The diameter of the giant coronary artery aneurysm is at least 4 times bigger than that of the normal coronary artery and 2-3 times bigger than that of the normal coronary artery aneurysm. Giant coronary artery aneurysm is rare in clinic with a reported morbidity which is less than 0.3%. Just like ordinary coronary artery aneurysm, coronary artery atherosclerosis is the main cause of the giant coronary artery aneurysm. Most giant coronary artery aneurysms are asymptomatic, but some patients may have heart-related clinical emergency in short term and may have thrombosis which can lead to embolism and fistula which can cause rupture in long term. Surgical treatment is the first chioce for giant coronary artery aneurysm now. However, the interventional therapy will also be an important way to treat the disease in the future. In this article, we review the diagnosis, clinical manifestation, treatment and other aspects of giant coronary artery aneurysm as follows.
The main cause of death in patients with end-stage renal disease (ESRD) is cardiovascular disease, and trimethylamine-N-oxide (TMAO) has been found to be one of the specific risk factors in the pathogenic process in recent years. TMAO is derived from intestinal bacterial metabolism of dietary choline, carnitine and other substances and subsequently catalyzed by flavin monooxygenase enzymes in the liver. The changes of intestinal bacteria in ESRD patients have contributed to the accumulation of gut-derived uremic toxins such as TMAO, indoxyl sulfate and indole-3-acetic acid. While elevated TMAO concentration accelerates atherosclerosis through mechanisms such as inflammation, increased scavenger receptor expression, and inhibition of reverse cholesterol transport. In this review, this research introduces the biological function, metabolic processes of TMAO and mechanisms by which TMAO promotes the progression of cardiovascular disease in ESRD patients and summarizes current interventions that may be used to reverse gut microbiota disturbances, such as activated carbon, fecal microbial transplantation, dietary improvement, probiotic and probiotic introduction. It also focuses on exploring intervention targets to reduce the gut-derived uremic toxin TMAO in order to explore the possibility of more cardiovascular disease treatments for ESRD patients.
Objective To investigate and analyze the relationships among glucagon-like peptide-1 (GLP-1) level, chronic inflammation, and atherosclerosis in patients with non-alcoholic fatty liver disease (NAFLD). Methods From October 2016 to February 2017, using cross-sectional investigation, the GLP-1 level, chronic inflammation, and atherosclerosis were investigated in 80 subjects (40 NAFLD patients in NAFLD group, and 40 non-fatty liver disease participants in control group) who underwent physical examination at Xi’an Road Community Hospital. Results Compared with those in the control group, GLP-1 fasting level in patients with NAFLD [(9.09±1.03) vs. (9.15±1.06) pmol/L, P=0.807] and postprandial plasma GLP-1 [(15.96±3.37) vs. (17.46±4.76) pmol/L, P=0.108] had no changes. The correlations of GLP-1 level with chronic inflammation and insulin resistance (IR) were not significant either. The increased risk of carotid intima-media thickness related cardiovascular disease (CVD) in the NAFLD group was greater than that in the control group, and the difference was statistically significant [22 (55.0%)vs.13 (32.5%), P=0.043]. When the plasma lipoprotein-associated phospholipase A2 level increased, the risk of NAFLD increased [odd ratio (OR)=1.16, 95% confidence interval (CI) (1.02, 1.32), P=0.023]. Plasma ceramide kinase (CERK) in the NAFLD group was lower than that in the control group, and the difference was statistically significant [(12.36±2.45) vs. (18.33±3.71) ng/mL, P<0.001]. When the plasma CERK level of the fasting plasma was elevated, the risk of NAFLD decreased [OR=0.30, 95%CI (0.12, 0.78), P=0.014]. The homeostasis model assessment of insulin resistance (HOMA-IR) in the NAFLD group was higher than that in the control group, and the difference was statistically significant (2.46±2.53 vs. 1.11±0.66, P=0.002). The Matsuda index in the NAFLD group was less than that in the control group, and the difference was statistically significant (5.88±4.09 vs. 10.46±7.90, P=0.002). When HOMA-IR increased, the risk of NAFLD increased [OR=2.75, 95%CI (2.49, 3.12), P=0.036]. Conclusions Plasma GLP-1 level is not a sensitive indicator of chronic inflammation and IR in patients with NAFLD. Patients with NAFLD are in an increased risk of atherosclerosis and CVD. It suggests that NAFLD might be involved in chronic inflammation and IR. Chronic inflammation can cause IR, and then chronic inflammation and IR can cause NAFLD and subclinical atherosclerosis. In return for this, NAFLD increases chronic inflammation and IR.
