ObjectiveTo investigate the quality of life in patients with severe aortic stenosis (AS) after transcatheter aortic valve replacement (TAVR) and analyze the related influencing factors. MethodsA total of 139 patients who had undergone TAVR in Department of Cardiovascular Medicine, West China Hospital, Sichuan University, were selected through the hospital electronic medical record system from April of 2012 to April of 2017. By using the General Information Questionnaire for Patients, Charlson＇s co-morbidity Index (CCI), Morisky Medication Adherence Scale, and China Cardiovascular Quality of Life Questionnaire (CQQC), their life quality were investigated and the influencing factors were analyzed. ResultsThe average score of CQQC after TAVR was (78.76±16.52), lower than the national norm. There were statistical difference in the scores of CQQC in patients with different ages, marital status, educational background, cardiac function preoperation, CCI weight, smoking status, drinking status, and regular exercise status(P＜ 0.05). Stepwise regression analysis indicated that, age,marital status, cardiac function preoperation, time of length postoperation and regular exercise could be included into the regression modal, accounting for 34.9% of variances. ConclusionsThe quality of life of patients after TAVR is low. Age, marital status, preoperative cardiac function, postoperative time and regular exercise will affect the quality of life of patients. It is suggested that medical staff should pay attention to the quality of life of TAVR patients after operation and carry out targeted nursing intervention and health education actively, as well as scientific rehabilitation exercise so as to improve the quality of life of TAVR patients after operation.

Objective:To study the relationship between zoledronic acid (ZOL) and vascular endothelial growth factor (VEGF) conformation so as to reveal the mechanism of bisphosphonates inhibiting angiogenesis.Methods:The binding structures of ZOL and VEGF were preprocessed and the molecular dockings were simulated through AutoDockTools, Discovery studio4 and AutoDockVina. The best binding conformation was accurately screened. The effects of various concentrations of ZOL (group A was 0 μmol/L, groups B, C and D were 25, 50 and 100 μmol/L, respectively) on human umbilical vein endothelial cell (HUVEC) proliferation, angiogenesis and angiogenic molecules were detected by using cell counting kit-8 (CCK-8) in vivo and in vitro angiogenesis, immunofluorescence and Western blotting. Results:There was a ZOL binding site on the target protein VEGF conformation. The affinity was -5.2 kcal/mol. This binding site consisted of the hydrophobic region composed of amino acids Cys26, 51, 57, etc. and the hydrogen bond binding region of the A chain (ASP34, SER50) and B chain (CYS61, 68, LEU66, GLY59). The results of CCK-8 showed that the levels of value A in groups B, C and D were significantly lower than that in group A at each time point from 3 to 6 days ( P<0.05). In vitro vascular experiments demonstrated that the numbers of budding in groups B, C and D [(208±28), (151±21) and (62±9), respectively] were significantly lower than that in group A (276±30) ( P<0.05). In vivo vascular experiments displayed that the ratio of Matrigel gel/plasma fluorescence in group A (0.003 1±0.000 3) was significantly higher than those in group B (0.002 1±0.000 2), group C (0.001 6±0.000 2) and group D (0.000 6±0.000 1) ( P<0.05). The results of Western blotting revealed that the expression of VEGF in groups B, C and D [(0.72±0.11), (0.41±0.07) and (0.24±0.04), respectively] were significantly lower than that in group A (1.01±0.02) ( P<0.05), and the expression levels of hypoxia-inducible factor-1α (HIF-1α) in groups B, C and D [(0.68±0.09), (0.55±0.06) and (0.43±0.08), respectively] were significantly lower than that in group A (0.96±0.04) ( P<0.05). Conclusions:ZOL could inhibit cell proliferation, in vivo and in vitro vascularization and expression of VEGF/HIF-1α. The binding site of ZOL with the conformation of VEGF was located in the hydrophobic region and hydrogen-bonding region of amino acids. Designing an antagonist targeting this site might potentially alleviate the effect of ZOL in inhibiting angiogenesis.