Reshaping bicuspid aortic valve stenosis with an hourglass-shaped balloon for transcatheter aortic valve replacement: A pilot study.

OBJECTIVES: We evaluated the safety and usefulness of preparatory anatomical reshaping with a geometric hourglass-shaped balloon to optimize transcatheter aortic valve replacement (TAVR) outcomes in bicuspid aortic valve (BAV) stenosis. BACKGROUND: TAVR has been increasingly performed for BAV stenosis; however, technical challenges remain. Procedural results are suboptimal given unfavorable valvular anatomies. METHODS: Eligible patients with BAV stenosis were enrolled to undergo aortic valve predilatation with the hourglass-shaped TAV8 balloon before TAVR using the self-expandable Venus A-Valve. Procedural details and outcomes were compared to a sequential group of patients with BAV who underwent TAVR with the same device following preparatory dilatation using a cylindrical balloon. RESULTS: A total of 22 patients were enrolled in the TAV8 group and 53 were included in the control group. Valve downsizing was less common in the TAV8 group (36.4 vs. 67.9%; p = .012). Stable valve release and optimal implant depth were consistently achieved in the TAV8 group with no requirement for a second valve (0 vs. 17.0%; p = .039) and with higher device success rates (100.0 vs 77.4%; p = .014). Residual aortic regurgitation graded as ≥mild was less common in the TAV8 group (13.6 vs 45.3%; p = .009). Mortality was similar (0 vs. 3.8%; p = 1); no major/disabling stroke or conversion to open-heart surgery was seen in either group within 30 days. CONCLUSIONS: Compared with standard cylindrical balloon valvuloplasty, preparatory reshaping with the hourglass-shaped balloon before self-expandable TAVR in BAV was associated with significantly better procedural results and may encourage more promising outcomes.

[Protective Effect of Activated Nrf2 against Hyperoxia-induced Lung Injury in Neonatal Rats].

OBJECTIVE: To observe the effect of nuclear factor erythroid 2-related factor 2 (Nrf2) agonist on the apoptosis of alveolar cell induced by hyperoxia and to explore whether Nrf2 activation could protect neonatal rats from hyperoxia induced lung injury. METHODS: 90 neonatal Sprague-Dawley rats were randomized into room air group (FiO2 =21%, N group), hyperoxia group (0 group) and Nrf2 group (n=30 each). Neonatal rats in the 0 group and Nrf2 group received saline 0. 2 mL and Nrf2 agonist 30 mg/kg respectively at the first and second day after birth, and were exposed in high concentration oxygen (95%) for 4 d. N group rats were fed in room air. The apoptotic index (AI) and Nrf2 expression of lung tissue were detected by TUNEL and immunohistochemistry staining respectively. RESULTS: Compared with 0 group (28. 8% ± 3. 0%), the AI of alveolar. cell was lower in N group (0. 7%±0. 6%) and Nrf2 group (7. 2% ± 0. 8%) (P<0. 01). The expression of Nrf2 was significantly higher in 0 group (926. 80 ± 130. 51) and Nrf2 group (1038. 40±151. 12) than that in N group (30. 03±9. 99) (P<0. 01). CONCLUSION: Nrf2 activation could reduce the alveolar cellular apoptosis and protect neonatal rats from hyperoxia induced lung injury.

Biotin-streptavidin cross-bridging: a novel and feasible approach for targeting transplanted cells to damaged tissue.

BACKGROUND: Accumulating evidence indicates the positive impact of endothelium-derived cell therapy in vascular repair. However, low cell transplantation efficiency inevitably and greatly reduces the treatment efficacy of cell transplants. PURPOSE: To modify the surfaces of cells with polypeptides or small-molecule proteins that specifically recognize and bind to damaged tissue. METHODS: We used a biotin-streptavidin binding approach to attach annexin V, which recognizes apoptotic cells, onto bEnd.3 cells that express vascular endothelial growth factor receptor 2 (VEGFR2) and verified that the modified cells could efficiently bind to dead cells in vitro. RESULTS: We analyzed biotinylated VEGFR2-bEnd.3 cells, streptavidin-biotinylated VEGFR2-bEnd.3 cells, and biotinylated annexin V-streptavidin-biotinylated VEGFR2-bEnd.3 cells. Our results from flow cytometry analysis and immunofluorescent examination demonstrated that we successfully labeled the cells in a three-step process. Furthermore, we determined that the positive binding rate correlated with reagent concentration. Immunofluorescent examination illustrated that adding the biotinylated annexin V-streptavidin-biotinylated VEGFR2-bEnd.3 cells to dead cells led to the clustering and aggregation of the modified cells and the dead cells. CONCLUSIONS: Annexin V can be attached to bEnd.3 cells using a biotin-streptavidin binding approach, and the modified cells can specifically recognize and bind to dead cells.