Objective To evaluate the relationship between COPD and atherosclerosis, and analyze the risk factors of atherosclerosis among COPD patients. Methods A total of 40 COPD patients and 43 normal subjects were enrolled in the study. Carotid intima-media thickness (IMT) and plaques were detected in both groups. Blood samples were collected to measure the concentration of high sensitive C-reactive protein (hs-CRP) , fibrinogen (Fbg) , total cholesterol (TC) , triglyceride (TG) , high density lipoprotein cholesterol (HDL-C) , low density lipoprotein cholesterol (LDL-C) , while smoking index was recorded. Multiple regression analysis was performed to evaluate the correlative factors of IMT among COPD patients. According to whether luminal stenosis appeared, the COPD patients were allocated into group A ( without luminal stenosis) and group B ( with luminal stenosis) . Age, gender, hs-CRP, Fbg, TC, TG, HDL-C, LDL-C, and smoking index of the two groups were compared respectively. Results Hs-CRP, Fbg, thickness of IMT, plaques detection rate, and smoking index in the COPD group were significantly higher than those in the control group ( Plt;0.05) . TC, HDL-C, LDL-C in the COPD group were significantly lower than those in the control group ( Plt;0. 05) .Multiple regression analysis of IMT correlative factors among COPD patients showed that age, hs-CRP, Fbg, TC, TG, LDL-C, HDL-C, and smoking index were in linear relationship with IMT thickening. Age, hs-CRP, TC, and smoking index were positively correlated with IMT ( Plt;0.05) . Hs-CRP and smoking index in the group A were lower than those in the group B ( Plt;0. 05) .While TC, TG, LDL-C, and HDL-C in the group A were higher than those in the group B ( Plt;0.05) . Conclusions Age, smoking index, hs-CRP, and TC are risk factors for thickening of carotid artery IMT in COPD patients. Furthermore, smoking index, hs-CRP, TC, TG, LDL-C, and HDL-C are related to the severity of IMT thickening. The ultrasound detection of carotid artery IMT can be a valuble tool to screen atherosclerosis in patients with COPD.
In recent years, high-resolution magnetic resonance imaging (HRMRI) has become a useful clinical and research tool. HRMRI can be used to observe intracranial vascular wall lesions in vivo, providing more valuable pathophysiological information, and providing guidance for the diagnosis, differential diagnosis and prognosis of intracranial atherosclerosis. For stenotic intracranial atherosclerosis, the morphology of the vessel wall can effectively differentiate various vascular stenosis diseases. Further, plaque composition, vessel wall enhancement, remodel mode provide information of plaque vulnerability. For non-stenotic intracranial atherosclerosis, the location of the plaque can reveal the pathophysiological mechanism. In addition, HRMRI can show the lesion in lenticulostriate artery. Therefore, this article will summarize the clinical application of HRMRI.
ObjectiveTo systematically review the safety and validity of the treatment of intracranial atherosclerosis diseases (ICAD) by using Wingspan stents, and to provide the reference for clinical practice and research. MethodsDatabases such as the PubMed, The Cochrane Library, EMbase, Cochrane Central Register of Controlled Trials, CBM, CNKI and VIP were searched for studies concerning the safety and validity of the treatment of intracranial atherosclerosis diseases (ICAD) by using Wingspan stents from January 1st, 2005 to January 10th, 2014. Randomized controlled trials (RCTs), non-randomized controlled trials, case-control studies, cohort studies and case series were all included. Two reviewers independently screened literature according to inclusion and exclusion criteria, extracted data. Then, meta-analysis was performed by using the R software. ResultsA total of 34 studies (2 RCTs, 22 cohort studies, and 10 case-control studies) involving 2 511 patients were included. The results of meta-analysis showed that:operation success rates was 96.75% (95%CI 95.82% to 97.48%), 30 day rates of the end point events was 8.75% (95%CI 7.61% to 10.04%), 1 year rates of the end point events was 13% (95%CI 11.47% to 14.70%), total mortality was 2.98% (95%CI 2.16% to 4.10%), incidence of in-stent restenosis was 21.76% (95%CI 18.27% to 25.71%), the ratio of the patients with symptomatic restenosis and total patients was 6.50% (95%CI 4.89% to 8.60%), and the ratio of the patients with symptomatic restenosis and total patients with restenosis was 26.06% (95%CI 19.94% to 33.29%). ConclusionCurrent evidence shows that treatment of ICAD by using Wingspan stents is effective and safe. However, this conclusion should be approved by further higher quality RCTs.
