100例冠心病的颈动脉彩色多普勒超声分析

目的 探讨冠状动脉粥样硬化心脏病变的颈动脉超声改变与其相关性，以及与血脂的关系。方法 对82例冠心病、18例心肌梗塞患和正常对照组20人的颈动脉作彩色多普勒超声检查以及血液中血脂测定。结果 91．5％冠心病人和100％心肌梗塞病人存在血管内膜-中层(IMT)增厚，斑块和管腔狭窄等变化。斑块以颈总动脉分叉处(BIF)多见、以硬斑为主。血脂检查示LDL-C增高和ApoAⅠ下降。结论 冠状动脉病变与颈动脉粥样硬化密切相关。测定血液中LDL-C和ApoAⅠ的含量，可作为提示颈动脉粥样硬化的危险因素。     

Comparison of laboratory parameters as risk factors for the presence and the extent of coronary or carotid atherosclerosis: the significance of apolipoprotein B to apolipoprotein all ratio.

We compared several "new" risk factors (autoantibodies to oxidatively modified low density lipoprotein (LDL), sialic acid content of LDL, bilirubin and C-reactive protein) with "conventional" risk factors (apolipoprotein (apo) AI, AII and B, lipoprotein(a), triglycerides, and total, LDL and high density lipoprotein (HDL) cholesterol) for the presence and the extent of coronary or carotid atherosclerosis. Forty male patients with angiographically proven coronary atherosclerosis and 31 male patients with ultrasound-proven extracranial carotid atherosclerosis were compared to 40 age matched (53+/-5 years) healthy males as control subjects, with negative parental history of atherosclerosis, no clinical signs of systemic or organ-related ischemic disease and normal extracranial carotid arteries. The apo B/apo All ratio most powerfully indicated the presence and the extent of coronary or carotid atherosclerosis. Elevated lipoprotein(a) contributed significant additional information in the assessment of the atherosclerotic risk. Increase in C-reactive protein indicated the presence (but not the extent) of coronary or carotid atherosclerosis with a similar power as lipoprotein(a). Decreased values of total bilirubin indicated the presence of atherosclerosis only in smokers. Autoantibodies to oxidatively modified LDL additionally described the atherosclerotic process, but were less important than apolipoproteins, lipoprotein(a), C-reactive protein or bilirubin. Sialic acid content of LDL added no information to the parameters discussed above. We demonstrated that in male patients apolipoproteins, especially the apo B/apo All ratio, were better indicators of the presence and the extent of coronary or carotid atherosclerosis than C-reactive protein, bilirubin, autoantibodies to oxidatively modified LDL or sialic acid content of LDL.     

Tissue factor in human coronary atherosclerotic plaques

The rupture or fissuring of a coronary atherosclerotic plaque and subsequent thrombosis is considered the key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque disruption frequently occurs during the evolution of atherosclerosis, only a minority of ruptured plaques develop thrombosis. The content and procoagulant activity of tissue factor in human coronary atherosclerotic plaques varies widely, and different studies confirm that it is higher in the plaques extracted from patients with unstable angina, myocardial infarction or histologic/angiographic evidence of coronary thrombosis than in those taken from patients with stable angina or uncomplicated coronary lesions. Variations in tissue factor content and activity may be responsible for the different thrombotic responses to human coronary atherosclerotic plaque rupture.     

颈部动脉粥样硬化与脑梗死的相关研究

目的评价颈部大动脉粥样硬化与脑梗死的相关性。方法对186例脑梗死患者进行颈部大动脉彩色多普勒检测,观察血管内膜情况,有无斑块形成,管腔是否狭窄及狭窄程度,与同期来院健康体检者40例对照。结果脑梗死患者颈动脉内膜中层厚度(IMT)、斑块的发生率及颈动脉狭窄程度较对照组明显增加,两组比较差异有显著性意义(P<0.05)。结论颈部大动脉粥样硬化形成与脑梗死发生密切相关。     

