调脂治疗与冠状动脉粥样硬化斑块消退

脂代谢紊乱、氧化应激和炎症反应在冠状动脉粥样硬化斑块的形成和发展中具有重要的作用。以往有关调脂治疗消退动脉粥样斑块已进行了大量动物实验研究和大规模随机、对照临床试验,结果证明,调脂治疗(尤其是强化他汀治疗)能显著降低血清低密度脂蛋白胆固醇(LDL-C)水平和增高高密度脂蛋白胆固醇(HDL-C)水平,有效阻止动脉粥样硬化进程,并有望稳定或消退粥样硬化斑块。但是,调脂治疗使何种类型斑块更易产生有效作用,以及新的影像技术在估价斑块消退中的价值,还需进一步研究。     

不稳定性冠状动脉粥样硬化斑块的研究进展

冠状动脉粥样硬化斑块的不稳定性是引发急性冠脉综合征 (包括不稳定型心绞痛、急性心肌梗死、心性猝死 )的主要原因 ,也是引起冠心病死亡的主要原因。大量研究表明 ,约 6 0 %～ 70 %的急性冠脉综合征是由于轻、中度狭窄的斑块破裂 ,继发血栓形成所致。冠状动脉血运重建虽可减轻冠脉狭窄程度 ,但与药物治疗相比 ,长期随访未明显减少急性冠脉事件发生率 ,主要原因是斑块的不稳定问题尚未解决。因此 ,认识不稳定斑块的内在特性、破裂机制、识别方法 ,探讨稳定斑块的方法具有重要的临床意义。　　动脉粥样硬化斑块的结构及其不稳定的内在特征1.…     

冠状动脉粥样硬化斑块的形成、发展和逆转

冠状动脉粥样硬化斑块形成是冠心病的病理基础,贯穿疾病发生与进展的整个过程。近年来国内外大量关于动脉粥样硬化的研究证实,降脂治疗不仅能稳定斑块,甚至能“逆转斑块”。本文对冠状动脉粥样硬化斑块逆转的机制、临床证据、治疗策略的最新研究进展进行概述。     

冠状动脉粥样硬化斑块组成成分与斑块破裂的关系

冠状动态粥样梗化斑块破裂是导致血栓形成引起急性缺血冠状动脉综合征的主要原因,斑块自身组成万分与斑块破裂的关系非常密切。本文概述了斑块组成成分在斑块破裂中所起的作用,并对易破斑块的识别和斑块破裂的预防作一简要叙述。     

冠状动脉粥样硬化斑块消退研究进展

冠状动脉粥样硬化的发生与低密度脂蛋白及炎症反应、内皮功能减退等有关。近年来多项临床试验证实早期强化应用他汀类药物可以通过降低低密度脂蛋白、抗炎、改善内皮功能等途径改善急性冠脉综合征患者的预后。其中他汀类药物发挥的抗炎症反应、改善内皮功能等多效性作用日益受到重视。而应用血管内超声的研究发现强化他汀类治疗能够显著遏制甚至消退冠状动脉粥样斑块。     

他汀降脂治疗冠状动脉粥样硬化斑块的影像学研究进展

脂质代谢紊乱是导致动脉粥样硬化的主要危险因素,低密度脂蛋白的作用尤为显著。他汀能使低密度脂蛋白降低,许多临床试验已证实他汀能显著减少心血管事件的发生。通过血管内超声评价他汀降脂治疗能够延缓冠状动脉斑块的进展甚至使其退缩的研究也越来越多,但应用冠状动脉计算机体层成像进行评价的研究尚少。在我国冠状动脉计算机体层成像的使用较血管内超声更广泛。目前就能使冠状动脉斑块明显退缩的低密度脂蛋白降低的水平或降低的程度仍无定论,还需要更多的研究来证实。     

稳定冠状动脉粥样硬化斑块新策略

冠状动脉粥样硬化斑块的生物学特性是决定其稳定的主要因素,不稳定斑块块破裂及继发血栓形成,冠脉血管闭塞,是引起包括不稳定型心绞痛,急性心肌梗死和冠脉性猝死在内的急性冠脉综合征的病理基础。与防治血栓和再血管化相比,稳定斑块具有更大的临床价值。降脂药物、抗氧化剂、β受体阻滞剂、血管紧张素转换酶抑制剂具有肯定的稳定斑块作用。促进斑块基质合成,阻止降解,抑制斑块内炎症,阻断基质金属蛋白酶的合成和活化以及应用     

