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@#Objective To evaluate the results of a hybrid procedure for treating Stanford type B1C aortic dissection. Methods In our center, 49 patients with Stanford type B1C aortic dissection underwent supra-arch branch vessel bypass and thoracic endovascular aortic repair (TEVAR) from December 2013 to December 2017. There were 33 males and 16 females with an average age of 60.4±5.5 years. Left common carotid artery to left subclavian artery bypass (n=29), right common carotid artery to left common carotid artery and left subclavian artery bypass (n=18), left common carotid artery to left subclavian artery and right common carotid artery to right subclavian artery bypass (n=2) were performed. Results Early mortality rate was 2.0% (1/49). Forty-eight patients survived postoperatively. The follow-up rate was 100.0% (48/48). The patients were followed up for 6 to 47 (26.8±11.9) months postoperatively. Chest pain relapsed in one patient 8 months after the operation. The whole aorta CTA showed type A1S aortic dissection in one patient 6 months after the operation, and the re-operation was satisfactory. There was no endoleak or paraplegia. Conclusion Initial results suggest that the one-stage hybrid procedure is a suitable therapeutic option for type B1C aortic dissection.
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@#Objective To summarize the clinical experience in the treatment of high-risk patients with severe aortic valve disease by transcatheter aortic valve implantation (TAVI) via heart apex approach and to evaluate the early efficacy. Method Five patients who underwent TAVI via heart apex approach from September 2017 to February 2019 in Henan Thoracic Hospital were retrospectively analyzed, including 3 males and 2 females, aged 65-84 (74.6±4.5) years. Result All operations were performed through a small left incision into the thoracic cavity (3-5 cm), and then through the J-Valve transport system, the aortic valve was successfully released via heart apex after precise positioning under digital subtraction angiography. One patient developed ventricular fibrillation during the operation, and the operation was completed with the assistance of emergency femoral arteriovenous catheterization cardiopulmonary bypass; one patient underwent percutaneous coronary intervention first because of severe coronary stenosis; one patient had paroxysmal atrial fibrillation during the perioperative period, and had hepatorenal insufficiency and thrombocytopenia after the operation, and was improved after medical treatment; one patient had perivalvular leak during the operation, and was improved after re-implantation of the valve; one patient was in stable condition during operation and recovered smoothly after operation. Surgery was successful in all 5 patients. The follow-up time was 2-19 months, and the early clinical effect was good. Conclusion The short-term clinical efficacy of TAVI via heart apex approach in the treatment of high-risk severe aortic valve disease is definite and safe, but the long-term and medium-term effects need to be further evaluated.
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@# Objective: To explore the resistance of CD133+ cells in HepG2 cell line to doxorubicin (DOX) and its mechanism. Methods: CD133+ cells were sorted by magnetic beads and CD133+ positive rate was detected by flow cytometry. MTT assay was used to detect the resistance to DOX-induced apoptosis of CD133+ cells. The expression of BCRP transporter mRNA was detected by RT-PCR. The expression of apoptosis-related proteins was detected by Western blotting. Immunofluorescence assay was used to detect the activation and transportation of P65 after DOX treatment. Results: Magnetic beads sorting could efficiently sort the CD133+ cells from HepG2 cells. MTT proliferation assay showed that CD133+ cells had stronger resistance to DOX than CD133- cells (P<0.05). Immunofluorescence showed that the activation rate and content of P65 in CD133+ cells were significantly higher than those in CD133- cells and HepG2 cells (P<0.05). The results of RT-PCR showed that the mRNA content of BCRP in CD133+ cells was significantly increased compared with CD133- cells and HepG2 cells (all P<0.05). Compared with HepG2 and CD133- groups, the expression of Bax and p53 in CD133+ cells was significantly decreased (P<0.05), while the expression of Bcl-2 and Survivin protein in CD133+ cells was significantly increased (P<0.05 or P<0.01). Conclusion: The molecular mechanism of high DOX-resistance of the CD133+ cell subsets in HepG2 cells is the high expression of the survival-related proteins NF-κB, Bcl-2, Survivin and the drug-resistance transporter BCRP, and low expression of apoptosis-promoting proteins p53 and Bax.