The long-term clinical outcomes of intravascular ultrasound-guided versus angiography-guided coronary drug eluting stent implantation in long de novo coronary lesions: A systematic review and meta-analysis.

Background: No meta-analysis has been conducted to compare the long-term clinical outcomes of intravascular ultrasound (IVUS)-guided versus angiographic-guided drug-eluting stent implantation in patients with long de novo coronary lesions. We attempted to compare the efficacy and safety of IVUS guidance versus angiography guidance in percutaneous coronary intervention (PCI) for long de novo coronary lesions. Materials and Methods: We performed a detailed meta-analysis from four randomized controlled trials (RCTs) and one observational study to compare long outcomes of IVUS versus angiography in guiding coronary stent implantation with long de novo coronary lesions defined as coronary stenosis which need stent implantation >28 mm in length. Data were aggregated for the endpoints measure using the fixed-effects model as pooled odds ratio (OR) with 95% confidence intervals. Clinical outcomes included major adverse cardiovascular events (MACE), all revascularization, including target lesion revascularization (TLR) and target vessel revascularization (TVR), all myocardial infarction (MI), all-cause death, and stent thrombosis (ST). Cochrane Library, Embase, PubMed, and Web of Science were searched. Results: Four RCTs and one observational study were included in our study with 3,349 patients (IVUS guidance = 1,708; Angiography guidance = 1,641). With mean follow-up of 2 years, the incidence of MACE, all myocardial infarction, all revascularization and stent thrombosis were significantly lower in IVUS-guided DES implantation of patients with long de novo coronary lesions than in angiography-guided patients; MACE [OR 0.41; 95% confidence interval (CI), 0.29-0.58; p < 0.00001], all myocardial infarction (OR 0.23; 95% CI, 0.09-0.58; p = 0.002), all revascularization (OR 0.48; 95% CI, 0.36-0.66; p < 0.00001), stent thrombosis (OR 0.32; 95% CI, 0.11-0.89; p = 0.03). There was no significant difference in all-cause mortality between the two groups (OR 0.82; 95% CI, 0.55-1.23; p = 0.34). Conclusion: During mean follow-up of 2 years, the incidence of MACE, stent thrombosis, all myocardial infarction and revascularization in patients with long de novo coronary lesions under IVUS-guided PCI were significantly lower than angiography-guided PCI, and there were no statistically significant differences in all-cause mortality.

Effects of miR-145-5p on cardiomyocyte proliferation and apoptosis, GIGYF1 expression and oxidative stress response in rats with myocardial ischemia-reperfusion.

This study aimed to investigate the effects of miR-145-5p on cardiomyocyte proliferation and apoptosis, GIGYF1 expression, inflammation, and oxidative stress in rats with myocardial ischemia-reperfusion injury (IRI). For this purpose, SPF male SD rats were used for IRI modeling. Experimental animals were subjected to specimen sampling and myocardial HE staining. The relative expression of miR-145-5p was detected by qRT-PCR; the protein expressions of GIGYF1, p-AKT, p53, Bax, p38MAPK, and ERK1/2 were detected by Western blot. Mouse embryonic cardiomyocytes H9C2 were used for H/R modeling, which was then subjected to cell transfection according to different grouping protocols. The target of miR-145-5p was confirmed to be GIGYF1 by dual-luciferase reporter assay. Further experiments were performed to detect the survival rate of transfected cells, the apoptosis of transfected cells, SOD activity determination, as well as IL-1ß and IL-6 concentrations. The results showed that the expression level of miR-145-5p was downregulated in H2C2 cells (P < 0.05). After 24h of transfection, there was a significant increase in the expression of miR-145-5p in the H/R+miR-145-5p mimic group (P < 0.05), but an evident decrease in the H/R+miR-145-5p inhibitor group (P > 0.05). Compared with the H/R+NC inhibitor group, the H/R+miR-145-5p mimic group had significantly increased cell proliferation, improved release of SOD, and upregulated expressions of ERK1/2 and p-AKT; but downregulated concentrations of IL-1ß and IL-6, and decreased expressions of P38MAPK, p53, and Bax (all P < 0.05). Also, the IRI+miR-145-5p agomir group had significantly upregulated expression of miR-145-5p and improved injury degree of heart tissue improved; a significant increase in the protein expressions ERK1/2 and p-AKT, but downregulated protein expressions of P38MAPK, p53, and Bax (all P < 0.05). Dual-luciferase reporter assay identified that GIGYF1 was the target gene of miR-145-5p. Furthermore, through the stimulated overexpression of miR-145-5p, there were significantly increased cell proliferation, improved release of SOD, and upregulated expressions of ERK1/2 and p-AKT; but downregulated concentrations of IL-1ß and IL-6, and decreased expressions of P38MAPK, p53, and Bax (all P < 0.05), while the above trends were reversed following the simultaneous upregulation of miR-145-5p and GIGYF1 (all P < 0.05). In general, our study confirmed a decreased expression of miR-145-5p and increased expression of GIGYF1 in the IRI or H/R model in vivo and in vitro. Overexpression of miR-145-5p can downregulate the expression of GIGYF1, further promote cell proliferation, inhibit cell apoptosis, alleviate inflammation and oxidative stress, and hence exert a protective role in myocardial infarction IRI.

