Outcomes of contemporary versus conventional reverse controlled and antegrade and retrograde subintimal tracking in chronic total occlusion revascularization.

BACKGROUND: Chronic total occlusion (CTO) lesions remain technically challenging for percutaneous coronary intervention (PCI). The introduction of a retrograde approach has allowed marked improvement in the success rate of CTO recanalization. Reverse controlled anterograde and retrograde sub-intimal tracking (reverse CART) is the predominant retrograde wire crossing technique and can be broadly classified into three categories: (1) conventional (2) contemporary and (3) extended. The present study aimed to compare the safety and efficacy of conventional and contemporary reverse CART techniques. METHODS: From March 2015 to May 2020, 303 patients achieving successful retrograde guidewire crossing with conventional or contemporary reverse CART during CTO PCI were included in the study. The patient characteristics, procedural outcomes and in-hospital and 1-year clinical events were compared between the conventional and contemporary groups. RESULTS: The distributions of the baseline and angiographic characteristics were similar in both study arms, except the CTO lesions of the conventional group were more complex, as reflected by borderline significantly higher mean J-CTO scores (3.4 ± 0.7 vs. 3.3 ± 0.8; p = 0.059). Recanalization using contemporary reverse CART was associated with a short procedure time (189.8 ± 44.4 vs. 181.7 ± 37.3 min; p = 0.044) and decreased procedural complications, particularly target vessel perforation (3.6% vs. 0.6%; p = 0.063) and major side-branch occlusion (36.7% vs. 28.0%; p = 0.051). Technical and procedural success and the in-hospital and 1-year outcomes were not significantly different between the groups. CONCLUSIONS: Contemporary reverse CART is associated with favorably high efficiency and low-complication rates and carries a comparable success rate and 1-year clinical outcomes as conventional reverse CART.

RBM15 Protects From Myocardial Infarction by Stabilizing NAE1.

RNA-binding proteins play multiple roles in several biological processes. However, the roles of RBM15-an important RNA-binding protein and a significant regulator of RNA methylation-in cardiovascular diseases remain elusive. This study aimed to investigate the biological function of RBM15 and its fundamental mechanisms in myocardial infarction (MI). Methylated RNA immunoprecipitation sequencing was used to explore the N6-methyladenosine (m6A) difference between MI and normal tissues. Our findings showed the elevated level of m6A in MI, and its transcription profile in both MI and normal tissues. RBM15 was the main regulator and its overexpression attenuated apoptosis in cardiomyocytes and improved cardiac function in mice after MI. Then, we used one target NEDD8 activating enzyme E1 subunit and its inhibitor (MLN4924) to investigate the impact of RBM15 targets on cardiomyocytes. Finally, the enhanced m6A methylation in the presence of RBM15 overexpression led to the increased expression and stability of NEDD8 activating enzyme E1 subunit. Our findings suggest that the enhanced m6A level is a protective mechanism in MI, and RBM15 is significantly upregulated in MI and promotes cardiac function. This study showed that RBM15 affected MI by stabilizing its target on the cell apoptosis function, which might provide a new insight into MI therapy.

The Identification and Validation of Hub Genes Associated with Acute Myocardial Infarction Using Weighted Gene Co-Expression Network Analysis.

Acute myocardial infarction (AMI), one of the most severe and fatal cardiovascular diseases, remains the main cause of mortality and morbidity worldwide. The objective of this study is to investigate the potential biomarkers for AMI based on bioinformatics analysis. A total of 2102 differentially expressed genes (DEGs) were screened out from the data obtained from the gene expression omnibus (GEO) database. Weighted gene co-expression network analysis (WGCNA) explored the co-expression network of DEGs and determined the key module. The brown module was selected as the key one correlated with AMI. Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses demonstrated that genes in the brown module were mainly enriched in 'ribosomal subunit' and 'Ribosome'. Gene Set Enrichment Analysis revealed that 'TNFA_SIGNALING_VIA_NFKB' was remarkably enriched in AMI. Based on the protein-protein interaction network, ribosomal protein L9 (RPL9) and ribosomal protein L26 (RPL26) were identified as the hub genes. Additionally, the polymerase chain reaction (PCR) results indicated that the expression levels of RPL9 and RPL26 were both downregulated in AMI patients compared with controls, in accordance with the bioinformatics analysis. In summary, the identified DEGs, modules, pathways, and hub genes provide clues and shed light on the potential molecular mechanisms of AMI.