Aim: We aimed to identify the expression profile and role of circular RNAs (circRNAs) in coronary heart disease (CHD). Materials & methods: We performed sequence analysis of circRNAs in peripheral blood mononuclear cells of 70 CHD patients and 30 controls. Eight selected circRNAs were validated using quantitative real-time polymerase chain reaction (qRT-PCR) in human atherosclerotic coronary arteries. Results: In total, 2283 downregulated and 85 upregulated circRNAs were identified in CHD. Parental genes of top 100 dysregulated-circRNAs are related to metabolism and protein modification, and 12 circRNAs might upregulate their CHD-related parental genes through miRNA sponges. Of the eight circRNAs validated in atherosclerotic coronary arteries by qRT-PCR, six were consistent with sequencing results of peripheral blood mononuclear cells. Conclusion: As potential ceRNAs, dysregulated circRNAs may be involved in CHD pathophysiology.

The present study aimed to clarify the effect of bolus intracoronary nicorandil on inflammatory, oxidative and adherent indicators in patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI). This randomized controlled trial (RCT) was performed to detect the inflammation and oxidative stress in intracoronary blood both before and after PCI. In total, 65 consecutive patients undergoing PCI were classified into a nicorandil therapy group (n=32) or a placebo group (n=33). All procedures were performed at Shandong University Qilu Hospital, China, during the period from March, 2016 to May, 2017. Intracoronary blood from patients who received nicorandil therapy during PCI showed no change in soluble CD40 ligand (sCD40L) concentration (1.86±0.08 vs. 1.90±0.09 ng/ml, P=0.12) but a significant increase was noted in the control group (1.87±0.17 vs. 2.82±0.26 ng/ml, P<0.01). This indicated a relative reduction in sCD40L level after PCI in the nicorandil group. We further demonstrated an increase in superoxide dismutase (SOD) activity (29.37±0.81 vs. 31.03±0.60 U/ml, P<0.001) and a reduction in lipid peroxidation (3.84±0.99 vs. 4.23±0.13 U/ml, P=0.001) in the nicorandil group but observed no change in the placebo group. ICAM-1 levels showed no change in the nicorandil group (69.54±6.89 vs. 72.01±8.25 ng/ml, P=0.83) but a significant increase in the control group after PCI in intracoronary blood (56.57±4.96 vs. 76.81±6.88 ng/ml, P=0.002). No changes were found in hs-CRP, TNFα and sVCAM-1 levels in coronary blood for both groups before and after PCI in ACS patients. Our findings demonstrate that intracoronary bolus nicorandil therapy has a significant effect on the inhibition of inflammatory indicators and oxidative stress in patients with ACS during PCI. This suggests a possible medical application of nicorandil for reducing inflammation and oxidative stress.

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Atrial septal defect (ASD) is one of the most common forms of congenital heart disease (CHD) and a major cause of childhood morbidity and mortality, with an estimated incidence of 100 per 100,000 live births. 1 The process of cardiomyogenesis is precisely and spatially regulated by signalling molecules. The regulation of this process involves a conservative network of tissue-specific transcriptional factors that are necessary for the morphogenesis of the atrioventricular septum. Any interruptions to this process can result in embryonic