彩超对颈动脉粥样硬化与缺血性脑血管疾病的研究

目的 :研究颈动脉粥样硬化与缺血性脑血管疾病的关系。方法 :彩超检查 1 4 0例缺血性脑血管疾病患者的颈动脉 ,测量血管的直径、内 -中膜的厚度 (intima- media thickness,IMT) ,血流的速度等参数 ,观察斑块的有无及形成情况 ,并检查 1 0 0例健康志愿者作为对照组。结果 :1 4 0例缺血性脑血管疾病患者中 ,颈动脉有粥样硬化、血管重构、IMT增厚、斑块形成、管腔狭窄等血管异常者占 1 2 0例 ,检出率达 85.7% ;对照组中有 IMT增厚和软斑形成 1 7例 ,检出率为 1 7.0 % ,二者比较有显著差异 (P<0 .0 1 )。结论 :缺血性脑血管疾病和颈动脉粥样硬化存在着线性关系 ;高分辨率彩超诊断技术 ,对颈动脉粥样硬化检出预报和疗效的观察、评价有重要意义     

Prevention of atherosclerosis. Excess of palmitic acid in food--a cause of hypercholesterolemia, inflammatory syndrome, insulin resistance in myocytes, and apoptosis

Unity of the pathogenesis of atherosclerosis, type 2 diabetes mellitus, and metabolic syndrome gives rise to impaired biological function of adaptation, altered biological function of exotrophy (external feeding) and endoecology ("purity" of the intercellular medium). Biological reactions of inflammation and hydrodynamic pressure, or blood pressure, are in vivo activated to compensate for intercellular debris accumulation by endogenous phlogogens--ligand-free low density lipoproteins (LDL). The biological reactions jointly remove LDL from blood to the intima of elastic type arteries, to interstitial tissue for the local pool of the intravascular medium. The causes of formation of aphysiological LDLs are a preponderance of palmitate-oleate-palmitate triglycerides in the latter and impaired hydrolysis upon exposure to post-heparin lipase to give rise to small, dense LDLs; intimal macrophages utilize the debris only partially and develop atheromatosis from polyenic fatty acids (FA) etherified by cholesterol alcohol. Excess of palmitic saturated fatty acid (sFA) is responsible for the lowered permeability of the plasma membrane, cell death via the mechanism similar to apoptosis. Aphysiological protein palmitoylation (covalent interaction with palmitic sFA) increased the debris accumulation of the intercellular medium and the activity of both biological reactions. Elevated plasma palmitic sFA and its enhanced passive absorption in the form of unetherified FA, as well as high C-reactive protein levels are a cause of insulin resistance. The only way to prevent atherosclerosis in the population is to normalize the biological function of exotrophy when the energy value ratio of FA, proteins and carbohydrates is 1:1:1 and that of sFA, monoenic, and polyenic FA is also 1:1:1. The lower amount of palmitic sFA and the higher concentration of essential polyenic FA, the lower blood levels of cholesterol alcohol and triglycerides are. At the same time, simultaneously activations and the biological function of locomotion are a level of physical activity.     

Plasma delipidation process induces rapid regression of atherosclerosis and mobilisation of adipose tissue

Cholesterol is a major component of atherosclerotic plaques. Cholesterol accumulation within the arterial intima and atherosclerotic plaques is determined by the difference of cellular cholesterol synthesis and/or influx from apo B-containing lipoproteins and cholesterol efflux. In humans, apo A-1 Milano infusion has led to rapid regression of atherosclerosis in coronary arteries. We hypothesised that a multifunctional plasma delipidation process (PDP) would lead to rapid regression of experimental atherosclerosis and probably impact on adipose tissue lipids. In hyperlipidemic animals, the plasma concentrations of cholesterol, triglyceride and phospholipid were, respectively, 6-, 157-, and 18-fold higher than control animals, which consequently resulted in atherosclerosis. PDP consisted of delipidation of plasma with a mixture of butanol-diisopropyl ether (DIPE). PDP removed considerably more lipid from the hyperlipidemic animals than in normolipidemic animals. PDP treatment of hyperlipidemic animals markedly reduced intensity of lipid staining materials in the arterial wall and led to dramatic reduction of lipid in the adipose tissue. Five PDP treatments increased apolipoprotein A1 concentrations in all animals. Biochemical and hematological parameters were unaffected during PDP treatment. These results show that five PDP treatments led to marked reduction in avian atherosclerosis and removal of lipid from adipose tissue. PDP is a highly effective method for rapid regression of atherosclerosis.     

