Se Jin Oh

Background: Endovascular aneurysm repair (EVAR) for abdominal aortic aneurysm (AAA) is associated with risks such as endoleaks and late aneurysm rupture, highlighting the importance of long-term survival prediction. Despite recent advancements in machine learning (ML), predictive models utilizing time-to-event analysis remain limited for AAA patients undergoing EVAR. We aimed to develop a stacking ensemble ML model to predict long-term outcomes in EVAR-treated AAA patients. Methods: From 2002 to 2019, a total of 12,312 patients underwent EVAR. The primary outcome was AAA-related mortality, with follow-up until December 31, 2019. Using 5 ML algorithms, we developed a model comprising 34 variables. Model performance was assessed using the time-dependent C-index and Brier score. Variable importance was evaluated through permutation-based and partial dependent plots. Results: The stacking ensemble model showed the best predictive performance among the tested models (time-dependent C-index: 0.759 at 30 days, 0.716 at 365 days). The time-dependent Brier scores generally increased slightly over time but remained stable across all ML algorithms. Important predictors included age, smoking status, duration between diagnosis and surgery, household income, renal function, and blood pressure. Variable importance differed over time, and each predictor presented a nonlinear relationship with AAA-related mortality risk. Conclusion: The stacking ensemble ML model for time-to-event prediction identified dynamic, time-varying changes in predictor importance, providing improved risk stratification and phase-specific management after EVAR.

Background: This randomized controlled trial was conducted to evaluate the impact of posterior pericardiotomy on the prevention of postoperative atrial fibrillation (POAF) in patients who underwent off-pump coronary artery bypass grafting (CABG). Methods: Adult patients who were scheduled to undergo isolated off-pump CABG were assessed for eligibility, and eligible patients were randomly assigned in a 1:1 manner to pericardiotomy or no intervention. Patients and postoperative caregivers were blinded to treatment assignment. The primary endpoint was the occurrence rate of POAF, and the secondary endpoints were the cumulative time spent in POAF and early outcomes, including operative mortality. Results: A total of 403 patients were screened for eligibility, and 270 patients were randomly assigned to the posterior pericardiotomy group (n=136) or control group (n=134). The mean age was 67.8±10.3 years, and 20.4% (55 of 270 patients) were female. There was no intergroup difference in baseline characteristics or surgical data. Off-pump CABG was performed as planned in all patients except one. All patients received the assigned treatment regarding pericardiotomy, and no intergroup crossover occurred. POAF occurred in 27.8% (75 of 270 patients) of patients at a median of 2 days (interquartile range 1–3 days) after surgery. There was no significant difference in the occurrence rate of POAF between the two groups (30.1% and 25.4% in the pericardiotomy and control groups, P =.38). There were no significant differences in the secondary endpoints between the two groups. Conclusions: Posterior pericardiotomy does not reduce the occurrence rate of POAF in patients undergoing off-pump CABG. ( NCT06159985 )

Background: Autologous venous conduits remain the mainstay of coronary artery bypass grafting (CABG); however, their long-term patency is limited by adverse vascular remodeling. While arterial and venous grafts undergo structural and molecular adaptation to arterial hemodynamics, the mechanisms underlying successful adaptation remain poorly characterized owing to the scarcity of functioning human graft tissues. Methods: We analyzed bypass grafts explanted en bloc during orthotopic heart transplantation, comprising patent vein grafts (VGP, n=19), occluded vein grafts (VGO, n=9), and patent arterial grafts (AGP, n=13), alongside freshly harvested controls (vein, n=23; artery, n=11). Quantitative histomorphometry, label-free LC-MS/MS proteomics, pathway analysis, and immunohistochemistry were performed. Results: While patent arterial and venous grafts exhibited medial elastin reinforcement, adventitial neovascularization, and organized intimal remodeling, occluded vein grafts demonstrated elastic layer disruption, medial degeneration, and collagen-dense fibrosis. Proteomic analysis revealed a convergent adaptive signature in patent grafts enriched for RNA metabolism, protein synthesis, cytoskeletal dynamics, and extracellular matrix organization, with shared activation of NR4A3, STAT1, and EGFR signaling. Vein-specific adaptation involved SRC-PTGES activation with concomitant STAT3 suppression, whereas arterial grafts engaged IGF1-RUNX2-associated proliferative programs. Failed venous grafts exhibited angiotensin-driven fibroinflammatory remodeling. Endothelial nitric oxide synthase expression was markedly upregulated in the luminal endothelium and adventitial neovessels of patent grafts. Conclusions: Despite distinct vascular origins, arterial and venous grafts converged toward a shared adaptive phenotype characterized by structural maturation and vasoprotective signaling. Targeting common adaptive pathways-including NR4A3, STAT1, EGFR, and adventitial eNOS-may offer therapeutic strategies to enhance long-term graft durability.