冠状动脉粥样硬化斑块的稳定性研究进展

本文概述了冠状动脉粥样硬化斑块的形成、发展和破裂的机理,以及增加斑块的稳定性、防治斑块破裂的措施。     

冠状动脉粥样硬化斑块的磁共振成像研究进展

急性冠状动脉综合征系由粥样硬化易损斑块的破裂进而血栓形成所致，因此，在斑块破裂之前进行冠脉管壁及斑块成像，并预测斑块稳定性，对于降低急性冠脉综合征的发生率具有重要意义。与其它影像学检查技术相比，MR成像优势明显，具有很大潜力。本文就冠脉粥样硬化斑块MR成像原理，以及目前冠脉粥样硬化斑块成像序列、MR对比剂研究现状进行综述，并探讨其对斑块成分的判定以及斑块稳定性评价的应用前景。     

冠状动脉粥样硬化斑块破裂的细胞与分子生物学研究进展

近 10年来对冠状动脉粥样硬化斑块生物学和动脉粥样硬化斑块破裂触发的认识迅速加深 ,已明确几种使斑块失稳定的分子和细胞学机制。将来血管病理生理学的研究应以稳定易破裂动脉粥样硬化斑块以及减少动脉粥样硬化斑块破裂后血栓形成为方向。本文介绍了近年来动脉粥样硬化斑块破裂的细胞学及分子生物学研究进展。     

颈动脉粥样硬化斑块及内-中膜厚度与冠心病的关系

目的：探讨冠心病患者颈动脉粥样硬化斑块及内-中膜厚度与冠心病的关系。方法：对58例冠心病患者的颈动脉内一中膜厚度及斑块进行超声检测，与35例具有动脉粥样硬化危险因素的患者作对照。结果：冠心病患者的颈动脉内-中膜厚度、斑块指数及斑块检出率明显高于对照组(P均＜0．01)，颈动脉内-中膜厚度与年龄，血总胆固醇、收缩压水平，高血压病呈正相关(r＝0．267-0．532，P＜0.05-0．01)。结论：年龄、甘油三酯、收缩压、高血压病程及斑块指数与颈动脉内-中膜厚度密切相关。     

颈总动脉粥样硬化斑块形成对心脑血管预后的影响

目的:评价颈总动脉粥样硬化斑块形成对心脑血管预后的影响。方法:198例有冠状动脉(冠脉)粥样硬化性心脏病(冠心病)危险因素并行冠脉造影的患者,依据颈动脉超声检测将有无颈总动脉粥样硬化斑块分为动脉粥样硬化组(AS组)(120例)和对照组(78例),随访、比较2组心脑血管不良事件发生率,应用Cox回归分析与心脑血管预后相关的独立因素。结果:基线时,AS组平均年龄大(P<0.001)、慢性肾病患者多(P<0.05)、冠心病患者多(P<0.001)、血清肌酐(Scr)水平高(P<0.05)、颈总动脉内膜中膜厚度(IMT)平均值大(P<0.001)、颈总动脉内径(C-Di)较高(P<0.05)、服用他汀类药物患者较多(P     

Tendon xanthomas as indicators of atherosclerotic burden on coronary arteries

The presence of tendon xanthomas is an almost certain indicator of familial hypercholesterolemia (FH). They also reflect coronary atherosclerotic burden and therefore must be treated aggressively. Tendon xanthomas also occur in two rare conditions, cerebrotendinous xanthomatosis and sitosterolemia, which are not easily confused with FH, can be easily differentiated with clinical history and biochemical tests.     

