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The aim of this study was to investigate the expression level of vascular cell adhesion molecule-1 (VCAM-1) in the aortic tissues of atherosclerotic patients and to explore the associated clinical implications. Full-thickness aortic wall tissue samples were collected from atherosclerotic patients. Biochemical analysis was used for the detection of the serum levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), lipoprotein (a) [Lp (a)], apolipoprotein (Apo) AI and Apo-B. Coronary angiography and SYNTAX scoring were used to determine the extent and severity of the disease. Immunohistochemistry was employed for the detection of the VCAM-1 protein expression levels in the arterial tissues. Significant differences were observed in the blood lipid levels between atherosclerotic patients and control subjects. Immunohistochemistry indicated that the aortic VCAM-1 expression level in atherosclerotic patients was 0.23±0.06 optical density (OD) units, which was significantly higher than that in the control subjects (0.08±0.03 OD units). In the atherosclerotic patients, the aortic VCAM-1 expression was positively correlated with the serum levels of TG (r=0.347), TC (r=0.469), LDL-C (r=0.463), Lp (a) (r=0.507) and Apo-B (r=0.384), while VCAM-1 and HDL-C were negatively correlated (r=-0.319). Furthermore, a higher SYNTAX score was accompanied by a higher VCAM-1 expression level (r=0.532), and an elevated aortic VCAM-1 expression was associated with certain cardiovascular risk factors. In conclusion, aortic VCAM-1 expression is associated with the severity of atherosclerosis and cardiovascular risk factors, indicating that VCAM-1 plays a role in the pathogenesis of atherosclerosis.

Objective To investigate the relationship between levels of toll-like receptor 4 (TLR4) protein in aortic tissue and the severity of atherosclerosis in patients undergoing coronary artery bypass graft (CABG) surgery. Methods Samples of ascending aorta and renal artery were collected from patients undergoing CABG surgery or kidney donation, respectively. TLR4 levels were determined by immunohistochemistry. Coronary angiography was performed to determine atherosclerosis severity via Gensini score. Results TLR4 was present at high levels in aortic tissues from patients ( n = 46), and was absent from renal artery tissue (controls; n = 11). There was a significant positive correlation between Gensini score and TLR4 level in the patient group. Conclusions TLR4 may play an important role in atherosclerosis and could be a potential therapeutic target for treatment of coronary artery disease. Discarded aortic tissue obtained during CABG surgery provides a new approach to the study of the pathogenesis of atherosclerosis.

Background Drug-eluting stent (DES) implantation has been proved more effective compared with bare-metal stent (BMS) implantation for ST-segment elevation myocardial infarction (STEMI) within medium follow up. However, limited information is available on the long-term safety and efficacy of DES. Methods We performed a meta-analysis of randomised controlled trials (RCT) comparing DES with BMS in patients with STEMI at long-term follow up, defined as five years or more. The clinical end points were target vessel revascularisation (TVR), death, recurrent myocardial infarction (MI), stent thrombosis and very late stent thrombosis. We calculated the pooled estimate based on a fixed-effects model using odds ratio (OR) for rare events. Results Four RCT were included, with a total of 1414 patients enrolled. Up to five years, DES showed a significant reduction in TVR (OR, 0.55; 95% confidence interval [CI], 0.55-0.77; P = 0.0005), but an increase in very late stent thrombosis (OR, 3.03; 95% CI, 1.28-7.18; P = 0.01), without increasing mortality (OR, 0.85; 95% CI, 0.59-1.20; P = 0.35), recurrent MI (OR, 1.05; 95% CI, 0.69-1.60; P = 0.80), and overall stent thrombosis (OR, 1.10; 95% CI, 0.66-1.82; P = 0.72). Conclusions At long-term follow-up, primary percutaneous coronary intervention with DES improved efficacy, without reducing overall safety. However, a trade-off must be made between the reduction of reintervention with DES and an increase in very late stent thrombosis.

The aim of the present study was to investigate the expression of NLRP3 in aorta of patients with coronary atherosclerosis and to explore the association between aortic expression levels of NLRP3 and atherosclerotic risk factors.We collected small pieces of ascending aorta from 36 patients undergoing coronary artery bypass graft (CABG) surgery, and the arterial tissues from 10 subjects without atherosclerosis through the kidney donation program were taken as control. The expression of NLRP3 of the research and control group was determined by immunohistochemistry. Gensini score was used to evaluate the severity of coronary atherosclerosis.NLRP3 was strongly expressed in aorta of CABG patients. The aortic NLRP3 expression was elevated in patients with hypertension or diabetes, and smokers. The NLRP3 expression in aorta was positively correlated with total cholesterol, low density lipoprotein cholesterol, and lipoprotein(a) (P0.05); but negatively correlated with high density lipoprotein cholesterol (P0.05). Spearman correlation revealed that aortic NLRP3 expression had significant correlation with Gensini coronary severity scores (P0.05).NLRP3 was overexpressed in aorta of patients with coronary atherosclerosis and the aortic NLRP3 expression is correlated with the severity of coronary artery disease and the atherosclerotic risk factors.