超声对冠状动脉粥样硬化与颈动脉粥样硬化的相关性研究

目的 探讨冠心病患者颈动脉粥样硬化与冠状动脉粥样硬化的相关性。方法 对冠状动脉造影确诊为冠心病的89例患者和正常对照组的80例患者行颈动脉超声检查,对比观察颈动脉内-中膜厚度（IMT）、颈动脉有无斑块及斑块类型;对冠心病组不同支病变间IMT、颈动脉斑块积分及斑块发生率进行比较分析。结果 ①冠心病组患者的颈动脉粥样硬化斑块发生率为87．64％,显著高于对照组（33．75％,P〈0．01）。②两组颈动脉斑块以软斑最多见,冠心病组软斑占37．12％,扁平斑占16．59％,混合斑占25．76％,硬斑块占20．53％;对照组软斑占34．09％,扁平斑占22．73％,混合斑占25．00％,硬斑占18．18％。③不同支数冠状动脉病变者之间IMT、颈动脉斑块积分和斑块发生率比较,差异有统计学意义。结论 通过超声了解颈动脉病变可间接反映冠状动脉粥样硬化病变的程度。     

Evaluation of carotid artery lesion by echography

The recent advance of the carotid artery echotomography indicates the intima media thickness(IMT) of the carotid artery as one of surrogate endpoints of atherosclerosis in subjects with multiple risk factors, such as hypertension, hyperlipidemia, and diabetes mellitus. IMT is shown to be increased in subjects with hyperlipidemia, type 1 and 2 diabetes mellitus, and other several diseases. Also, increase in IMT is related with the prevalence of cerebral infarction and coronary artery diseases. The carotid artery plaques including soft or calcified plaques were shown to predict appearance of strokes. Several drugs, such as anti-diabetogenic drugs(insulin-sensitizer, biguanides, and alfa-glucosidase inhibitor), hypotensive drugs(ACEI, Ca-blocker), and anti-platelet drugs were shown to attenuate the progression of IMT. Recently, we have shown that an anti-platelet drug arrested the progression of IMT and significantly reduced appearance of asymptomatic cerebral infarction in subjects with type 2 diabetes. These data clearly indicate the usefulness of the carotid artery echography in subjects with atherosclerosis and IMT could evaluate the effects of treatment for atherosclerosis.     

颈动脉斑块与缺血性脑血管病及其危险因素的关系

目的探讨缺血性脑血管病患者颈动脉粥样硬化斑块特点及其与缺血性脑血管病之间的关系,寻找颈动脉斑块危险因素。方法对115例颈内动脉粥样硬化缺血性脑血管病患者进行颈动脉超声检查,并检查血清甘油三酯、总胆固醇、高密度脂蛋白、低密度脂蛋白,分析引起颈动脉粥样硬化的危险因素。结果超声检查颈动脉粥样硬化斑块检出率为81.7%(94例),颈动脉中重度狭窄发生率为7.8%(9例)。缺血侧颈动脉斑块发生率(67.7%),其中软斑发生率(33.1%),均高于非缺血侧(48.5%,其中软斑20.4%,P<0.05)。斑块组发生高血压病的比例(85.1%)明显高于无斑块组(57.1%,P<0.05);且在软斑组长期烟酒史及男性比例高于稳定性斑块组(P<0.05)。结论缺血性脑血管病患者颈动脉粥样硬化以斑块居多,软斑为重要危险因素,高血压病在斑块发生发展中起重要作用。多因素分析表明,年龄、甘油三酯、总胆固醇和低密度脂蛋白影响颈动脉斑块的形成,而性别、烟酒史可能会影响斑块的稳定性。     

彩色多普勒超声对高血压合并脑梗死颈动脉的临床分析

目的　探讨颈动脉粥样硬化与高血压合并脑梗死的关系。方法　使用百胜 AU4彩色多普勒超声仪 ,对 78例高血压患者 (排除合并脑梗死 )及 82例高血压合并脑梗死患者 ,观察其颈动脉内 -中膜厚度 (IMT)及斑块形成情况。结果　高血压合并脑梗死患者组的颈动脉 IMT、斑块积分、发生率及溃疡斑的检出率显著大于高血压患者 (排除合并脑梗死 ) (P<0 .0 1)。溃疡斑是高血压合并脑梗死患者组的主要栓子来源。结论　彩色多普勒超声可清晰显示颈动脉 IMT情况 ,在高血压合并脑梗死的预防及防治监测上有重要临床意义。     

Correlation of lipemia level after fat loading with manifestation of atherosclerosis in coronary arteries

