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.
ObjectiveTo summarize the progress on the injury mechanism of vascular endothelial cells in atherosclerosis.MethodsThe latest progress was reviewed in recent literatures.ResultsAll kinds of etiological factors have activated NF-kappa B and cytokines in the development of atherosclerosis, which lead to expression of cell adhesive molecules and adhesion of monocytes to vascular endothelial cells.A variety of inflammatory mediums are released, which can directly damage endothelial cells.Besides, the inflammatory mediums make monocytes and neutrophils attach to endothelial cells by immune mechanisms, which injure the endothelial cells more severely. Meanwhile the damaged membrance structure leads to the production of AECA which activates the complementary system. Then the vascular endothelial cell injury is aggravated and the development of atherosclerosis accelerated. ConclusionIt is very important to recognize the injury mechanism of vascular endothelial cells in the development of atherosclerosis for prevention and treatment of atherosclerosis.
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 explore the methods of early diagnosis of arteriosclerosis obliterans of lower extremity (ASOLE). Methods The related literatures on ASOLE detection means adopted clinically were reviewed, and their advantages and disadvantages were compared.Results Asymptomatic ASOLE could be discovered by determination of ankle brachial index (ABI) and toe brachial index (TBI), which was a good index for arterial function assessment of lower extremity. Pulse wave velocity (PWV) was more vulnerable and less sensitive than ABI, and therefore more suitable for screening of a large sample. ASI was an index to assess arterial structure and function, and it had a good correlation with PWV. Flow-mediated dilation (FMD) was a measurement evaluating the function of endothelial cell; Pulse wave measurement was simple, sensitive, and its result was reliable. Color Doppler ultrasonography could localizate the lesion and determine the degree of stenosis at the same time. Multiple-slice CT angiography (MSCTA) was more accurate than color Doppler ultrasonography, but its inherent shortcomings, such as nephrotoxicity of contrast agent, was still need to be resolved. 3D-contrast enhancement magnetic resonance angiography (CEMRA) had little nephrotoxicity, but a combination of other imaging methods was necessary. Microcirculation detections required high consistency of the measurement environment, but they were simple, sensitive and noninvasive, and therefore could be used for screening of ASO. Conclusion Publicity and education of highrisk groups, and reasonable selection of all kinds of detection means, are helpful to improve the early diagnosis of ASOLE.
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.
【Abstract】ObjectiveTo investigate the effects of CO2 pneumoperitoneum on blood flow of carotid arteries in atherosclerosis rabbits.MethodsFifty Japan white rabbits were randomly divided into control group and three atherosclerosis groups. In atherosclerosis group, the rabbits were randomly subjected to CO2 pneumoperitoneum with an intraabdominal pressure of 0 mm Hg, 10 mm Hg or 15 mm Hg for 2 hours, after the model were created by feeding the rabbits with high fatty diet. The blood flow of the common carotid arteries were measured by electromagnetic blood flowmeter. Artery blood samples were collected for blood gas analysis at 30 minute intervals. ResultsHigher insufflation pressures and longer duration of CO2 pneumoperitoneum were associated with greater increase in blood flow of common carotid arteries. Compared with those in control group and atherosclerosis group with 0 mm Hg CO2 pneumoperitoneum, there were statistically significant increases in blood flow of the common carotid arteries during CO2 pneumoperitoneum in 10 mm Hg and 15 mm Hg pneumoperitoneum group, the changes in 15 mm Hg pneumoperitoneum group were more significant than those in 10 mm Hg pneumoperitoneum group (Plt;0.05). When compared with the blood flow before insufflation, those in 10 mm Hg and 15 mm Hg pneumoperitoneum group also increased significantly during CO2 pneumoperitoneum, even at 30 minute after desufflation (Plt;0.05). However, those in control group and 0 mm Hg pneumoperitoneum group did not change significantly (Pgt;0.05). There were significant decrease in pH and significant increase in PCO2 in both 10 mm Hg and 15 mm Hg groups, when compared with presufflation values or those in control group and 0 mm Hg pneumoperitoneum group(Plt;0.05). The changes in pH and PCO2, however, were no significant at any time point in control group and 0 mm Hg pneumoperitoneum group (Pgt;0.05). HCO3- did not change significantly in either group(Pgt;0.05).ConclusionUnder atherosclerosis conditions, CO2 pneumoperitoneum has an adverse influence on the blood flow of the common carotid arteries which may be associated with increased intrabdominal pressure,absorbed CO2 gas.
