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 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.
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.
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.
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 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 study the characteristics of carotid atherosclerotic plaque and investigate the relationship between visfatin and plaque stabilization. Methodsfifty-six patients with carotid stenosis were divided into symptomatic group (n=31) and asymptomatic group (n=25) based on the clinical manifestation and onset time.All plaque specimens were stained with HE and Masson trichrome staining and studied pathologically.The plaques were grouped into stable and unstable plaques based on thickness of the fibrous cap and the area of lipid-rich core in the plaques.The expression of visfatin was detected by immunohistochemistry staining. Results①The proportion of unstable plaques were significantly higher in symptomatic group than in asymptomatic group (67.74% vs 36.00%, P < 0.05).②Compared with stable plaques, unstable plaques had thinner fibrous cap, larger lipid necrotic core, and higher proportion of hemorrhage: (49.87±8.75)μm vs (74.54±6.80)μm (P < 0.001), (65.63±12.97)% vs (31.81±5.13)% (P < 0.001), and 63.33% vs 30.77% (P < 0.05).③The integral optical density value of expressed visfatin in unstable plaques was significantly more than in stable plaques (84 165.47±9 183.12 vs 55 694.08±4 818.57, P < 0.001). ConclusionsThe plaque destabilization is closely related to the clinical symptoms of atherosclerosis.The thickness of fibrous cap, area of lipid-rich core, and hemorrhage play an important role in the plaque stabilization.The visfatin is related to atherogenesis and plaque destabilization.
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.
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.