斑块稳定性与炎症反应在急性冠状动脉综合征中作用的研究

目的 探讨冠状动脉（冠脉）粥样斑块稳定性和炎症反应在急性冠状动脉综合征（ACS）中的作用。方法 对28例ACS和13例稳定性心绞痛（SA）患者“罪犯”冠脉进行血管内超声（IVUS）检查,同时测定外周血清高敏C反应蛋白（hs-CRP）、基质金属蛋白酶-9（MMP-9）、组织型基质金属蛋白酶抑制剂-1（TIMP-1）、可溶性CD40L（sCD40L）含量。结果 ACS患者冠脉病变处以软斑块为主71．4％（20／28）,SA患者冠脉病变处以硬斑块为主76．9％（10／13）,差异有统计学意义（P=0．004）。与sA组比较,ACS组病变处斑块面积大（P=0．004）、斑块负荷重（P=0．048）、以正性重构为主（P=0．013）。ACS组血清hs—CRP、MMP-9、sCIMOL含量均高于SA组,TIMP-1含量在ACS组和SA组之间差异无统计学意义（P=0．234）,ACS组hs-CRP与MMP-9（r=0．671,P=0．000）、sCIMOL（r=0．494,P=0．008）呈正相关。结论 冠脉“罪犯”病变处结构性易损斑块是ACS发作基础,CIMOL和MMP-9参与的炎症反应导致斑块功能性不稳定和不同临床表现。     

冠状动脉斑块消退的调脂治疗策略

4项他汀类药物治疗冠心病患者,以血管内超声评价冠状动脉(冠脉)斑块变化的临床试验(RE-VERSAL、ASTEROID、COSMOS和SATURN)结果一致显示,他汀治疗显著降低LDL-C,同时升高Apo-A1和HDL-C,才能观察到冠脉粥样硬化斑块的消退。适度调脂指通过他汀类药物治疗,达到减少胆固醇流入斑块的目标值:降低LDL-C>45%(达到1.81～2.46mmol/L),同时达到增加胆固醇流出斑块的目标值:升高Apo-A1>9%(达到3.50～3.89mmol/L)和HDL-C>8%(达到1.17～1.42mmol/L),实现冠脉斑块的消退。     

动脉粥样硬化不稳定斑块的研究现状

随不稳定斑块发展而继发的血栓形成是导致急性冠状动脉综合征的重要原因。在内外因素的共同作用下,不稳定斑块可能发生破裂、糜烂以及钙化等现象。斑块中存在许多直接和间接的致血栓形成的物质,它们同血液一起促进了血栓的产生。人们已经建立多种自发或诱发的不稳定斑块的动物模型。针对各种不同的影响斑块稳定性的因素,人们正从不同角度寻找能有效的稳定斑块的治疗方法。     

Perinatal and infant early atherosclerotic coronary lesions

OBJECTIVE

Because the fetal origin of coronary artery lesions is controversial, early atherosclerotic coronary artery lesions in late fetal stillborns and infants, as well as the possible atherogenic role of maternal cigarette smoking, were studied.

METHODS

Twenty-two fetal death and 36 sudden infant death syndrome victims were examined by autopsy. In 28 of 58 cases, the mothers were smokers. Serially cut sections of coronary arteries were stained for light microscopy and immunotypified for CD68, CD34, alpha-smooth muscle actin, proliferating cell nuclear antigen, c-fos and apoptosis.

RESULTS

Multifocal coronary lesions were detected in 10 of 12 fetuses and in 15 of 16 infants whose mothers smoked. Arterial lesions in infants with nonsmoking mothers were observed in only five cases (two of 10 fetuses and three of 20 infants) (P<0.001). Alterations ranged from focal areas with mild myointimal thickening in prenatal life to early soft plaques in infants. Smooth muscle cells infiltrated into the subendothelium. These early lesions demonstrated c-fos gene activation in the smooth muscle cells of the media, and in some of these, positivity for apoptosis was observed, suggesting that c-fos overexpression may promote proliferation, as evidenced by proliferating cell nuclear antigen-positive cells.

CONCLUSIONS

Early intimal alterations of the coronary arteries are detectable in the prenatal and infancy period, and may be significantly associated with maternal smoking.     

Relationship of coronary artery plaque composition to coronary artery stenosis severity: results from the prospective multicenter ACCURACY trial

Objectives

The purpose of this study was to determine the relationship of coronary artery plaque composition as detected by coronary computed tomographic angiography (CCTA) to luminal diameter stenosis severity quantified by quantitative coronary angiography (QCA) in individuals without known coronary artery disease (CAD) presenting with stable chest pain syndrome.