ObjectiveTo investigate the pathogenesis of atherosclerosis (AS) by detecting different expression genes between normal Wistar rats and rats with atherosclerosis through the technology of gene chip. MethodsThe rats were treated with standard diet with saline injection (control group) or high-cholesterol diet with vitamin D3 injection and balloon injury (model group). Total cholesterol (TC) and triglyeride (TG) in serum were detected 90 days later to ensure the success of establishment of the atherosclerosis model. Abdominal aorta was isolated and stained with HE. Total RNA was isolated from the aorta for gene chip analysis to explore the differential gene expression. ResultsCompared with the control group, the TC and TG level in the model group were highly advanced (P<0.05). AS model was confirmed by pathological observation. Gene chip detection showed that 511 genes were up-regulated and 1 219 ones were down-regulated which were interrelated with lipid metabolism, inflammatory reaction, oxidative stress and apoptosis as well. ConclusionThe expression change with multiple gene in AS suggests that the nosogenesis of AS is adjusted and controlled complicatedly. Intensive study of some important genes will contribute to the prevention and improvement of prognosis of AS.
Objective To review research advances in atherosclerosis of removal mechanisms of apoptotic cells.Method The literatures about the removal mechanisms of the apoptotic cells were reviewed．Results The removal factors of apoptotic cells， such as transglutaminase 2， milk fat globule-EGF-factor 8， complement system，c-Mer proto-oncogene tyrosine protein kinase，and Fas，might cause the lipid core of the atherosclerotic plaque if one of them was defective phagocytic clearance．Conclusion How to remove the surplus of the phagocytosis and study the common pathways of the downstream signal of its receptor were the future direction of development．
ObjectiveTo explore the relationship between plasma homocysteine level and intracranial artery atherosclerosis in patients with cerebral infarction. MethodsA total of 120 patients with cerebral infarction diagnosed between January and December 2013 were selected.Plasma homocysteine level was analyzed and intracranial artery was detected by DSA. ResultsIntracranial artery atherosclerosis can be found in most of patients with cerebral infarction.Moreover,Plasma Hcy level of patients with large cerebral artery atherosclerosis was much higher than others (P<0.05).The much higher Plasma Hcy level,the severe intracranial artery atherosclerosis were found in internal carotid artery and cerebral middle artery (P<0.05). ConclusionIntracranial artery atherosclerosis is common in patients with cerebral infarction.Occurrence of intracranial artery atherosclerosis is positively correlated with plasma homocysteine level.Plasma homocysteine level may be a risk factor of intracranial artery atherosclerosis in patients with cerebral infarction.
ObjectiveTo observe the frequency and severity of carotid atherosclerotic stenosis in senior chronic obstructive pulmonary disease (COPD) patients and explore the related risk factors in order to provide a theoretical basis for the effective prevention of cardiovascular comorbidity in COPD. MethodsStable COPD out-patients followed up in Sichuan Provincial People's Hospital were prospectively enrolled between August 2012 and August 2015, who had carotid atherosclerosis confirmed by cervical vascular color ultrasonic inspection within 3 months. All the patients were divided into a carotid stenosis group and a non-carotid stenosis group. Demographic and laboratory data were extracted and compared between two groups. Pearson correlation and Logistic regression analysis were performed to analyze the risk factors related to carotid stenosis. ResultsOf 380 consecutive senior patients with COPD and carotid atherosclerosis, 199 (52.37%) had carotid stenosis. Compared with those without carotid stenosis, the patients in the carotid stenosis group had significantly higher levels of hypersensitive C reactive protein (hs-CRP), uric acid (UA), brain natriuretic peptide (BNP) and smoking index (P < 0.05). Lower levels of forced expiratory volume in one second (FEV1%) and body mass index (BMI) were also observed in the carotid stenosis group (P < 0.05). Pearson correlation and logistic regression analysis showed that hs-CRP (OR 1.040, 95%CI 1.011-3.070), UA (OR 1.003, 95%CI 1.000-2.006), FEV1 (OR 0.899, 95%CI 0.200-5.722), smoking index (OR 1.002, 95%CI 1.001-2.904) and BMI (OR 0.955, 95%CI 0.312-4.866) were associated with carotid stenosis. ConclusionsCarotid atherosclerotic stenosis is common in senior COPD patients. Higher levels of hs-CRP, UA and smoking index and lower levels of FEV1 and BMI may be independent risk factors for carotid stenosis in COPD.