The Relationship between Plasma Soluble Receptor for Advanced Glycation End Products and Coronary Artery Disease.

BACKGROUND: Inflammation is involved in the development and progression of coronary artery disease (CAD). The role of the receptor for advanced glycation end products (RAGE) in the development of CAD has been recognized. The expression of sRAGE and S100A12 in patients with coronary artery disease from different studies was inconsistent. We attempted to determine the expression of sRAGE and S100A12 and their relationship in the subjects with different severity levels of CAD. METHODS: A total of 259 patients undergoing coronary angiography were enrolled from the Department of Geriatric Cardiology in the First Affiliated Hospital of Nanjing Medical University from January 2014 to December 2016. Groups were divided as follows: normal coronary artery (control group), nonobstructive coronary atherosclerosis (<50% stenosis in all coronary vessels, NOCA group), stable angina (SAP group), and acute coronary syndrome (ACS group). During CAG or PCI, peripheral arterial blood was collected from all the patients. Plasma sRAGE and S100A12 levels were measured by ELISA. We calculated the SYNTAX score of each patient with CAD according to the result of CAG. RESULTS: The levels of sRAGE were significantly elevated in the ACS group compared with those in the control group, the NOCA group, and the SAP group. sRAGE levels were similar among the control group, the NOCA group, and the SAP group. Plasma S100A12 levels were significantly higher in the ACS group than in the control group and the NOCA group. Baseline correlations between plasma levels of sRAGE and plasma S100A12 in the ACS group were significant. Plasma sRAGE concentration was increasing in patients with ACS and was significantly positively correlated with the increasing SYNTAX score. ROC curve analysis revealed that the combination of sRAGE and S100A12 had a good performance in the prediction of high-risk CAD patients. CONCLUSION: The plasma levels of sRAGE and S100A12 can be increased in patients with ACS. The elevated sRAGE concentration may be independently associated with the severity of CAD and the inflammatory process. sRAGE combined with S100A12 may be used as a predictor of severe coronary heart disease.

Remote Ischemic Postconditioning Protects against Myocardial Ischemia-Reperfusion Injury by Inhibition of the RAGE-HMGB1 Pathway.

BACKGROUND: The aim of the present study was to observe the effect of RAGE-HMGB1 signal pathway on remote ischemic postconditioning in mice with myocardial ischemia reperfusion injury. METHODS: Mice model of MIRI was established and randomly divided into three groups: control group, ischemia reperfusion group, and remote ischemic postconditioning group. Infarction size was detected by Evans blue and TTC staining. Cardiac function was detected by echocardiography measurement. The protein levels of RAGE, HMGB1, P-AKT, and ERK1/2 were detected by Western blot 120 min following reperfusion. RESULTS: RIPostC could decrease the infarct size and increase LVEF and FS compared with I/R group. Two hours after myocardial ischemia reperfusion, the levels of RAGE and HMGB1 were significantly decreased in RIPostC group compared with those in I/R group. The level of p-AKT was significantly higher in the RIPostC group than in the I/R group. LY294002 significantly attenuated RIPostC-increased levels of Akt phosphorylation. CONCLUSION: RIPostC may inhibit the expression of RAGE and HMGB1 and activate PI3K/Akt signaling pathway to extenuate ischemic reperfusion injury in mice. It could further suppress the oxidative stress, have antiapoptosis effect, and reduce inflammatory reaction, but this effect has certain timeliness.

Effect of Remote Ischemic Preconditioning on Perioperative Cardiac Events in Patients Undergoing Elective Percutaneous Coronary Intervention: A Meta-Analysis of 16 Randomized Trials.

BACKGROUND: The main objective of this meta-analysis was to investigate whether remote ischemic preconditioning (RIPC) reduces cardiac and renal events in patients undergoing elective cardiovascular interventions. METHODS AND RESULTS: We systematically searched articles published from 2006 to 2016 in PubMed, EMBASE, Web of Science, Cochrane Library, and Google Scholar. Odds ratios (ORs) with 95% confidence intervals (CIs) were used as the effect index for dichotomous variables. The standardized mean differences (SMDs) with 95% CIs were calculated as the pooled continuous effect. Sixteen RCTs of 2435 patients undergoing elective PCI were selected. Compared with control group, RIPC could significantly reduce the incidence of perioperative myocardial infarction (OR = 0.64; 95% CI: 0.48-0.86; P = 0.003) and acute kidney injury (OR = 0.56; 95% CI: 0.322-0.99; P = 0.049). Metaregression analysis showed that the reduction of PMI by RIPC was enhanced for CAD patients with multivessel disease (coef.: -0.05 [-0.09; -0.01], P = 0.022). There were no differences in the changes of cTnI (P = 0.934) and CRP (P = 0.075) in two groups. CONCLUSION: Our meta-analysis of RCTs demonstrated that RIPC can provide cardiac and renal protection for patients undergoing elective PCI, while no beneficial effect on reducing the levels of cTnI and CRP after PCI was reported.