Diagnosis, clustering, and immune cell infiltration analysis of m6A-related genes in patients with acute myocardial infarction-a bioinformatics analysis.

Background: Accurate myocardial infarction (AMI) is one of the leading causes of mortality worldwide. N6-methyladenosine (m6A) modification plays an important role in the development of cardiac remodeling and the cardiomyocyte contractile function. The aim of this study is to analyze the m6A-related molecular biological mechanisms of AMI in terms of accurate diagnosis and prognosis. Methods: The platform data and probe data of the GSE66360 data set were downloaded. The differential analysis was conducted by combining the m6A-related gene expression. Thereafter, a diagnostic model was established using the random-forest method. The diagnostic accuracy of the diagnostic models was assessed by using the area under the receiver operating characteristic (ROC) curve (AUC). Next, the patients with AMI were clustered by unsupervised machine learning using the R software. Finally, an immune cell clustering analysis for each cluster was conducted to determine the correlations between m6A-related gene expression and the infiltration amount of the immune cells. The case and control groups were not matched in terms of demographics. Results: The GSE6636 data set comprised 99 participants (49 patients with AMI and 50 without in control group). The differential analysis identified 10 m6A-related genes: 5 writers [Methyltransferase-like 3 (METTL3), Methyltransferase-like 14 (METTL14), Wilms tumor 1-associated protein (WTAP), Zinc Finger CCCH-Type Containing 13 (ZC3H13), and Casitas B-lineage proto-oncogene like 1 (CBLL1)], 4 readers [YT521-B homology domain-containing family 3 (YTHDF3), Fragile X mental retardation type 1 (FMR1), YT521-B homology-domain-containing protein 1 (YTHDC1), and insulin-like growth factor binding protein 3 (IGFBP3)] and 1 eraser [fat mass and obesity associated (FTO) gene]. The Mean Decrease Gini (MDG) values of these 10 genes were greater than 2. The FTO, WTAP, YTHDC1, IGFBP3, and CBLL1 were included in the model with a C index of 0.842. METTL3, ZC3H13, WTAP, and CBLL1 were highly expressed in Type A, and YTHDF3 was highly expressed in Type B. Conclusions: A diagnostic model of AMI was established based on the genes of FTO, WTAP, YTHDC1, IGFBP3, and CBLL1. Additionally, 2 molecular subtypes were successfully identified from the above-mentioned gene. Our findings could provide a novel method for the accurate diagnosis of AMI.

Varying correlation between 18F-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI in carotid atherosclerosis: implications for plaque inflammation.

BACKGROUND AND PURPOSE: (18)F-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI have been proposed to quantitatively assess plaque inflammation by probing macrophages and neovessels, respectively. We examined their correlation to study the in vivo relationship between macrophage and neovessel activities in atherogenesis. METHODS: Forty-one patients (34 men; aged 65±12 years) with a total of 68 carotid plaques (thickness ≥2 mm on ultrasound; 20 symptomatic) were assessed by both (18)F-fluorodeoxyglucose positron emission tomography/computed tomography and dynamic contrast-enhanced MRI within 2 weeks, measured as target-to-background ratio and transfer constant (K(trans)), respectively. RESULTS: Overall, the correlation between target-to-background ratio and K(trans) was weak and marginal (r=0.22; P=0.068). They were correlated in the symptomatic plaques (r=0.59; P=0.006) but not in the asymptomatic plaques (r=0.07; P=0.625; P=0.033 for difference in r). Neither target-to-background ratio nor K(trans) was significantly higher in the symptomatic plaques, but both showed an inverse relationship with time since last neurological event (r=-0.94 and -0.69 for target-to-background ratio and K(trans), respectively). CONCLUSIONS: The correlation between (18)F-fluorodeoxyglucose positron emission tomography and dynamic contrast-enhanced MRI measurements varied with clinical conditions, pointing to a complex interplay between macrophages and neovessels under different pathophysiological conditions. The moderate correlation shown only in symptomatic plaques indicates the presence of acute plaque inflammation with increased metabolic activity and cytokine production by inflammatory cells.