Heart failure (HF), particularly acute decompensated heart failure (ADHF), remains a significant health challenge, with limited long‐term therapeutic options to alleviate congestion and improve cardiac function. Pharmacological treatments focus on reducing congestion, but many patients are discharged with persistent symptoms, leading to poor outcomes. Current device‐based solutions, such as balloon catheters, offer some relief from fluid overload but require hospitalization, a driveline, and direct blood contact, limiting long‐term use. A s uperior‐vena‐cava (SVC) c ompressive s hape‐memory‐alloy (SMA) implantable device, “SCS” is presented, which is designed to wrap around the SVC and externally compress it to regulate blood flow, alleviating ADHF symptoms. The SCS device, actuated by biocompatible SMA actuators, adjusts the SVC's cross‐sectional area to control blood flow. Unlike existing solutions, the SCS device operates without direct blood contact, minimizing thrombosis and endothelial damage while offering a long‐term implantable solution. Benchtop tests verified the SCS's effectiveness in flow regulation (68% decrease in flow rate) while maintaining a safe surface temperature (<40 °C). In‐vivo tests in a porcine heart failure model demonstrated the device's ability to reduce left ventricular preload, observed through a leftward shift in the pressure‐volume loop (18.6% reduction in end‐diastolic volume), validating its potential as a long‐term solution for ADHF.

Choi HJ, et al. J Korean Med Sci. 2025 Aug;40(45):e238. https://doi.org/10.3346/jkms.2025.40.e238

Dong Jae Han, M.D., You Jung Ok, M.D., Ph.D., Se Jin Oh, M.D., Ph.D., Jae-Sung Choi, M.D., Ph.D., Yong Won Seong, M.D., Hyeon Jong Moon, M.D.. J Chest Surg 2024;57:477-83. https://doi.org/10.5090/jcs.24.026

Sangil Yun, M.D., You Jung Ok, M.D, Ph.D., Se Jin Oh, M.D., Ph.D., Jae-Sung Choi, M.D., Ph.D., Hyeon Jong Moon, M.D., Yong Won Seong, M.D.. J Chest Surg 2024;57:329-38. https://doi.org/10.5090/jcs.23.161

Background Abdominal aortic aneurysm (AAA) is a potentially lethal condition that often remains asymptomatic until it ruptures. Recent research suggests that immune-inflammatory processes are associated with AAA development, yet the exact mechanisms remain unclear. Serum C-reactive protein (CRP) serves as a prognostic marker for AAA and various cardiovascular diseases. When CRP accumulates in damaged tissues, it transforms into a monomeric form, exacerbating tissue damage. Our previous study confirmed the presence of CRP deposition in eroded AAA and atherosclerosis regions, accompanied by an increased infiltration of inflammatory cells. However, a comprehensive understanding of the specific changes in the inflammatory cellular landscape attributable to CRP deposition is lacking. Here, we aimed to explore cellular-level alterations in AAAs associated with varying CRP levels. Methods We categorized AAA patients into High-CRP (≥0.1 mg/dL, and ≥3+ CRP IHC score, n=6) and Low-CRP (≤0.1 mg/dL, and ≤1+ CRP IHC score, n=3), and used normal aorta specimens as a baseline control. The cellular landscape of immune and stromal components was characterized using Co-Detection by Indexing (CODEX) tissue imaging with 31 DNA-barcoded antibodies, followed by single-cell-based analysis and GPU-accelerated unsupervised clustering. Results We identified 51 distinct immune and stromal cell types in the cohort and revealed significant differences in protein expression patterns among the groups. In AAA, stromal cells decreased significantly, while immune cell proportions sharply increased. Lag3+ T cell regulators decreased, leading to an increase in CD3+ T cells. The composition of immune cells within atherosclerotic plaques was associated with the degree of CRP deposition in AAA. The High-CRP group showed increased M1 and Ki67+ proliferating macrophages, while the Low-CRP group exhibited intensified fibrosis with M2 macrophages. Conclusions Our study found significant variations in immune cell distribution within AAA walls based on CRP levels. These findings suggest a potential link between CRP-related immune changes and AAA progression. HIGHLIGHTS By performing CODEX (co-detection by indexing) multiplexed imaging on paraffin-embedded, formalin-fixed archived abdominal aortic aneurysm (AAA) tissue samples with varying CRP levels, we segmented 415,365 cells into 51 distinct clusters. In AAA, the presence of CRP deposition led to variations in the spatial relationships, distances, and enrichment patterns among immune and stromal cells.. In AAA-High CRP, there was an intensified infiltration of M1 macrophages and various immune cells observed in the atherosclerotic plaque. In AAA-Low CRP, severe stromal fibrosis was associated with M2 macrophages. Our results suggest that the deposition of CRP into the atherosclerotic plaque alters the immune-stromal landscape in AAA.