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find Author "ZHENG Fuzhen" 2 results
  • Risk factors and prognosis of new-onset conduction block following transcatheter aortic valve implantation

    Objective To analyze predictive factors, clinical implications and prognosis effects of new-onset conduction block after transcatheter aortic valve implantation (TAVI). Methods The clinical data of 86 patients who underwent TAVI through transfemoral approach from 2019 to 2021 in Fujian Provincial Hospital were retrospectively analyzed, including 59 males and 27 females with an average age of 72.9±8.0 years. The patients were divided into a normal group and a new-onset conduction block group according to whether there was new-onset conduction block after operation, and then the new-onset conduction block group was subdivided into a left bundle branch block (LBBB) group (28 patients) and a complete atrioventricular block (CAVB) group (11 patients). We compared the hemodynamics and TAVI-related complications between the postoperative and early follow-up periods, and used the multivariate logistic regression models to identify risk factors for the new-onset conduction block. Results The median EuroSCORE of all patients were 8 (2) points before the operation. In the postoperative and early follow-up periods, the hemodynamics and TAVI-related complications had no statistical difference between the new-onset conduction block group and the normal group (P>0.05). The incidence of permanent pacemaker implantation (81.8%, 9/11) and mortality due to cardiac causes (18.1%, 2/11) in the CAVB group were significantly higher than those in the normal group and theLBBB group (P<0.05). Female, severe calcification of the aortic valve, too large valve size and deep valve implants were the risk factors for new-onset conduction block after TAVI. ConclusionThe incidence of LBBB and CAVB is high after TAVI, however, both of them do not significantly effect the hemodynamics of the patients. Higher incidence of permanent pacemaker implantation is found in the CAVB group which affects the rate of rehospitalization and mortality. Female patients, severe calcification of the aortic valve, too large valve size and deep valve implants are the risk factors for the new-onset conduction block after TAVI.

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  • Effects of ginkgolide B on Caspase-3/PTEN/Akt pathway and cell proliferation and apoptosis in hypoxia/reoxygenation cardiomyocytes

    Objective To investigate the effect of ginkgolide B (GB) on cysteinyl aspartate specific proteinase-3 (Caspase-3)/chromosome 10 deletion phosphatase-tension protein homologue (PTEN)/protein kinase B (Akt) pathway and cell proliferation and apoptosis in hypoxia/reoxygenation cardiomyocytes. Methods H9C2 cells were cultured in vitro. A control group was cultured in serum-free DMEM high glucose medium at 37°C and 5% CO2 for 28 hours. The remaining groups were prepared with hypoxia/reoxygenation models. A GB low-dose group and a GB high-dose group were treated with GB pretreatment with final concentration of 50 μmol/L and 200 μmol/L respectively at 1 h before hypoxia/reoxygenation. A carvedilol group was treated with carvedilol of a final concentration of 10 μmol/L at 1 h before hypoxia/reoxygenation. The proliferation and apoptosis of H9C2 cells were detected, and the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), reactive oxygen species (ROS), PTEN, Akt, phosphorylated Akt (p-Akt) and Caspase-3 in H9C2 cells were also detected. Results Compared with the control group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in other groups decreased, and the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 increased (P<0.05). Compared with the hypoxia/reoxygenation group, the proliferation rate of H9C2 cell, and the levels of PTEN, Akt and p-Akt in all GB dose groups and the carvedilol group increased; the apoptosis rate, and the levels of LDH, MDA, ROS and Caspase-3 decreased, and the effect of GB was in a dose dependent manner; however, the effect of GB was not as strong as carvedilol (P<0.05). Conclusion GB can inhibit H9C2 cell apoptosis and promote H9C2 cell proliferation by activating Caspase-3/PTEN/Akt pathway.

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