Association of early elevated cardiac troponin I concentration and longitudinal change after off-pump coronary artery bypass grafting and adverse events: a prospective cohort study.

BACKGROUND: The elevation of troponin after coronary artery bypass grafting (CABG) is common This study aimed to investigate the association between very early cardiac troponin I (cTnI) concentration and its longitudinal change within 24 hours after CABG and 30-day adverse events. METHODS: This study prospectively enrolled 633 patients who underwent isolated off-pump CABG from January 2019 to May 2019. Serum cTnI levels were measured in all patients at two examinations within 24 hours postoperatively (1 hour and 12-18 hours), and a proportional hazards model was used to determine the association between cTnI levels and their change with adverse events, which were defined as a composite of 30-day mortality, stroke, heart failure, myocardial infarction (MI), and ventricular fibrillation. RESULTS: cTnI levels of the two examinations and absolute change of cTnI levels were significantly higher in the event group than in the non-event group (P<0.01, both). Earlier and later cTnI concentrations were associated with 30-day complications [adjusted hazard ration (HR) 1.598, 95% confidence interval (CI), 1.158-2.204 and HR 1.499, 95% CI, 1.228-1.831, respectively]. With regard to longitudinal change in cTnI levels, participants with persistently high levels of cTnI and those with progression from a low level to high level concentration experienced a significantly increased risk of adverse events than did participants who had a trend of persistently low cTnI levels (HR 3.105, 95% CI, 1.748-5.517 versus HR 2.944, 95% CI, 1.488-5.824). CONCLUSIONS: Longitudinal change in cTnI levels within 24 hours and early cTnI concentrations, even less than 1 hour after CABG, are associated with adverse events. These data will be useful in identifying patients at an increased risk of complications.

MicroRNA-16 is putatively involved in the NF-κB pathway regulation in ulcerative colitis through adenosine A2a receptor (A2aAR) mRNA targeting.

MicroRNAs (miRNAs) act as important post-transcriptional regulators of gene expression by targeting the 3'-untranslated region of their target genes. Altered expression of miR-16 is reported in human ulcerative colitis (UC), but its role in the development of the disease remains unclear. Adenosine through adenosine A2a receptor (A2aAR) could inhibit nuclear factor-kappaB (NF-κB) signaling pathway in inflammation. Here we identified overexpression of miR-16 and down-regulation of A2aAR in the colonic mucosa of active UC patients. We demonstrated that miR-16 negatively regulated the expression of the A2aAR at the post-transcriptional level. Furthermore, transfection of miR-16 mimics promoted nuclear translocation of NF-κB p65 protein and expression of pro-inflammatory cytokines, IFN-γ and IL-8 in colonic epithelial cells. Treatment with miR-16 inhibitor could reverse these effects in cells. The A2aAR-mediated effects of miR-16 on the activation of the NF-κB signaling pathway were confirmed by the A2aAR knockdown assay. Our results suggest that miR-16 regulated the immune and inflammatory responses, at least in part, by suppressing the expression of the A2aAR to control the activation of the NF-κB signaling pathway.