgical repair for TAPVC from 1981 to 2016. The anatomic TAPVC subtypes in this study were as follows: 114 supracardiac (44.5%), 56 cardiac (21.9%), 64 infracardiac (25.0%) and 22 mixed (8.6%) types. The follow-up for the entire study ranged from 1.6 months to 28.2 years (median 10.4 years). Preoperative PVO was present in 128 patients (50.0%). All patients with TAPVC with single-ventricle anatomy were excluded from the analysis. Data were retrospectively reviewed. RESULTS: Seven (2.7%) early deaths and 26 (10.1%) late deaths occurred. The actuarial survival rate at 20 years postoperatively was 85.3%. The preoperative predictors of operative mortality were younger age and the era of TAPVC repair (before 1998). In addition to these variables, associated cardiac anomalies were predictors of late mortality. Those for postoperative PVO were younger age, lower weight and being an emergency case. The actuarial survival rate at 20 years was 38.6% for patients with postoperative PVO and 92.2% for patients without postoperative PVO (P < 0.001). CONCLUSIONS: The long-term outcomes after TAPVC repair in patients with biventricular anatomy were satisfactory. Mortality was significantly associated with the rate of progression of postoperative PVO, and careful follow-up was required especially within 6 months after the primary operation.

Thoracic endografting increases cardiac afterload and leads to left ventricular hypertrophy in dogs.

OBJECTIVES: Aortic endografting can cause aortic stiffening. We aimed to determine the chronic effect of thoracic endografting on cardiac afterload, function and remodelling. METHODS: Eleven dogs were included, and all except 1 was successfully assessed [endograft, n = 5; sham operation (control), n = 5]. We deployed a stent graft in the descending aorta. The ascending aortic pressure and flow were measured, and aortic input impedance was obtained by frequency analysis to determine characteristic impedance and arterial compliance. Left ventricular pressure-volume relations were measured with an admittance catheter. Measurements were performed before, 10 min after and 3 months after endografting. Following euthanasia, we weighed the left ventricle of each dog and measured the cardiomyocyte cell size. RESULTS: Arterial compliance decreased from 0.47 ± 0.07 to 0.36 ± 0.06 and to 0.31 ± 0.05 ml/mmHg (both P < 0.01 versus baseline), and characteristic impedance increased from 0.11 ± 0.04 to 0.19 ± 0.05 and to 0.21 ± 0.04 mmHg/ml/s (both P < 0.01 versus baseline) 10 min and 3 months after endografting, respectively. Pressure-volume relation analysis showed that arterial elastance increased from 5.3 ± 1.0 to 6.7 ± 1.6 (at 10 min) and to 6.8 ± 1.0 mmHg/ml (at 3 months) (both P < 0.05 versus baseline), but end-systolic elastance and ventriculo-arterial coupling remained unchanged. Left ventricular weight to body weight ratio and left ventricular cardiomyocyte cell width in the endograft group were larger compared with the control's results (5.06 ± 0.27 g/kg vs 4.20 ± 0.49 g/kg, P = 0.009, 15.1 ± 1.7 µm vs 13.9 ± 1.5 µm, P = 0.02, respectively). CONCLUSIONS: The mid-term effect of the descending aortic endografting on left ventricular contractility and efficiency in canine normal hearts was minimal. However, endografting resulted in increased cardiac afterload and left ventricular hypertrophy.

Surgical repair of ostial obstruction of the coronary artery for quadricuspid aortic valve in an infant.

A congenital quadricuspid aortic valve accompanied by ostial obstruction of the left coronary artery is extremely rare and has not yet been reported in an infant. We herein describe an infant with ostial obstruction of the left coronary artery caused by a small left coronary cusp that formed a pouch. The patient's cardiac function deteriorated due to progressive myocardial ischaemia, and translocation of the ostium of the left coronary artery was performed. Postoperative coronary angiography revealed good filling of the left coronary artery.

Usefulness of 18F-FDG-PET/CT in aortic graft infection: two cases.

Diagnosis of vascular graft prosthesis infection is crucial, but not straightforward. Here we report two cases in which [(18)F] fluoro-2-deoxy-D-glucose positron emission tomography/computed tomography ((18)F-FDG PET/CT) was very useful in the diagnosis of aortic graft infection. Case 1: A 77-year-old Japanese man, two months status post aortic arch graft surgery, suffered from repeated fevers. Blood cultures revealed bacteremia. (18)F-FDG-PET/CT ruled out graft infection and diagnosed lumbar pyogenic spondylitis, which was treated with antibiotics, sparing the patient a possible reoperation. Case 2: A 53-year-old Japanese man, seven years status post replacement of the aortic root and ascending aorta, had been suffering from an ostensibly aseptic fistula for over a year and a half. Although repeated CT findings had been negative, (18)F-FDG-PET/CT clearly demonstrated communication between the fistula and the ascending aortic graft. He was treated with repeat ascending aortic replacement, omentopexy, and antibiotics. Our experience supports (18)F-FDG-PET/CT as a promising modality in cases of suspected vascular graft infection.