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.
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.
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.
ObjectiveTo systematically review the interventional effects of Simiao Yong'an decoction on atherosclerosis animal models.MethodsDatabase including CNKI, WanFang Data, VIP, PubMed, The Cochrane Library, and Web of Science were searched to collect animal experiments on atherosclerosis model intervention by Simiao Yong’an decoction from inception to October 2020. Two reviewers independently screened the literature, extracted data, and used the SYRCLE animal experiment bias risk assessment tool to evaluate risk bias of included studies, and then used RevMan 5.4.1 software for meta-analysis.ResultsA total of 14 animal experiments were included. The results of meta-analysis showed that compared with the blank model group, the Simiao Yong’an decoction group could reduce the aortic plaque area (SMD=−2.04, 95%CI −3.35 to −0.74), the ratio of aortic plaque to lumen area (SMD=−1.72, 95%CI −2.48 to −0.97), total cholesterol level (SMD=−0.97, 95 %CI −1.72 to −0.22), triglyceride level (SMD=−1.21, 95%CI −1.82 to −0.60), low-density lipoprotein cholesterol level (SMD=−1.82, 95%CI −3.12 to −1.53), tumor necrosis factor-α level (SMD=−3.36, 95%CI −4.21 to −2.52), monocyte chemotactic factor-1 level (SMD=−2.98, 95%CI −4.60 to −1.35) and C-reactive protein level (SMD=−0.60, 95%CI −1.08 to −0.11); however, in the high-density lipoprotein cholesterol level (SMD=0.66, 95%CI −0.10 to 1.42) and the level of interleukin 1 (SMD=−1.41, 95%CI −4.11 to 1.30), the differences were not statistically significant.ConclusionsThe existing evidence shows that the intervention of Simiao Yong’an decoction in the atherosclerosis model can reduce the aortic plaque area and the ratio of the aortic plaque to the lumen area, reduce total cholesterol, triglycerides, and low-density lipoprotein cholesterol levels, and reduce tumor necrosis factor-α, monocyte chemotactic factor-1, and C-reactive protein levels. Due to limited quality of included studies, more high quality studies are required to verify the above conclusions.
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.
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 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.
【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.
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 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.