Objectives. The role of the NLRP3 inflammasome in atherosclerosis remains controversial. The aim of this study was to determine whether inhibition of NLRP3 signaling by lentivirus-mediated RNA interference could reduce atherosclerosis and stabilizes plaques. We also tried to explore the mechanisms of the impact of NLRP3 inflammasome on atherosclerosis.Methods. Apolipoprotein E-deficient mice aged 8 weeks were fed a high-fat diet and were injected with NLRP3 interfering or mock viral suspension after 4 weeks. Lentivirus transfer was repeated in 2 weeks. Four weeks after the first lentivirus injection, we evaluated the effects of NLRP3 gene silencing on plaque composition and stability and on cholesterol efflux and collagen metabolism, by histopathologic analyses and real-time PCR.Results. Gene silence of NLRP3 prevented plaques progression and inhibited inductions of proinflammatory cytokines. Moreover, this RNA interference reduced plaque content of macrophages and lipid, and increased plaque content of smooth muscle cells and collagen, leading to the stabilizing of atherosclerotic plaques.Conclusions. NLRP3 inflammasomes may play a vital role in atherosclerosis, and lentivirus-mediated NLRP3 silencing would be a new strategy to inhibit plaques progression and to reduce local inflammation.

Inflammation plays an Important role In the pathophysiology of the metabolic syndrome (MS). We determined whether the overexpression of interleukin (IL)-18 could aggravate left ventricular (LV) remodeling and diastolic dysfunction in fructose-fed rats (FFRs). To create an animal model for MS, male Wistar rats received 10% fructose in water for 8 months. We used an adenovirus encoding rat IL-18 to overexpress IL-18 in FFRs by intravenous administration. IL-18 overexpression led to increases in collagen volume fraction and collagen deposition. LV systolic function was unaltered. But the LV end-diastolic pressure and the time constant of isovolumic relaxation (tau) were increased. Peak negative value of time derivative of LV pressure (−dp/dt) was decreased. Isovolumic relaxation time and myocardial index, as assessed by echocardiography, were increased. Overexpression of IL-18 leads to aggravated LV remodeling and dysfunction in FFRs. Attenuation of the inflammatory process may provide a novel therapeutic strategy in treating metabolic cardiomyopathy.

Aim To evaluate creatine kinase-MBmass (CK-MBmass) for the early diagnosis of infarct-related artery (IRA) patency after thrombolysis and the hierarchical diagnosis of related artery reperfusion (RAR). Patients and methods CK-MBmass and creatine kinase-MBactivity (CK-MBactivity) were measured kinetically in 48 patients treated with thrombolysis and 96 patients treated with routine drugs. Results In the continuous-RAR (CRAR) group, the peak values of CK-MBmass and CK-MBactivity appeared at ⩽12 h, the peak durations were maintained for ⩽8 h before decreasing to normal at ⩽42 h, which occurred more quickly than those values in the non-RAR (NRAR) group. In the temporary-RAR (TRAR) group, the peak values appeared at ⩽12 h, but no significant differences were found between the TRAR and NRAR groups in the time that the peak durations lasted before decreasing to normal values. In the reobliteration group after RAR, the peak values appeared at ⩽12 h, and the peak durations were maintained for ⩽8 h. After returning to the normal, a second peak appeared, and the time required for the values to return to normal was prolonged significantly. Conclusions CK-MBmass could be used as an indicator of RAR after thrombolysis; and the kinetic changes of serum CK-MBmass could be used for the hierarchical diagnosis of RAR in acute myocardial infarction.

As a novel vasoactive peptide, plasma coupling factor 6 (CF6) was shown to be elevated in patients with diabetes mellitus, yet the mechanism involved is unknown. We studied CF6 protein release and its potential mechanism in human umbilical vein endothelial cells (HUVECs) incubated with high glucose levels. High glucose level enhanced CF6 expression and peptide secretion in HUVECs in a time- and concentration-dependent manner, which was independent of increased osmolarity. PKC or p38 MAPK inhibition significantly suppressed high glucose-mediated CF6 release in HUVECs, and the inhibition rate was -45% and -30%, respectively. Also, high glucose-induced CF6 production was antagonized by insulin treatment. Hence, high glucose increases the expression and secretion of CF6 in endothelial cells and appears to be mediated by PKC and p38 MAPK activity.