AIM: To examine relationships between lipemia, atherogenicity of blood lipoproteins spectrum after fat loading (FL) and severity of angiographic manifestations of coronary atherosclerosis. MATERIAL AND METHODS: The study enrolled 72 males free of ischemic heart disease (IHD)--group 1; 60 IHD patients with moderate affection of the coronary arteries (CA), i.e. maximal narrowing of one CA 50%--group 2; 107 IHD patients with severe CA affection, i.e. CA narrowing > 50%--group 3. FL was given by J. R. Patsch technique, blood sampling was made before meal, 3 and 6 hours after FL. RESULTS: It was shown that intake of food fats in IHD and IHD-free patients stimulated development of postprandial lipemia of different severity and duration. It appeared due to increased fraction of lipoproteins rich in triglycerides. In group 2 and 3 there was a definite and up to 6 hours in duration postprandial hypertriglyceridemia associated with proatherogenic deviations in lipid and protein components (LDL and HDL) by FL hour 6: growing of LDL cholesterol, apoB, apoB/apoAI and lowering of HDL cholesterol and apoAI. Patients with severe CA atherosclerosis (> 50% narrowing of three CA) had the most severe atherogenic affections in the postprandial lipoprotein spectrum. CONCLUSION: Postprandial lipemia/hypertriglyceridemia and atherogenic changes in the spectrum of lipoproteins after FL correlate directly with angiographic manifestations of coronary atherosclerosis.     

Oxidized low‐density lipoprotein in inflammation‐driven thrombosis

Summary

Thrombosis is the defining feature of the most prevalent causes of cardiovascular mortality, such as myocardial infarction, stroke, and pulmonary artery embolism. Although platelet activation and activation of the plasmatic coagulation system are the hallmarks of thrombus formation, inflammatory processes and the cellular responses involved are increasingly being recognized as critical modulators of thrombosis. In the context of many chronic inflammatory diseases that are associated with a high thrombotic risk, oxidized lipoproteins represent a prominent sterile trigger of inflammation. Oxidized low‐density lipoprotein and its components play a central role in the initiation and progression of atherosclerotic plaques, but also in other processes that lead to thrombotic events. Moreover, dying cells and microvesicles can be decorated with some of the same oxidized lipid components that are found on oxidized lipoproteins, and thereby similar mechanisms of thromboinflammation may also be active in venous thrombosis. In this review, we summarize the current knowledge on how oxidized lipoproteins and components thereof affect the cells and pathways involved in thrombosis.

     

血清脂蛋白相关磷脂酶A2及C反应蛋白与颈动脉粥样硬化斑块易损性的关系

目的探讨脂蛋白相关磷脂酶A2（Lipoprotein—associated phospholipase A2,Lp—PLA2）、C反应蛋白（C—reactive protein,CRP）与急性前循环脑梗死患者颈动脉粥样硬化斑块易损性的关系。方法100例急性前循环脑梗死患者（脑梗死组）和40例体检健康者（对照组）,检测2组血清Lp—PLA2、CRP水平;应用彩色多普勒超声评估脑梗死患者颈动脉粥样硬化程度,并对进行神经功能缺损评分。结果脑梗死组血清Lp—PLA2、CRP水平高于对照组（P〈0．01）;随着脑梗死患者颈动脉粥样硬化程度及病情程度加重,易损斑块组、稳定斑块组、内膜增厚组、内膜正常组,以及重度组、中度组、轻度组血清Lp—PLA2、CRP水平依次降低,组间差异均有统计学意义（P〈0．05）。结论急性脑梗死患者血清Lp—PLA2、CRP水平可反映颈动脉粥样硬化斑块性质和稳定性,可作为脑梗死病情严重程度的敏感指标。     

多层螺旋CT评价颈动脉粥样硬化与脑梗死的关系

目的探讨多层螺旋CT评价颈动脉粥样硬化与脑梗死的关系。方法MSCT检测48例脑梗死患者的颈动脉,测量粥样斑块的厚度;并检查37例无脑梗死患者作为对照组。结果在脑梗死组,共有26例发现有斑块形成,检出率为54.2%;对照组共有5例发现有斑块形成,检出率为13.5%,两者有显著差异﹝P<0.01﹞。颈动脉粥样斑块最常见于颈动脉分叉处,其次为颈内动脉起始段。结论颈动脉粥样硬化程度与脑梗死发生率呈正比。MSCT在检出颈动脉粥样硬化斑块和临床疗效观察方面是一种有用的技术手段。     

