运用中西医理论探讨动脉粥样硬化研究进展

动脉粥样硬化是动脉内壁因有胆固醇积聚而引致黄色粥样病灶，受累动脉内膜先后有多种病变存在，包括局部脂质和复合糖类积聚，出血和血栓形成，平滑肌细胞（smooth muscle cell，SMC）增生，引致硬化现象。主要累及大中型动脉，以主动脉、冠状动脉及脑动脉为多见，常导致管腔闭塞或管壁破裂出血等严重后果，是导致心脏病与中风的元凶。本病多见于40岁以上男性和绝经后女性，为中老年人主要致死原因之一，全球每年约有1200万人死于与动脉栓塞相关的疾病。     

黄芩苷对动脉粥样硬化作用机制的研究进展

动脉粥样硬化(AS)主要累及大动脉及中动脉,特别是冠状动脉、脑动脉和主动脉,其他常见的AS类型还有小动脉硬化和动脉中层硬化.其特点是受累动脉的病变从内膜开始,先后有多种病变合并存在,其基本病变是动脉内膜的脂质沉积、内膜灶性纤维灶、粥样斑块形成,导致管壁变硬、管腔狭窄,并引起斑块内出血、斑块破裂及局部血栓形成等一系列继发性病变,特别是发生在心和脑等器官,可引起缺血性改变.     

PCSK9致动脉粥样硬化的作用机制研究进展

<正>动脉粥样硬化(AS)是众多致死性和致残性血管事件发生的前期病理基础。AS的病理变化主要累及全身大中型肌弹力型动脉,受累动脉病变始于内膜,渐累及动脉中层,先后有多种病变合并存在,使动脉壁增厚变硬,以致管壁失去弹性、管腔缩小,进而使受阻动脉远端缺血而导致局部组织坏死、纤维化。临床表现为冠状动脉、颅脑动脉、四肢动脉、肾动脉及其他内脏     

动脉粥样硬化研究的当前问题

进入21世纪以来，动脉粥样硬化(AS)性心血管疾病已成为严重危害人类健康的第一位杀手。AS是以进行性脂质沉积、纤维组织增生和炎性细胞浸润为特征的累及全身大、中型弹性和肌性动脉的慢性疾病。病理学研究证明，主动脉、冠状动脉、脑动脉、肾动脉和下肢动脉是AS的易患部位。     

相关炎症因子与动脉粥样硬化

动脉粥样硬化(atherosclerosis,As)是一组主要累及全身大、中型弹力型动脉的血管硬化性疾病,以主动脉、冠状动脉和脑动脉多见,其特征是动脉内膜的脂质沉积和粥样斑块形成,且发病机制与高血压、血脂紊乱及血管内皮损伤等因素密切相关。近年来,各种细胞炎症因子与动脉粥样硬化的关系引起愈来愈多研究者的重视,现谨就择要作综述。     

踝臂指数在老年冠状动脉粥样硬化中的诊疗意义

动脉粥样硬化常可累及主动脉、冠状动脉及脑动脉,可导致管腔闭塞或管壁破裂出血等严重后果[1].如发生部位为冠状动脉则称为冠状动脉粥样硬化.准确及时地判断患者的疾病严重程度和预后是治疗的前提[2].临床上可以通过介入技术对该病进行明确诊断及分级,但介入是一种有创的检查方法,往往不易被初发或症状较轻的患者所接受.踝臂指数(ABI)常用于诊断外周动脉疾病.本研究试将ABI应用于冠心病严重程度的诊断中.     

联合他汀类与普罗布考抗动脉硬化斑块的研究进展

动脉粥样硬化(AS)是以富含脂肪的斑块聚积在大动脉壁为特征的疾病,其病变起始于动脉内膜中层的退变,先后有脂质和复合糖类聚积、纤维组织增生和钙化沉着。斑块内出血、斑块破裂及局部血栓形成是AS的继发病变。AS可累及全身动脉如:主动脉、冠状动脉、脑动脉、颈动脉、下肢动脉等。AS斑块形成是心脑血管事件的重要危险因素。     

动脉硬化在耳、眼、舌部的蛛丝马迹

动脉硬化是指人体的大型及中型动脉(如主动脉、冠状动脉、脑动脉等)的管腔内膜沉积了不等量的脂质,特别是胆固醇,它使内膜表明凸凹不平,凸出于血管腔内,有的还伴有钙质沉淀物及纤维形成。很显然,动脉管壁内膜增厚,加上纤维化及钙质沉着,使血管也变硬了。目前,世界上每年约有800万～1000万人死于动脉硬化所引起的心血管病和脑中风。动脉硬化是个隐形杀手,疾病发生时不知不觉,进展缓慢,难以引起人们关注,一旦     

