Purpose: We identified the risk factors for remnant gastric cancer (RGC) based on remnant gastric mucosal characteristics and gastritis morphology in patients undergoing distal gastrectomy. Materials and Methods: This multicenter retrospective study included 100 patients with RGC after distal gastrectomy and 550 patients without RGC treated between 2013 and 2020.Endoscopic findings, including anastomotic redness, red streaks, enlarged folds, bile reflux as anastomotic findings, as well as disappearance of the regular arrangement of collecting venules (RAC), atrophic gastritis, and intestinal metaplasia as background gastric mucosal findings, were evaluated. Disease risk score matching (1:1) was adjusted for baseline characteristics. Logistic regression analysis was used to develop a risk score model to stratify RGC risk into low, moderate, and high categories. Results: After matching, 96 patients with RGC and 96 controls were analyzed. Anastomotic redness and red streaks, as well as the disappearance of RAC and atrophic gastritis, were significantly more frequent in the RGC group than in the control group, whereas enlarged folds and bile reflux showed no significant differences. Risk scores were assigned as follows:anastomotic redness, 2; red streaks, 3; disappearance of RAC, 7; and atrophic gastritis, 3. The total score stratified patients into high (≥15), moderate (7–14), and low risk (≤6). The positive and negative predictive values were 67.7% and 83.3%, respectively. Conclusions The endoscopic findings of anastomotic redness, red streaks, RAC disappearance, and atrophic gastritis were significantly associated with RGC development.The proposed risk-scoring model could serve as a stratification tool for RGC surveillance.

We report two surgical cases with corrected transposition of the great arteries associated with ventricular septal defect and pulmonary atresia undergoing total correction including reconstruction of the central pulmonary artery after reconstruction of the left pulmonary artery for non-confluent pulmonary arteries. Both patients underwent reconstruction of the left pulmonary artery using 13 or 12mm diameter heterologous pericardial conduit at age of 5 year, respectively. At surgery, after the left pulmonary artery was exposed between the upper and lower lobe of the left lung, the conduit was connected with the left pulmonary artery along the pericardium. Continuity between the conduit and the left subclavian artery or the ascending aorta was established with 5 or 6mm diameter Micronit grafts, respectively. Total correction was performed at 2 years and 10 months after the initial surgery, respectively. In a patient with {I, D, D} type corrected transposition of the great arteries, the central pulmonary artery was established with another 16mm diameter heterologous pericardial conduit, which ran in front of the left superior vena cava. The ventricular septal defect was closed via the right atrium. In another patient with {S, L, L}, the central pulmonary artery was established with the reconstructed conduit of the left pulmonary artery, which ran behind the left phrenic nerve. The ventricular septal defect was closed via the right atrium with the De Leval procedure. In both patients, continuities between the left ventricle and the central pulmonary artery were established with tricuspid valved porcine pericardial conduit and equine pericardial conduit. Postoperatively both patients had uneventful recovery with left ventricular/right ventricular systolic pressure ratios of 0.4 and 0.35, respectively.