Effect of Dapagliflozin on Ventricular Remodeling and Prognosis in Patients with Coronary Atherosclerotic Heart Disease Undergoing Percutaneous Coronary Intervention.

Objective: Acute coronary syndrome (ACS) is a common cardiovascular complication in patients with type 2 diabetes mellitus (T2DM) and significantly increases the risk of disability and death in T2DM patients. Dapagliflozin inhibits blood glucose reabsorption, improves insulin resistance, and reduces the occurrence of long-term adverse cardiovascular events, indicating the importance of Dapagliflozin as a drug for type 2 diabetes patients and its close relationship with coronary atherosclerotic heart disease. At present, there are few studies on the effects of Dapagliflozin intervention on ventricular remodeling and myocardial microperfusion in patients with ACS combined with T2DM after PCI. Methods: Between January 2019 and August 2023, a total of 35 patients diagnosed with Coronary atherosclerotic heart disease and T2DM were chosen as the observation group using a multi-stage cluster sampling method. Concurrently, 35 patients with similar age, height, weight, and healthy physical examination results were selected as the control group during the same time frame. We collected demographic data, symptoms and underlying diseases of the two groups Before enrollment and 6 months after discharge and compared the data between the two groups. Subsequently, multivariate logistic regression analysis was employed to identify indicators with statistically significant differences and to summarize the potential risk factors that could impact ventricular remodeling in patients with Coronary atherosclerotic heart disease and T2DM. Results: There was significant difference in LDL-C between the two groups, and the difference was statistically significant (P < .05). After treatment, the levels of hs-CRP, FBG, HbAlc and IL-6 in both groups were significantly decreased, and the decrease was more obvious in the observation group, with statistical significance (P < .05). These results indicated that Dapagliflozin intervention could significantly inhibit postoperative inflammation in patients with ACS combined with T2DM after PCI. LVMI of Observation group patients was significantly higher than Comparison group, LVEDD and ESVI of Observation group patients were significantly lower than Comparison group. The difference was statistically significant (P < .05). These results indicated that Dapagliflozin intervention could significantly inhibit the improvement of blood glucose index, ventricular remodeling and myocardial microperfusion in patients with ACS combined with T2DM after PCI. After treatment, TIMI Flow Count Frame Count (CTFC) level and Myocardial Perfusion (TMPG) level in the observation group were significantly lower than those in the comparison group, and the difference was statistically significant (P < .05). These results indicated that Dapagliflozin intervention could significantly inhibit ventricular remodeling and improve myocardial microperfusion in patients with ACS combined with T2DM after PCI. Conclusion: Dapagliflozin intervention can significantly inhibit inflammatory indexes in patients with Coronary atherosclerotic heart disease combined with T2DM after PCI, promote the improvement of blood glucose indexes, ventricular remodeling and myocardial microperfusion, and reduce the risk of occurrence.

Associations between genetic variations in microRNA and myocardial infarction susceptibility: a meta-analysis and systematic review.

BACKGROUND: Current genetic association studies have reported conflicting results regarding the association between miRNA polymorphisms and myocardial infarction (MI) risk METHODS: Relevant studies were retrieved from the PubMed, EMBASE, ISI Web of Science, and Scopus databases. Eligible studies determining the association between miRNA polymorphisms and MI susceptibility were included and a meta-analysis was performed to quantify the associations between miRNA polymorphisms and MI risk. RESULTS: A total of eight studies with 2507 MI patients and 3796 healthy controls were included, dealing with nine miRNA genes containing 11 different loci, including miR-149 (rs71428439 and rs2292832), miR-126 (rs4636297 and rs1140713), miR-146a (rs2910164), miR-218 (rs11134527), miR-196a2 (rs11614913), miR-499 (rs3746444), miR-27a (rs895819), miR-26a­1 (rs7372209), and miR-100 (rs1834306). miR-146a rs2910164 and miR-499 rs3746444 were determined to have a significant association with MI susceptibility, a finding that was supported by the meta-analysis (rs2910164: GG/CC, odds ratio [OR]: 1.40, 95% confidence interval [95% CI]: 1.05-1.74, p < 0.001; rs3746444: AA + AG/GG, OR = 2.04, 95% CI: 1.37-2.70, p < 0.001). Limited or conflicting data were found for the relationship between the other miRNA polymorphisms (rs71428439, rs4636297, rs1140713, rs11134527, rs11614913, rs895819, rs7372209, rs1834306, rs2292832) and MI risk. CONCLUSION: There was a significant association between rs2910164 and rs3746444 and MI susceptibility. Further studies are required to investigate the role of miRNA polymorphisms in MI risk.

Ultrasound-Targeted Microbubble Destruction-Mediated miR-206 Overexpression Promotes Apoptosis and Inhibits Metastasis of Hepatocellular Carcinoma Cells Via Targeting PPIB.

BACKGROUND: Ultrasound-targeted microbubble destruction (UTMD) has been found to be an effective method for delivering microRNAs (miRNAs, miRs). The current study is aimed at discovering the potential anti-cancer effects of UTMD-mediated miR-206 on HCC. METHODS: In our study, the expressions of miR-206 and peptidyl-prolyl cis-trans isomerase B (PPIB) in HCC tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). PPIB expressions in HCC and adjacent normal tissues were analyzed by gene expression profiling interactive analysis (GEPIA). MiR-206 mimic and mimic control were transfected into HCC cells using UTMD. Potential binding sites between miR-206 and PPIB were predicted and confirmed by TargetScan and dual-luciferase reporter assay, respectively. Cell migration, invasion, and apoptosis were detected by wound healing assay, Transwell, and flow cytometry, respectively. The expressions of apoptosis-related proteins (Bax, Bcl-2), Epithelial-to-mesenchymal (EMT) markers (E-cadherin, N-cadherin and Snail) and PPIB were measured by Western blot. RESULTS: MiR-206 expression was downregulated while PPIB expression was upregulated in HCC, and PPIB was recognized as a target gene of miR-206 in HCC tissues. UTMD-mediated miR-206 inhibited HCC cell migration and invasion while promoting apoptosis via regulating the expressions of proteins related to apoptosis, migration, and invasion by targeting PPIB. CONCLUSION: Our results suggested that the delivery of UTMD-mediated miR-206 could be a potential therapeutic method for HCC treatment, given its effects on inhibiting cell migration and invasion and promoting cell apoptosis.