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 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．
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.
The way of intravenous drug abuse is to puncture the peripheral blood vessels and inject the drug directly into the blood. Therefore, this method has an impact on the peripheral artery and venous system of the users, and can cause a variety of peripheral vascular diseases, such as phlebitis, deep vein thrombosis, chronic venous insufficiency, phlebangioma, atherosclerosis, acute arterial ischemia, pseudoaneurysm, etc. However, due to the particularity of drug abusers, the vascular complications caused by intravenous drug abuse have not attracted enough attention. This paper reviewed the types and pathogenesis of peripheral vascular diseases caused by intravenous drug abuse, so as to improve the clinical understanding of peripheral vascular diseases caused by intravenous drug abuse, improve the prognosis of patients, reduce occupational exposure of medical staff, and play a certain role in social warning.
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 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.
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.
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 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.
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.