| Background and Objective: There are not only excessive activation ofneuroendocrine system, but also the interactions between inflammatory reaction andoxidative stress, during the development and progression of heart failure（HF）.Activated inflammatory mediators, reactive oxyradical and neuroendocrine systemconstitute an interactive network, which can change cellular structure and destroy itsstability, lead to apoptosis, necrosis and fibrosis hyperplasia of myocardial cells,promote ventricular remodeling and progressive deterioration of cardiac function, andparticipate in the process of development and progression of heart failure. Some studiessuggest that when receptor for advanced glycation end product（sRAGE）is activated andcombined with its ligand in patients with heart failure, it could promote the activation ofNF-κB, raise the expression of numerous cytokines and inflammatory factors, produceoxidative stress and inflammatory reaction, cause remodeling and even necrosis ofmyocardial cells, and eventually result in ventricular dysfunction of contractility andrelaxation. Endogenous secretory receptor for advanced glycation endproducts(esRAGE)that can compete binding with the ligands of RAGE to block thetissue injury of RAGE-ligands is the isoform of RAGE. Studies have shown that thelevel of esRAGE is significantly decreased in patients with heart failure, and it isnegatively correlated with the inflammatory factor high-sensitivity C-reactiveprotein(hs-CRP). However，there is fewer studies which committed to discuss therelationship of esRAGE and the severity and prognosis of heart failure. However, fewclinical studies were performed about esRAGE in the pathophysiology of HF. Our aimis to study the association between serum esRAGE levels and cardiac structure, reducedand preserved ejection fraction, clinical value in patients with heart failure. To evaluatethe clinical prognostic value of serum esRAGE in patients with heart failure,180daysfollow-up was done by telephone. Methods:79patients with NYHA functional class I (n=12), class II (n=17), classIII (n=22), IV (n=28) were included. The baseline clinical data were collected includingage, gender, body weigh, blood pressure, previous history and orally taken drugs. SerumesRAGE, hs-CRP, N-terminal pro-brain natriuretic peptide（NT-proBN）and heart colordoppler ultrasound were examined. Existent age was performed to the Web-basedSHSM software. esRAGE concentration was detected by enzyme linkedimmunosorbent assay (ELISA).180days after discharge, telephone follow-up wasperformed to the HF patients to document the adverse events, such as death orreadmission. Statistical analysis was performed by SPSS17.0software. Level forstatistical difference was P<0.05.Results:1. esRAGE showed remarkable reduce in patients with New York HeartAssociation（NYHA）ClassⅠcompared with these of the patients of Class II~IV(P<0.05). In addition, esRAGE in patients with NYHA Class II showed remarkablehigher than those of Class III~IV patients (P<0.05).2. esRAGE levels of patients with left ventricular end-diastolic dimension(LVEDD) less than50mm were higher than those of LVEDD more than50mm(P<0.05).3. Correlation analysis indicated esRAGE level was negative correlated withNYHA classification (r=-0.575，P<0.001), NT-proBNP (r=-0.404，P<0.001) andLVEDD (r=-0.244, P<0.05).4. During the180days telephone follow-up, esRAGE level and SHFM of patientswith adverse events were lower than those without adverse events (P<0.05), butNT-proBNP、hs-CRP were higher than those without adverse events (P<0.05).5. esRAGE level was positively correlated with SHFM (r=-0.575，P<0.05)，hs-CRP level was negative correlated with SHFM(r=-0.233, P=0.034).No correlationwas detected between NT-proBNP and SHFM (P>0.05).Conclusions:1.esRAGE level reduce gradually with the deterioration of heartfunction, indicating that esRAGE is associated with the extent of heart failure.2.esRAGE is associated with the progress of left ventricular remodeling.3.One of the predictors of short-term prognosis is the levles of esRAGE in patientswith heart failure. |
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