Vascular endothelial cell(VEC) is a kind of simple squamous epithelium lined on the inner surface of blood vessels. VEC is an important barrier between the blood and tissue and it also plays a key role in regulating inflammation, thrombosis, endothelial cells mediated vasodilatation and endothelial regeneration. These processes should be controlled by a variety of complex mechanism which requires us to find out. With results of the researches in vascular endothelial cell function, the important roles that microRNA in vascular endothelial cell function draws more and more researchers' attention. MicroRNAs control gene expression in post-transcriptional level and affect the function of endothelial cells. This review focuses on the research progress on regulatory mechanism of microRNA to endothelial cell inflammation, thrombosis, vasodilation and endothelium regeneration.
Objective To provide the anatomical basis for detecting distal outflow tract in late atherosclerosis obliteration in lower extremities. Methods Ten lower extremities that were amputated above knees because of late atherosclerosis obliteration were used in this experiment. The blood vessels in the residual bodies were perfused to run blood vessel cast mould to observe the anatomical and pathological change of the popliteal artery, the anterior and posterior tibial arteries and their collateral vessels. The number and distribution of those collateral vessels were also observed. Results The popliteal artery, anterior and posterior tibial arteries were all occluded due to atherosclerosis. However, there were three types of those collateral arteries: ① Atheromatous plaque in bole stretched into collateral arteries and led to occlusion. ② Obliteration was only observed at the initial segment, with no obstruction at the distal end but extenuated. ③ The collateral arteries originated from the bole artery symmetrically, keeping communicative with each other through punctiform interspaces. The last two types were mainly distributed at the inferior segment of popliteal artery, the superior segment of anterior and posterior tibial arteries, forming vascular anastomosing network in the whole cnemis muscle group. Conclusion Un-obstructed collateral arteries in certain places can be still found, though atherosclerosis obliteration is formed in popliteal artery, anterior and posterior tibial arteries in lower extremities. Therefore, it may be possible to construct collateral outflow tracts if endo-membrane stripping operation is performed.
Objective To investigate theory guidance for preoperative appraisal of advanced stage lower limb arteriosclerosis obliterans and clinical application of arteriae surales. Methods From September 2007 to June 2008, one hundred cases without obviously arteriosclerosis were collected to accepted color Doppler ultrasonography, and parameters of the arteriae surales were observed， such as location, macro-body morphous, caliber, and blood parameters value, meanwhile the caliber and blood parameters value of anterior tibial artery and posterior tibial artery were also measured. Results Detection rate of arteriae surales was 96% (96/100). Arteriae surales located midpiece sequentiae of popliteal fossa, and above flatfish tendinous arch, which in 89 cases were geminous branched from popliteal artery; in the remaining 7 cases, popliteal artery diverged a bole, walked 1-3 cm, then diverged two branches and ingressed gastrocnemius. Diameter and cross section area of arteriae surales were smaller than those of anterior tibial artery and posterior tibial artery (P＜0.05）, but peak flow rate of systolic phase, maximum positive direction flow rate of relaxing period and mean flow rate were not significantly differents between arteriae surales and anterior tibial artery or posterior tibial artery （P＞0.05）. The flow of geminous arteriae surales was 63.1% of anterior tibial artery, and 59.1% of posterior tibial artery. Conclusion Through the ultrasonic study, it is significant for clinical therapy to master the normal anatomy, blood parameters value and flow of arteriae surales.