BackgroundLong noncoding RNAs (lncRNAs) are involved in numerous physiological functions. However, their mechanisms in acute myocardial infarction (AMI) are not well understood.MethodsWe performed an RNA-seq analysis to explore the molecular mechanism of AMI by constructing a lncRNA-miRNA-mRNA axis based on the ceRNA hypothesis. The target microRNA data were used to design a global AMI triple network. Thereafter, a functional enrichment analysis and clustering topological analyses were conducted by using the triple network. The expression of lncRNA SNHG8, SOCS3 and ICAM1 was measured by qRT-PCR. The prognostic values of lncRNA SNHG8, SOCS3 and ICAM1 were evaluated using a receiver operating characteristic (ROC) curve.ResultsAn AMI lncRNA-miRNA-mRNA network was constructed that included two mRNAs, one miRNA and one lncRNA. After RT-PCR validation of lncRNA SNHG8, SOCS3 and ICAM1 between the AMI and normal samples, only lncRNA SNHG8 had significant diagnostic value for further analysis. The ROC curve showed that SNHG8 presented an AUC of 0.850, while the AUC of SOCS3 was 0.633 and that of ICAM1 was 0.594. After a pairwise comparison, we found that SNHG8 was statistically significant (P SNHG8-ICAM1 = 0.002; P SNHG8-SOCS3 = 0.031). The results of a functional enrichment analysis of the interacting genes and microRNAs showed that the shared lncRNA SNHG8 may be a new factor in AMI.ConclusionsOur investigation of the lncRNA-miRNA-mRNA regulatory networks in AMI revealed a novel lncRNA, lncRNA SNHG8, as a risk factor for AMI and expanded our understanding of the mechanisms involved in the pathogenesis of AMI.

Background: Statins reduce the incidence of cardiovascular events after percutaneous coronary intervention (PCI), but no clinical studies have investigated the role of statins in ischemia-reperfusion injury after PCI. Hypothesis: Rosuvastatin could reduce ischemia-reperfusion injury in patients with acute coronary syndrome treated with PCI. Objectives: We investigated the effects of rosuvastatin on ischemia-reperfusion injury in patients with acute coronary syndrome after PCI and evaluated short-term prognosis. Methods: Patients scheduled for emergent PCI were given either rosuvastatin for ≥6 months (10 mg/d, every night; n = 55) or no statins (control group; n = 65). Serum superoxide dismutase activity, malondialdehyde, brain natriuretic peptide (BNP), and high-sensitivity C-reactive protein (hs-CRP) were determined before and after PCI, as well as left ventricular ejection fraction and left ventricular end-diastolic volume. Major adverse cardiac events were observed at follow-ups for 6 months. Results: Superoxide dismutase activity in the rosuvastatin-treated group was higher than that of the control group; serum levels of malondialdehyde were lower. BNP and hs-CRP levels in the rosuvastatin-treated group were lower than that of the control group. Four weeks after PCI, the left ventricular ejection fraction in the treatment group was higher than that of the control group, and the left ventricular end-diastolic volume was lower. At the 6-month follow-up, there was no difference in major adverse cardiac events between the 2 groups. Conclusions: Rosuvastatin before PCI reduced ischemia-reperfusion injury in patients with acute coronary syndrome, which suggests the importance of application of rosuvastatin before PCI for early intervention.

This study aims to evaluate the association of serum growth differentiation factor 15 (GDF-15) with in-hospital mortality and arrhythmic risks in patients with acute myocardial infarction (AMI). A total of 296 consecutive patients with AMI were enrolled in our hospital from Jan. 2018 to Dec. 2020. Serum GDF-15 levels were measured at baseline. The primary endpoint was in-hospital all-cause mortality, and the secondary endpoint was major adverse cardiac events (MACEs) during hospitalization, defined as a composite of cardiovascular death, heart failure, sustained ventricular arrhythmias (ventricular tachycardia or ventricular fibrillation), and bleeding. During hospitalization, patients with a higher GDF-15 level had significantly higher incidences of in-hospital mortality (7.4% vs 1.4%; P = .02) and MACEs (9.5% vs 20.9%, P < .01) than those with a lower GDF-15 level. Multivariate logistic regression analysis showed that a higher GDF-15 level was significantly associated with increased risks of in-hospital mortality (OR = 1.92, 95% CI: 1.44-2.50; P < .01) and MACEs (OR = 2.19, 95% CI: 1.56-2.77; P < .01). In conclusion, GDF-15 was associated with the risks of in-hospital mortality and MACEs, indicating that it should be a prognostic biomarker for patients with AMI.

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