Objective To investigate the safety and effectiveness of perventricular device closure (PDC) for congenital ventricular septal defects (VSD) by a meta-analysis.Methods PubMed, The Cochrane Library, EMbase and China Biology Medicine (CBM) databases were searched for studies on PDC of VSD up to October 2018 by computer. We included studies only with more than 80% patients diagnosed with perimembranous VSD. A meta-analysis was performed to obtain pooled estimates of success rate and incidences of complications with 95% confidence interval (CI). Subgroup analysis stratified by percentage of perimembranous VSD was performed. Risk difference (RD) was used in the comparison of perioperative data with follow-up data. Results Fifteen studies (2 randomized controlled trials, 3 retrospective cohorts, and other 10 retrospective single-arm studies) involving 4 164 patients (3 848 patients with perimembranous VSD) were included in this meta-analysis. The pooled success rate was 95.4%. Incidences of residual shunt, aortic insufficiency, tricuspid insufficiency, and third-degree atrioventricular block were 5%, 0.1%, 3%, and less than 0.001% respectively. Improvements of residual shunt and aortic insufficiency were confirmed in follow-up patients. Conclusion PDC of congenital perimembranous VSDs is safe and yields good results. Because some limitations can not be overcomed, multicenter randomized controlled trials are needed to confirm our results.
This study aimed to explore the role of miR-130a-3p in cardiomyocyte hypertrophy and its underlying mechanisms. Pressure-overload induced myocardial hypertrophy mice model was constructed by thoracic aortic constriction (TAC). In vitro, norepinephrine (NE) was used to stimulate neonatal rat cardiomyocytes (NRCMs) and H9c2 rat cardiomyocytes to induce hypertrophic phenotypes. The expression of miR-130a-3p was detected in mice hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. The mimics and inhibitors of miR-130a-3p were transfected into H9c2 cells to observe the role of miR-130a-3p on the hypertrophic phenotype change of cardiomyocytes separately. Furthermore, whether miR-130a-3p regulated hypertrophic related signaling pathways was explored. The results showed that the expression of miR-130a-3p was significantly decreased in hypertrophic myocardium, hypertrophic NRCMs and H9c2 cells. After transfection of miR-130a-3p mimics, the expression of hypertrophic marker genes, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and β-myosin heavy chain (β-MHC), and the cell surface area were notably down-regulated compared with the control group (mimics N.C. + NE group). But after transfection of miR-130a-3p inhibitor, the expression of ANP, BNP and β-MHC in H9c2 cells increased significantly, and the cell area increased further. By Western blot, it was found that the protein phosphorylation level of Akt and mTOR were down-regulated after over-expression of miR-130a-3p. These results suggest that miR-130a-3p mimics may alleviate the degree of cardiomyocyte hypertrophy, meanwhile its inhibitor can further aggravate cardiomyocyte hypertrophy. Over-expression of miR-130a-3p may attenuate cardiomyocytes hypertrophy by affecting the Akt pathway.