主动脉瓣硬化和颈动脉斑块对冠心病的诊断价值

动脉粥样硬化广泛累及全身性动脉系统,主要累及大、中型动脉,特别是中型动脉,如冠状动脉和颈动脉,表现为斑块沉积和管腔狭窄,以不规则性瓣膜增厚为主要表现的主动脉瓣硬化（AVS）与动脉粥样硬化有关，被认为是动脉粥样硬化在血管壁以外的另一种表现形式，     

颈动脉粥样硬化与心血管疾病的关系

动脉粥样硬化是一种脂质在血管内膜沉积、内皮细胞受损、血小板和白细胞（单核细胞）黏附浸润伴平滑肌细胞和胶原纤维增生的慢性炎症过程。一般认为动脉硬化先由弹性大的主动脉发生,以后逐渐累及到小动脉（如四肢动脉、冠状动脉、颅内动脉等）。     

Atherosclerosis and its evolution in childhood

Cardiovascular risk factors in childhood are related to arterial wall changes that lead to atherosclerotic coronary artery disease in later life. Atherosclerosis begins early in life. The observations of early arterial wall connective tissue changes and accompanying early lipid deposition show the importance of understanding cardiovascular risk factors in children. Since risk factors found in childhood are potentially predictive of adult coronary heart disease, methods for prevention of atherosclerosis should begin in children. Rational strategies should be directed to removing atherogenic forces that work in a child at high risk. Primary prevention of atherosclerosis has its maximal potential when begun before advanced irreversible lesions can occur. Consideration needs to be directed to how cardiovascular connective tissue changes and lipid and calcium deposition can be modulated in the injury and healing processes. It is important to recognize that adult coronary artery disease is really a major pediatric problem.     

Diffusion of gamma globulin into the arterial wall identifies localized entry of lipid and cells in atherosclerosis

BACKGROUND: The localization of atheromatous lesions in vulnerable arteries and their relatively rare occurrence in other arteries of the same subject cannot be explained by current theories of the aetiology of atherosclerosis. OBJECTIVE: To determine whether abnormal diffusion of gamma globulin into the arterial wall from the lumen will identify defects of barrier function allowing localized entry of lipid and cells in atherosclerosis. METHODS: Paraffin sections of left anterior descending coronary arteries and corresponding internal thoracic arteries from 80 human subjects aged 1-65 years were stained for gamma globulin by the immunoperoxidase technique. Duplicate sections were stained with orcein to demonstrate the elastin structure. RESULTS: The barrier function of the luminal surface of the thickened intima was associated with the presence of an elastin lamina beneath the endothelial cells. With advancing age, the coronary arteries exhibited breakdown of this barrier function in localized areas with entry into the arterial wall of gamma globulin, lipid and cells. This was rare in the internal thoracic artery. CONCLUSION: Lack of continuity or incomplete formation of this sub-endothelial lamina, which was seen particularly in the coronary artery, was associated with localized entry into the arterial wall of gamma globulin, lipid and cells from the circulating blood and with the development of atheromatous lesions.     

The relation of coronary and peripheral arterial disease to the severity of femoral atherosclerosis in hypercholesterolaemia

Abstract. Objectives. The extent of atherosclerosis in the superficial femoral artery and the severity of arterial disease in the aorto-iliac and femoro-popliteal arterial districts were related to clinical diagnosis of coronary and peripheral atherosclerosis in hypercholesterolaemic patients. Design. The study constitutes baseline cross-sectional data of a randomized double-blind clinical trial on Probucol, using both computer based and visual estimations of angiographies as endpoints. Subjects. Two hundred and ninety men and women (mean age 54 years) with hypercholesterolaemia. Main outcome measures. Atherosclerosis was estimated with arteriographies. Lumen volume and edge roughness (vessel inner wall irregularity) of a 20 cm segment of the femoral artery were estimated by computer. A visual atherosclerosis score of the abdominal aorta to the popliteal arteries was made on both sides. Results. Patients with peripheral arterial disease had significantly more advanced disease according to all three angiographic variables than those without symptoms of peripheral vascular disease. Both men and women with coronary artery disease had significantly lower femoral lumen volume and higher roughness values than patients without. Men with previous myocardial infarction had significantly higher mean visual scores of atherosclerosis than those without, while lumen volume and roughness did not differ in either sex. Conclusions. Femoral atherosclerosis is an expression of a generalized disease, associated with clinical symptoms of coronary artery disease. Femoral atherosclerosis is often accompanied by atherosclerosis also in the coronary arteries.     

