Abstract:Acute aortic dissection (AAD) is a very dangerous cardiovascular emergency. Although some progress has been made in diagnosis and treatment, the mortality rate of AAD is still high. AAD is a multi-factor involved disease, and its pathophysiological mechanism has not been fully explained, so its clinical treatment effect is limited and its mortality rate is extremely high. A large number of studies have shown that serum amyloid A (SAA), as a major inflammatory protein produced in the acute phase response, is closely related to the occurrence and development of cardiovascular diseases.Therefore, SAA may become a candidate target for the diagnosis and treatment of AAD. This review discusses the relationship between SAA and inflammatory response, vascular dysfunction, thrombosis and extracellular matrix remodeling, and the possibility of SAA as a potential biomarker of AAD.

Abstract:Aim To study the diagnostic value of serum heparin-binding epidermal growth factor (HB-EGF) and serum amyloid A (SAA) in hypertensive patients with carotid atherosclerosis (CAS). Methods A total of 100 hypertensive patients were selected and divided into hypertension group (n＝42) and hypertension CAS group (n＝58); another 50 healthy subjects who underwent physical examination during the same period were selected as the healthy control group.The serum HB-EGF, SAA levels and CIMT in healthy control group, hypertension group and hypertension CAS group were compared. Pearson correlation analysis was used to test the correlation between serum HB-EGF, SAA levels and CIMT.Logistic regression analysis was used to analyze the risk factors of CAS. ROC curve was used to analyze the diagnostic value of serum HB-EGF and SAA levels for CAS in hypertensive patients. Results Compared with the healthy control group, the serum levels of HB-EGF and SAA in the hypertension group and the hypertension CAS group were significantly increased (P＜0.05), and the CIMT was significantly increased (P＜0.05). Compared with the hypertension group, the serum HB-EGF and SAA levels in the hypertension CAS group were significantly increased (P＜0.05), and the CIMT was significantly increased (P＜0.05). Pearson correlation analysis showed that serum HB-EGF and SAA levels were positively correlated with CIMT (r＝0.7,5%CI:0.7257～0.8662, P＜0.001; r＝0.5,5%CI:0.6688～0.8357, P＜0.001). Logistic regression analysis showed that high HB-EGF and high SAA were both risk factors for CAS in hypertensive patients (P＜0.05). The ROC curve showed that the optimal cut-off points of serum HB-EGF and SAA levels for diagnosing CAS were 19.84 μg/L and 8.97 mg/L, respectively. The AUC for diagnosing CAS alone and in combination were 0.1,0.810 and 0.875, respectively, the value of combined diagnosis of the two was higher than that of single diagnosis. Conclusion Serum HB-EGF and SAA levels were significantly increased in hypertensive CAS patients, and both were positively correlated with CIMT, which has high diagnostic efficacy for hypertensive CAS.

Abstract:Aim To investigate the cholesterol efflux capacity(CEC) of plasma high-density lipoprotein(HDL) in coronary heart disease(CHD) patients with diabetes and its influencing factors. Methods 140 patients who were diagnosed as CHD by coronary angiography had one or more artery lesion degree ＞50%. They were divided into two groups:the CHD with diabetic mellitus(DM) group(n＝70) and the CHD without DM group(n＝70), patients without CHD confirmed by coronary angiography was taken an controls(n＝25). The capacity of HDL to induce cellular cholesterol efflux was determined by measuring the transfer of [3H] cholesterol from J774 macrophages to the medium containing the ApoB-deleted plasma. The levels of myeloperoxidase(MPO) and serum amyloid A protein (SAA) in plasma were measured to evaluate the level of oxidative stress and inflammation. The correlation between CEC and the above indexes (MPO, SAA) was analyzed. Results The cholesterol efflux capacity in CHD patients with diabetes was significantly lower than that in CHD patients without diabetes (P＜0.05); The level of SAA was increased in CHD patients with diabetes than that in CHD patients without diabetes, but the difference was not statistically significant (P＞0.05). And plasma SAA level in CHD patients with diabetes were negatively correlated with CEC (r＝－0.260,P＜0.05). Moreover, the level of MPO in CHD patients with diabetes was not higher than that in CHD patients without diabetes, there was no correlation between MPO and CEC in CHD patients with diabetes. Conclusion CHD patients with diabetes has more impaired CEC compared with those without diabetes. Inflammation is a possible mechanism of CEC decline caused by abnormal glucose metabolism in patients with CHD.

Abstract:Serum amyloid A has a significant effect on the formation of atherosclerosis as an acute reaction, leading to inflammation by stimulating the release of inflammation factors. It is vital for atherosclerosis that serum amyloid A combined with lipoprotein changes the physiological function of high density lipoprotein. Serum amyloid A can affect the function of vascular endothelium and smooth muscle, and also cause thrombosis,which all promote the development of atherosclerosis.

Abstract:High density lipoprotein (HDL) is mainly composed of apolipoprotein A1 (ApoA1), lipid and related regulatory factors. Its structural and functional abnormalities are closely related to the occurrence and development of cardiovascular diseases. HDL mainly transports cholesterol from the macrophages under the endothelium of blood vessels to the liver and expels it through the reverse cholesterol transport pathway, regulating the lipid balance in the body. It is found that the structure and metabolism of HDL have changed in patients with cardiovascular disease, including the abnormal modification of ApoA1, serum amyloid A instead of ApoA1 and the change of miRNA content carried by HDL. This article reviews the structure, metabolism and function of HDL, which provides a new way for the diagnosis and treatment of lipid metabolism related diseases.

Abstract:High density lipoprotein-cholesterol (HDLC) is regarded as an important protective factor against cardiovascular disease. There is an inverse relationship between its serum levels and risk of cardiovascular disease. However, in cardiovascular disease, diverse components of the high density lipoprotein(HDL) proteins,lipids or microRNAs suffer alterations, which propel a shift towards a dysfunctional state, where HDL becomes proatherogenic, prooxidant, and proinflammatory. This review is to summarize the structural and functional changes of the dysfunctional high density lipoprotein.