脑梗死患者颈动脉粥样硬化的特点及其对血流动力学的影响

目的 探讨脑梗死患者颈动脉粥样硬化的特点及其对血流动力学的影响.方法 根据颈动脉超声检查将研究对象分为有颈动脉粥样硬化组和无颈动脉粥样硬化组,观察粥样斑块的部位、性质,比较两组管腔内径、SPV、EDV以及RI.结果 BIF、CCA、ICA斑块的发生率依次是60.4%、29.2%和10.4%;软斑、硬斑及扁平斑、溃疡斑的发生率依次是58.3%、34.4%和7.3%.两组CCA和ICA内径及SPV无显著性差异:在CCA有斑块组EDV显著低于无斑块组,而RI显著高于无斑块组;在ICA两组EDV及RI无显著性差异.结论 脑梗死患者颈动脉粥祥硬化斑块的好发部位依次是BIF,CCA,ICA;斑块性质依次为软斑,硬斑及扁平斑,溃疡斑.颈动脉粥样硬化可以导致颈动脉的血流动力学改变.     

冠状动脉不稳定斑块血管内超声特征的临床研究

目的　探讨冠状动脉不稳定斑块的血管内超声 (IVUS)的特点。方法　在 31例急性冠脉综合征 (ACS,其中不稳定心绞痛 19例 ,急性心肌梗死 12例 )和 12例稳定性心绞痛患者中进行冠状动脉造影及 IVUS检查。应用 IVUS分别观察比较冠状动脉内斑块的性质 ,同时测量冠脉病变部位及其参考部位的血管外弹力膜面积 (EEMA)、管腔面积 (L A)、斑块面积 (PA)及管腔面积狭窄率 ,并计算斑块的偏心指数 (EI)及血管的重构指数(RI)。结果　在 4 3例患者中发现 ,不稳定心绞痛与急性心肌梗死中脂质斑块分别占 73.7% (14 / 19)及 75 .0 % (9/ 12 ) ,而稳定性心绞痛主要为纤维性斑块及混合性斑块 ,脂质斑块仅占 8.3% (1/ 12 )。同时发现 9例急性冠脉综合征患者发生斑块破裂及血栓形成。与稳定性心绞痛的斑块相比较 ,不稳定心绞痛的斑块具有较大的偏心性 (P<0 .0 5 ) ,EEMA、 PA及管腔面积狭窄率明显大于前者 ,具有显著的统计学意义 (P均 <0 .0 0 1) ,不稳定斑块呈现明显的正性重构 ,占 74 .2 % (2 3/ 31) ,而稳定斑块主要表现为负性重构 ,占 75 .0 % (9/ 12 )。结论　 IVUS能够准确地识别 AS不稳定斑块 ,本研究为早期发现不稳定斑块并预测斑块破裂奠定了基础。     

Macrophage: pathogenesis in the progression of atherosclerosis

Atherosclerotic changes in aorta or coronary arteries involve the accumulation and activation of macrophages, which this type of cell is present not only in plaques of intima but in the outer-media and adventitia. Macrophages play important roles in the progression of atherosclerosis by exhibiting unique characteristics under the various stimuli, evolving the plaque instability, thrombus formation and remodeling. Recent studies have shown the molecules-associated with metabolism, such as sirtuin-1 and peroxisome proliferator -activated receptor gamma in macrophages, appear to be involved to modulate the atherosclerotic process. In addition, macrophages work coordinately with other immune cells like mast cells. Thus, modulation of activation and function in macrophages might be a potential therapeutic target in attenuating the atherosclerosis-based cardiovascular diseases.     

Risk factors for coronary artery disease: a study comparing hypercholesterolaemia and hypertriglyceridaemia in angiographically characterized patients

Fifty-two male patients undergoing coronary angiography were allocated to four groups each consisting of 13 subjects: group I had normal coronary arteries and patients in groups II-IV exhibited coronary artery disease. In group II, plasma cholesterol was below 250 mg dl-1 and triglycerides below 160 mg dl-1; in group III, cholesterol was above 270 mg dl-1 and triglycerides under 160 mg dl-1; and in group IV, cholesterol was under 270 mg dl-1 and triglycerides above 180 mg dl-1. The hypertriglyceridaemic group IV had the highest coronary score. In addition, it had lowest lipoprotein lipase activity, lowest HDL-cholesterol and lowest high-density lipoproteins-2 (HDL-2) levels, suggesting that this type of hypertriglyceridaemia is caused--at least in part--by lipoprotein lipase deficiency with impaired removal of the triglyceride-rich lipoproteins and increased catabolism of HDL-2. Our findings point towards a type of hypertriglyceridaemia strongly associated with coronary artery disease which should therefore be treated accordingly.