Effect of TEVAR Combined with Drugs and Drug Therapy Alone on the Efficacy and Safety of Stable Standford B Aortic Dissection.

Objective: Stanford type B aortic dissection is a condition in which the intima of the aorta tears, and TEVAR is an interventional treatment to manage this dissection through intimal repair. To evaluate the medium-term clinical efficacy of endovascular repair (TEVAR) for Aortic dissection and drug Conservative management for Stanford B Aortic dissection aneurysms and further explore whether the former is superior to drug Conservative management in the medium-term efficacy. Methods: The clinical data of 70 patients with stable Standford type B Aortic dissection admitted to our hospital from March 2016 to March 2020 were retrospectively analyzed. They were divided into the treatment group (n = 47) and the control group (n = 23). The control group patients were treated solely with medication, while the treatment group patients were treated with TEVAR on the basis of the control group patients. The treatment efficacy and safety of the two groups of patients were compared and analyzed. All patients will be followed up once a month for 12 months after discharge and every 2 months thereafter (for a total of 3 years). Results: The findings highlight the need to carefully weigh the benefits and harms in the treatment of Stanford type B aortic dissection, especially when considering TEVAR surgery. Future research should focus on reducing postoperative complications to optimize treatment strategies and improve overall patient outcomes.TEVAR surgery significantly reduces hospital mortality, but is also associated with significantly increased postoperative complications, emphasizing the complexity of treatment decisions. This finding provides critical information about weighing the risks and survival benefits of surgery, helping medical teams and patients make informed treatment choices. The hospital mortality rate of patients in the treatment group was 12.77%, while the hospital mortality rate of patients in the control group was 21.74%. The difference between the two groups was statistically significant (P < .05). The incidence of postoperative complications in the treatment group was 23.40%, while the control group did not experience any major complications. The difference between the two groups was statistically significant (P < .05). The mortality rate of patients in the treatment group within 30 days of discharge was 0%, while the mortality rate of patients in the control group within 30 days of discharge was 11.11%. The difference between the two groups was statistically significant (P < .05). The Kaplan Meier curve showed that the survival rates at 3 years of the control and treatment groups were 56.52% and 95.12%, respectively. The log-rank test showed a statistical difference between the two groups. Univariate and multivariate regression analysis showed that postoperative neurological complications (HR = 32.41; P = .00) and preoperative Aortic valve regurgitation (HR = 3.91; P = .00) were risk factors for medium-term death. Conclusion: The TEVAR combination drug is a safe and effective treatment for stable Stanford B Aortic dissection. It can reduce mortality. Compared with drug treatment, it has obvious advantages in medium-term treatment effects. Early rising for high-risk patients can make them have better long-term outcomes. Limitations of the study include its retrospective nature and the use of data from only a single medical center, which may limit the external generalizability of the results.

Qishen Yiqi dropping pills improve cardiomyocyte hypertrophy via the lncRNA TINCR/miR-193b-3p/RORA axis.

Background: This study was designed to explore the therapeutic effect and mechanism of action of Qishen Yiqi dropping pills (QYDP) in chronic heart failure (CHF) via a long non-coding RNA (lncRNA)-microRNA (miRNA)-messenger RNA (mRNA) axis. Here, the mechanism of action of the lncRNA terminal differentiation-induced non-coding RNA (TINCR), miR-193b-3p, and RAR-related orphan receptor A (RORA) mRNA was analyzed in an angiotensin (Ang) II-induced H9C2 cardiomyocyte hypertrophy model treated with QYDP. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to analyze the gene expression changes of lncRNA, miRNA, and mRNA in H9C2 induced by QYDP on Ang II. The Gene Expression Omnibus (GEO) was used to analyze differentially expressed genes (DEGs) potentially affecting CHF progression. Cell Counting Kit-8 (CCK-8) was used to analyze the effect of QYDP on the proliferation of H9C2, RNA pull-down was used to analyze the binding of lncRNA and miRNA, and dual luciferase was used to analyze the targeting of miRNA and lncRNA or mRNA. Results: Ang II induced TINCR and RORA downregulation, miR-193b-3p upregulation, and hypertrophy in the H9C2 cardiomyocytes, which were alleviated by QYDP. In contrast, TINCR inhibition reversed the effects of QYDP by increasing miR-193b-3p expression and downregulating RORA expression. According to subsequent double luciferase and RNA pull-down experiments, TINCR adsorbed miR-193b-3p by acting as a competitive endogenous RNA sponge and miR-193b-3p directly targeted RORA. Lastly, we showed that the Ang-II-induced inhibition of TINCR and RORA expression and promotion of cardiac hypertrophy were both reversed by a TINCR overexpression plasmid (ov-TINCR), whereas the effects of ov-TINCR were suppressed by a miR-193b-3p mimic. Conclusions: Administration of QYDP improves Ang II-induced H9C2 cardiomyocyte hypertrophy and increase cell proliferation rate through the TINCR/miR-193b-3p/RORA axis.