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1.
Arch Gynecol Obstet ; 2024 May 25.
Artigo em Inglês | MEDLINE | ID: mdl-38795137

RESUMO

PURPOSE: Cesarean section may result in adverse psychosocial and behavioral outcomes because women put considerable emphasis on the process of birth. Virtual reality treatment has been shown by many studies to reduce anxiety and improve patient satisfaction. Therefore, we designed a randomized controlled trial to investigate whether the application of virtual reality technology during cesarean section can reduce maternal anxiety and improve satisfaction. METHODS: We recruited 128 women undergoing elective cesarean delivery with proposed spinal anesthesia and randomly assigned them to either virtual reality or routine care. The virtual reality intervention was a virtual reality program tailored specifically for women undergoing cesarean section. Primary outcome was the change in anxiety score (change = preoperative-intraoperative score). Secondary outcomes included patient satisfaction score, requirement of intraoperative sedative and analgesic drugs, and respiratory rate. RESULTS: The change in anxiety score in the virtual reality group was significantly higher than that in the routine care group (30 [20, 47.5] vs 10 [- 10, 23.8], respectively; P < 0.001, with Hodges-Lehmann median difference estimate of 20 (95% confidence interval CI, 15-30)). There were no significant differences between the two groups in patient satisfaction scores, the requirement of intraoperative sedative and analgesic drugs, and respiratory rate and side effects. CONCLUSION: Virtual reality treatment could reduce the anxiety of women undergoing elective cesarean section, which is beneficial to the mother and baby. Trial registration This study was registered at the Chinese Clinical Trial Registry (ChiCTR2200061936) on July 11, 2022, and can be reached at https://www.chictr.org.cn/showprojEN.html?proj=173329.

2.
Ann Palliat Med ; 11(3): 1017-1027, 2022 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-35365031

RESUMO

BACKGROUND: infarction (AMI) can be reduced by the use of sacubitril/valsartan. However, the therapeutic effects of sacubitril/valsartan in clinical settings are inconsistent. In this paper, the related research on the application of sacubitril/valsartan in AMI was comprehensively searched, in order to explore the clinical efficacy and safety of early application of sacubitril/valsartan after AMI. METHODS: English databases, including American National Library of Medicine, Medline, and Embase, and Chinese databases, including Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure (CNKI), Wanfang, and VIP, were searched using a combination of the following search terms: AMI, acute ST-segment elevation myocardial infarction (STEMI), acute non-ST-segment elevation myocardial infarction (NSTEMI), sacubitril/valsartan sodium tablets, and angiotensin receptor enkephalinase inhibitors. The experimental group was given Sacubitril/Valsartan sodium tablets, while the control group was given angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB). Cochrane Handbook 5.0 risk assessment table were used for quality assessment and bias risk assessment. RESULTS: A total of 5 articles were included in the meta-analysis. The total incidence of adverse cardiovascular events in the sacubitril/valsartan group was significantly lower than that in the control group {relative risk (RR) =0.61 [95% confidence interval (CI): 0.46, 0.82], significance testing Z=3.36, and P=0.0008}. The difference between the rehospitalization rate of the sacubitril/valsartan group and control group was statistically significant [RR =0.67 (95% CI: 0.47, 0.95), significance testing Z=2.23, and P=0.03]. The difference in low blood pressure between the sacubitril/valsartan group and the control group was statistically significant [RR =1.28 (95% CI: 1.18, 1.40), significance testing Z=5.58, and P<0.00001]. The difference in left ventricular ejection fraction (LVEF) between the sacubitril/valsartan group and control group was statistically significant [mean difference (MD) =3.09 (95% CI: 1.69, 4.49), significance testing Z=4.33, and P<0.0001]. DISCUSSION: Sacubitril/valsartan was found to inhibit ventricular remodeling after AMI, improve cardiac function, and reduce the incidence of adverse cardiovascular events after myocardial infarction, the rehospitalization rate, and the mortality rate.


Assuntos
Insuficiência Cardíaca , Infarto do Miocárdio , Aminobutiratos , Antagonistas de Receptores de Angiotensina/farmacologia , Antagonistas de Receptores de Angiotensina/uso terapêutico , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Compostos de Bifenilo , Insuficiência Cardíaca/tratamento farmacológico , Humanos , Infarto do Miocárdio/tratamento farmacológico , Volume Sistólico/fisiologia , Tetrazóis/farmacologia , Tetrazóis/uso terapêutico , Estados Unidos , Valsartana/farmacologia , Valsartana/uso terapêutico , Função Ventricular Esquerda
3.
Panminerva Med ; 2021 Apr 28.
Artigo em Inglês | MEDLINE | ID: mdl-33908728

RESUMO

BACKGROUND: To explore the role of Atorvastatin in rescuing pulmonary artery hypertension (PAH) via inhibiting the AKT/ERK-dependent PDGF-BB/HIF-1α axis. METHODS: PAH model in rats was established by MCT induction, followed by Atorvastatin intervention. Pulmonary hemodynamic measurement and pulmonary morphological evaluation in rats were conducted. Human pulmonary artery smooth muscle cells (hPASMCs) were subjected to hypoxic exposure or PDGF-BB treatment, followed by Atorvastatin induction. Relative levels of HIF-1α, p-ERK and p-Akt were detected. Viability and apoptosis were respectively determined by cell counting kit-8 (CCK-8) assay and flow cytometry. RESULTS: Atorvastatin protected PAH-induced increases in RVSP and Fulton's index in rats. Meanwhile, it inhibited vascular remodeling following PAH by downregulating HIF-1α and PDGF-BB. Hypoxia or PDGF-BB treatment in hPASMCs resulted in upregulation of p-ERK and p-Akt, and viability increase, which were partially abolished by Atorvastatin intervention. In addition, Atorvastatin triggered apoptosis in hypoxia or PDGF-BB-induced hPASMCs. CONCLUSIONS: Atorvastatin inhibits the activation of HIF-1α and proliferative ability, and triggers apoptosis in hPASMCs exposed to hypoxia or PDGF-BB treatment through inactivating the AKT/ERK pathway.

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