Stiffness of systemic arteries in patients with myocardial infarction. A noninvasive method to predict severity of coronary atherosclerosis

The static elastic properties of arterial tree (abdominal aorta and common carotid artery) were studied in 19 normal subjects and in 49 patients with myocardial infarction with an ultrasonic phase-locked echo-tracking system that allows continuous transcutaneous measurement of the arterial diameter. The stiffness index beta, which represented the mechanical properties in the arterial wall, was calculated from the relation between systemic blood pressure and the diameter of the artery. Patients with myocardial infarction underwent coronary angiography in their convalescent period to determine involved vessels. In 11 patients, coronary artery was patent; 15 patients had one-vessel disease, 12 had two-vessel disease, and the remaining 11 patients had three-vessel disease. In normal subjects, increasing age was associated with an increase in arterial stiffness. An average value of the stiffness index of the abdominal aorta was 8.58 +/- 3.02 (mean +/- SD) and that of common carotid artery was 9.17 +/- 2.22. In patients with three-vessel disease, these values were significantly higher (22.37 +/- 4.29 in abdominal aorta and 13.17 +/- 4.56 in common carotid artery) than those in normal subjects. Stiffness index of patients with two- or one-vessel disease was also increased but lower than those in patients with three-vessel disease (p less than 0.05). Forty-four of 49 patients with infarction had an arterial stiffness index of abdominal aorta higher than the 95% confidence limits of the normal data (p less than 0.05). Twenty-eight patients were outside the nomogram of common carotid artery (p less than 0.05). The mechanical properties of these elastic arteries provided sufficiently reliable information on changes caused by atherosclerosis.     

Giant aneurysm of the left main coronary artery in Takayasu aortitis

Takayasu aortitis is a chronic inflammatory vasculitis characterised by stenosis or obliteration of large and medium sized arteries. Although coronary arteries are affected in approximately 10% of cases, most of the lesions are luminal narrowing, and coronary aneurysm formation is extremely rare. A case is described of giant aneurysm of the left main coronary artery complicated with Takayasu aortitis in a 46 year old Japanese woman who was followed until her death at age 71. Pronounced intimal proliferation and adventitial fibrous thickening of the involved arterial wall usually induce constriction or occlusion at the orifice of the main branch of the aorta in Takayasu aortitis. However, systemic hypertension, which resulted from renovascular stenoses in this case, is likely to have enlarged the vessel lumen before replacement of medial and adventitial fibrosis after extensive destruction of medial elastic fibres in the left main coronary artery. Moreover, associations such as autoimmune hepatitis, chronic thyroiditis, and Sjögren syndrome strongly suggests that Takayasu aortitis may be an autoimmune disease.

Keywords: giant coronary aneurysm; Takayasu aortitis; renovascular hypertension; autoimmune disorders     

The genesis of atherosclerosis and risk factors: a review

Atherosclerosis constitutes the most common medical and surgical problem. This can be manifested clinically as stroke, coronary artery disease, or peripheral vascular disease. In the present review the microscopic appearance of the normal arterial wall, the definition of atherosclerosis and the five theories of atherogenesis are described. These are: the lipid theory, the hemodynamic theory, the fibrin incrustation theory, the nonspecific mesenchymal hypothesis and the response to injury hypothesis. Based on the above theories the sequence of events in atherogenesis is analyzed. The classification of the atherosclerotic lesions according to Stary (types I-VI) and their characteristics appear in a table. The epidemiology and the role of the following risk factors are presented in detail: age, sex, lipid abnormalities, cigarette smoking, hypertension, diabetes mellitus, physical inactivity, alcohol consumption, obesity, and hemostatic factors. In addition, less common genetically determined associations like homocystinuria, Tangier disease, Hutchinson-Gilford syndrome (progeria), Werner's syndrome, radiation induced atherosclerosis and the implications of Chlamydia pneumoniae on the arterial wall are discussed.     

Chlamydia pneumoniae (TWAR) in coronary arteries of young adults (15-34 years old).

