Exosomes are attracting considerable interest in the cardiovascular field as the wide range of their functions is recognized in acute myocardial infarction (AMI). However, the regulatory role of exosomal long non‐coding RNAs (lncRNAs) in AMI remains largely unclear. Exosomes were isolated from the plasma of AMI patients and controls, and the sequencing profiles and twice qRT‐PCR validations of exosomal lncRNAs were performed. A total of 518 differentially expressed lncRNAs were detected over two‐fold change, and 6 kinds of lncRNAs were strikingly elevated in AMI patients with top fold change and were selected to perform subsequent validation. In the two validations, lncRNAs ENST00000556899.1 and ENST00000575985.1 were significantly up‐regulated in AMI patients compared with controls. ROC curve analysis revealed that circulating exosomal lncRNAs ENST00000556899.1 and ENST00000575985.1 yielded the area under the curve values of 0.661 and 0.751 for AMI, respectively. Moreover, ENST00000575985.1 showed more significant relationship with clinical parameters, including inflammatory biomarkers, prognostic indicators and myocardial damage markers. Multivariate logistic model exhibited positive association of ENST00000575985.1 with the risk of heart failure in AMI patients. In summary, our data demonstrated that circulating exosomal lncRNAs ENST00000556899.1 and ENST00000575985.1 are elevated in patients with AMI, functioning as potential biomarkers for predicting the prognosis of pateints with AMI.

Blood pressure (BP) changes with age. We conducted a cross-sectional study in rural Chinese adults to investigate: (1) what is the relationship between age, arterial stiffness, and BP in Chinese men and women; and (2) to what degree can the age–BP relationship be explained by arterial stiffness, controlling for other covariables. These analyses included a total of 1688 subjects (males/females: 623/1065), aged 40 to 88 years. Among them, 353 (20.9%) had hypertension (defined as systolic blood pressure (SBP) ≥140 mm Hg or diastolic blood pressure (DBP) ≥90 mm Hg). Arterial stiffness was measured by brachial–ankle pulse wave velocity (baPWV). baPWV appeared to be more strongly correlated with BP (including SBP, DBP, mean arterial pressure [MAP], pulse pressure [PP]) than age (P < 0.001 for comparisons between Spearman correlation coefficients). Furthermore, baPWV was associated with BP (including SBP, DBP, MAP, and PP) and risk of hypertension in a dose–response fashion, independent of age; in contrast, the age–BP associations were either attenuated or became negative after adjusting for baPWV. Arterial stiffness appears to be an independent contributor to hypertension, even after adjusting for age and other covariables. In contrast, age–BP associations became attenuated or negative after adjusting for baPWV. The utility of baPWV as a diagnostic, prognostic, and therapeutic indicator for hypertension warrants further investigation.

The expression profile of long noncoding RNA (lncRNA) in human epicardial adipose tissue (EAT) has not been widely studied. In the present study, we performed RNA sequencing to analyze the expression profiles of lncRNA and mRNA in EAT in coronary artery disease (CAD) patients with and without heart failure (HF). Our results showed RNA sequencing disclosed 35673 mRNA and 11087 lncRNA corresponding to 15554 genes in EAT in total, while 30 differentially expressed lncRNAs (17 upregulated and 13 downregulated) and 278 differentially expressed mRNAs (129 upregulated and 149 downregulated) were discriminated between CAD patients with and without HF (P2); lncRNA ENST00000610659 drew specific attention for it was the top upregulated lncRNA with highest fold change and corresponded to UNC93B1 gene, which was proved to be related to HF and encoded UNC93B1 protein regulating toll-like receptor signaling, and both of them significantly increased in HF patients in qRT-PCR validation; the top significant upregulated enriched GO terms and KEGG pathway analysis were regulation of lymphocyte activation (GO:0051249) and T cell receptor signaling pathway (hsa04660), respectively. The current findings support the fact that EAT lncRNAs are involved in the inflammatory response leading to the development of HF.

Background Recent studies have reported circular RNA (circRNA) expression profiles in various tissue types; however, circRNA expression profile in human epicardial adipose tissue (EAT) remains undefined. This work aimed to compare circRNA expression patterns in EAT between the heart failure (HF) and non-HF groups. Methods RNA-sequencing was carried out to compare circRNA expression patterns in EAT specimens from coronary artery disease cases between the HF and non-HF groups. Quantitative real-time polymerase chain reaction was performed for validation. Comparisons of patient characteristics between the two groups were using t test, Mann-Whitney U test, and Chi-squared test. Results A total of 141 circRNAs substantially different between the HF and non-HF groups (P < 0.05; fold change >2) were detected, including 56 up-regulated and 85 down-regulated. Among them, hsa_circ_0005565 stood out, for it had the highest fold change and was significantly increased in HF patients in quantitative real-time polymerase chain reaction validation. The top highly expressed EAT circRNAs corresponded to genes involved in cell proliferation and inflammatory response, including GSE1, RHOBTB3, HIPK3, UBXN7, PCMTD1, N4BP2L2, CFLAR, EPB41L2, FCHO2, FNDC3B, and SPECC1. The top enriched Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway were positive regulation of metabolic processes and insulin resistance, respectively. Conclusion These data indicate EAT circRNAs may contribute to the pathogenesis of metabolic disorders causing HF.

Background: There is currently no evidence regarding the role of plasma Sirtuin2 (SIRT2) level in acute myocardial infarction (AMI) yet. This study assessed the role of plasma SIRT2 in AMI, and investigated the association of plasma SIRT2 level with major adverse cardiovascular events (MACE) and heart failure after AMI. Methods: This is a prospective observational study. A total of 129 AMI patients (mean age: 62.2±12.7 years old, male/female: 96/33) were included. Cox proportional hazards regression models were used to estimate the association of different SIRT2 levels with MACE and heart failure after AMI. Results: According to the 75th percentile value of plasma SIRT2 level, we divided all the AMI patients into two groups: high-level group (plasma SIRT2 level ≥109.0 pg/mL) and low-level group (plasma SIRT2 level <109.0 pg/mL). Compared with the low-level group, the high-level group had higher percentage of Killip class ≥3 (P<0.001), left ventricular ejection fraction (LVEF) <50% (P=0.007) or even <40% (P=0.012), use of breathing machine(P=0.003), and higher plasma brain natriuretic peptide (BNP) level (P=0.006). Multivariate Cox regression analysis showed that there were higher risks of MACE [hazard ratio (HR) 11.20, 95% confidence interval (CI): 3.18–39.52, P<0.001)] and heart failure (HR 27.10, 95% CI: 4.65–157.83, P<0.001) in the high-level group. Conclusions: The present study suggested that plasma SIRT2 level is a promising biomarker to predict heart failure and MACE after AMI.