Background

While CCTA has been previously evaluated for its ability to detect and exclude coronary artery stenosis, CCTA also permits assessment of other important plaque characteristics, including plaque composition. Identification of the relationship between plaque composition by CCTA and plaque severity by invasive angiography may provide valuable insight into the pathophysiology of coronary artery plaque.

Methods

Patients enrolled in the ACCURACY trial, a 16-site multicenter study of patients with stable chest pain syndrome but without known CAD undergoing both CCTA and invasive coronary angiography (ICA), comprised the study population. CCTAs were scored on a per-segment basis for plaque composition and graded as non-calcified (>70% non-calcified), calcified (>70% calcified) or “mixed” (30–70% non-calcified or calcified) by concordance of ≥2 of 3 readers. CCTAs were also scored on a per-patient basis, and individuals were categorized as possessing primarily non-calcified plaques, primarily calcified plaques or primarily mixed plaques. Quantitative coronary angiography (QCA) was performed in all patients, used as the reference standard for stenosis severity, and interpreted blinded to patient characteristics and CCTA results.

Results

230 subjects comprised the study population (59.1% male, 57 ± 10 years). QCA was performed in all subjects following CCTA (mean inter-test interval 5.9 ± 4.3 days), and demonstrated obstructive CAD in 24.8% and 13.9% at the 50% and 70% stenosis severity threshold, respectively. On a per-segment based analysis, obstruction by QCA at both the 50% and 70% stenoses thresholds was more often for mixed composition plaques by CCTA (69.1% and 67.9%, respectively), as compared to non-calcified plaques (24.7% and 28.6%, respectively) and calcified plaques (6.1% and 3.6%, respectively) [p < 0.01 for comparisons]. On a per-patient basis, patients with mixed plaque or mixtures of plaque types more often exhibited obstructive coronary stenosis by QCA at the 50% level (39/96; 40.6%) compared to those with primarily non-calcified (12/43; 27.9%) or primarily calcified (4/29; 13.8%) plaques [p = 0.02].

Conclusions

In this multicenter trial of chest pain patients without known CAD, QCA-confirmed obstructive coronary stenosis was associated with mixed plaque composition by CCTA at both the per-segment and the per-patient levels. Coronary artery segments exhibiting calcified plaque were rarely associated with obstructive coronary stenosis.     

钙结合蛋白S100A12与冠状动脉粥样斑块稳定性的相关性

目的 探讨冠心病患者血清钙结合蛋白S100A12的表达及其与冠心病的相关性,评价其作为预测斑块稳定性的外周血生物学指标的临床意义.方法 选择依据临床症状及冠脉造影结果冠心病诊断明确的患者91例,其中稳定型心绞痛（SAP组）18例、不稳定型心绞痛（UAP组） 37例、急性心肌梗死（AMI组）（包括ST段抬高型心梗和非ST段抬高型心梗） 36例.对照组为冠脉造影正常或微小病变＜50%排除冠心病的患者34例.观察血清S100A12水平在各组间的变化.通过介入手术模拟斑块破裂,比较术前、术后S100A12水平变化,评价其预测斑块稳定性的临床意义.结果 ①冠心病患者（SAP组、UAP组、AMI组）血清S100A12水平显著高于对照组（P＜0.05）;与SAP组比较,UA组及AMI组血清S100A12水平显著升高,且差异有统计学意义（P＜0.05）;UAP组与AMI组比较血清S100A12水平差异无统计学意义（P＞0.05）.②根据是否行支架置入术分为单纯行选择性冠脉造影组（CAG组）与选择性冠脉造影＋内支架置入术组（PCI组）.在CAG组中,血清S100A12术后与术前即刻相比差异无统计学意义（P＝0.064）;在PCI组中,术后血清S100A12水平与术前即刻相比显著升高,差异有统计学意义（P＜0.01）.③入院至手术前住院期间药物对血清S100A12水平的影响：所有对象入院时与术前即刻血清S100A12水平相比差异无统计学意义（P＞0.05）.结论 钙结合蛋白S100A12可能参与动脉粥样硬化的形成,并且可能成为外周血中预测斑块稳定性的生物学指标.