An association of Chlamydia pneumoniae with atherosclerosis of coronary and carotid arteries and aorta has been found by seroepidemiology and by demonstration of the organism in atheromata. Age-matched control tissue from persons without atherosclerosis was usually not available. We studied autopsy tissue from young persons, many with no atherosclerosis, to determine whether C. pneumoniae is present in atheroma in young persons with early atherosclerosis and to compare the findings in age- and sex-matched persons without atherosclerosis. A left anterior descending coronary artery sample, formalin-fixed, from 49 subjects, 15-34 years of age, from the multicenter study called Pathobiological Determinants of Atherosclerosis in Youth (PDAY), was examined by immunocytochemistry and the polymerase chain reaction (PCR) for the presence of C. pneumoniae and by PCR for cytomegalovirus. A hematoxylin/eosin-stained section was used to determine disease present in the studied sample. Seven of the artery samples were found to have atheromatous plaque, 11 had intimal thickening, and 31 had no lesions. Eight of the samples were positive for C. pneumoniae by immunocytochemistry (n = 7) and/or PCR (n = 3). Six of the 7 (86%) atheroma, 2 of the 11 (18%) with intimal thickening, and none of the 31 normal-appearing coronary samples were positive. Four were positive by PCR for cytomegalovirus, 2 from diseased arteries and 2 from normal arteries. Examination of the adjacent left coronary artery sample with a fat stain found abnormalities in 25 of the patients, but 19 still showed no evidence of atherosclerosis as a result of either examination. Thus, C. pneumoniae is found in coronary lesions in young adults with atherosclerosis but is not found in normal-appearing coronary arteries of both persons with and without other evidence of atherosclerosis.     

Interrelation between the extent of atherosclerosis in the thoracic aorta, carotid intima-media thickness and the extent of coronary artery disease

Intima-media thickness (IMT) of the common carotid artery and atherosclerosis of the thoracic aorta have been shown to correlate with coronary artery disease (CAD). This study compares the relation between wall changes in the thoracic aorta and the carotid arteries and the angiographic severity and extent of atherosclerotic lesions in the coronary arteries in patients with verified CAD. Atherosclerotic wall changes in the carotid arteries and the thoracic aorta were measured by B-mode ultrasonography and transesophageal echocardiography (TEE), respectively, in 37 subjects aged 65+/-10 years with angiographically verified CAD. The mean value of the common carotid IMT of the right and left sides was 0.87+/-0.21 mm. All subjects had carotid plaques. TEE detected grades II-IV atherosclerotic plaques in the thoracic aorta in 32 of the 37 (86%) patients. A significant correlation was seen between the extent of coronary artery stenosis and aortic plaques score (r=0.46, p=0.008). Mean carotid IMT was also significantly correlated with coronary artery stenosis extent score (r=0.44, p=0.007). Moreover, a significant correlation was seen between the aortic plaque score and the mean carotid IMT (r=0.39, p=0.02). In conclusion, we found a clear and significant relationship between wall changes in the thoracic aorta, common carotid IMT and the angiographic extent of coronary artery stenosis in patients with severe CAD. These findings indicate a potential of B-mode ultrasonography of the carotid arteries and transesophageal echocardiographic aortic examination in the diagnostic and prognostic evaluation of patients with suspected CAD.     

Imaging of atherosclerosis using magnetic resonance: State of the art and future directions

Atherosclerosis is the leading cause of morbidity and mortality in industrialized societies, and its incidence is projected to increase in the future. Because the atherosclerotic process begins in the vessel wall, the focus of cardiovascular imaging is shifting from the arterial lumen to imaging of the vessel wall, with the goal of detecting preclinical atherosclerosis. MRI, because of its high resolution, three-dimensional capabilities, noninvasive nature, and capacity for soft tissue characterization, is emerging as an important modality to assess the atherosclerotic plaque burden in the arterial wall and can monitor atherosclerosis in different arterial beds, including the carotid arteries, aorta, and more recently, the coronary arteries. Furthermore, it has also been successfully utilized to monitor plaque regression following therapeutic interventions. Finally, the emergence of high-resolution MRI and development of sophisticated contrast agents offers tremendous promise for in vivo molecular imaging of the atherosclerotic plaque.     

ACE insert/delete polymorphism and atherosclerosis

We report on the results of a large autopsy study focusing upon the hypothesis that deletion of the Alu insert in the angiotensin converting enzyme (ACE) gene is associated with: (a) greater prevalence or extent of atherosclerosis in the aorta and coronary arteries; and (b) microscopic qualities of established atherosclerotic plaques in the coronary arteries. This study was conducted in young US black (n=290) and white (n=379) males using available materials and data from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study, a multi-center cooperative autopsy study organized in 1985 to explore the relationships of known cardiovascular risk factors to atherosclerosis in victims of accidents, homicides, or suicides in the age range of 15-34 years. The results provide strong evidence that ACE genotype may not be a predictor of either the prevalence or the extent of the lesions of atherosclerosis in the right coronary artery or the aorta of young adults, an observation that confirms previous studies that estimated the prevalence and extent of atherosclerosis using coronary angiography. In addition, the results suggest that ACE genotype does not contribute to the formation of atherosclerotic lesions that have the characteristics of vulnerable plaques in the left anterior descending coronary artery of young adults.