动脉粥样硬化和高血压PPT课件

4.对血小板的作用 可引起血小板黏附、聚集，促进
血栓形成
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sLDL：LDL亚型中的小颗粒低密度脂蛋白：具 有经LDL受体清除缓慢、易粘附于血管壁及抗氧 化能力低等特点
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2. 甘油三脂增高
冠心病↑、 LDL↑、HDL 高血压、肥胖、糖尿病
3.脂蛋白（a）和载脂蛋白B100增高
ApoB100： LDL的主要组成部分 介导LDL的摄取
1.对内皮细胞的作用 使内皮细胞损伤，诱导内皮细 胞表达多种黏附分子，增强单核细胞和T淋巴细胞黏附 及向内皮下移行
2.对单核巨噬细胞的作用 促使单核细胞向巨噬细胞 转化，吞噬脂质形成泡沫细胞。
3.对平滑肌细胞的作用 使平滑肌细胞由收缩型向合 成型转变，并促使平滑肌细胞游走；诱发细胞增殖的 基因表达，促进平滑肌细胞增生
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稳定斑块（stable plaque） 不稳定斑块（unstable plaque）
指脂质核较大、病变偏心、纤维 帽较薄、炎症细胞浸润较重、在受到 外力作用时容易破裂的斑块，又称脆 性斑块（vulnerable plaque）。
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oxLDL可能参与动脉粥样硬化发生发展的全过程：
第七讲 动脉粥样硬化和高血压
Atherosclerosis and Hypertension
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心血管疾病
（cardiovascular disease, CVD ）
发病率和死亡率居所有疾病之首
发病率↑：90年代-200万/年以上 2000年-1700万，总死亡人数1/3 2020年-2500万 80%在发展中国家
The core is rich in extracellular lipids, which are formed by trapping blood-derived lipids, notably low-density lipoprotein, or by lipid-filled macrophages, known as foam cells. The plaque destabilizes due to inflammation by foam cells and other inflammatory mediators that make the plaque more vulnerable to rupture. This commonly occurs at the junction of the plaque and the less diseased vessel wall. As a result, the lipid core may be exposed to flowing blood leading to platelet-mediated thrombus formation.
LP（a）： 与LDL结构类似 与ApoB100相结合
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（四）糖尿病
“胰岛素抵抗”—“代谢综合症”
（糖尿病、动脉粥样硬化、高血压等）
（五）其他因素
年龄，性别，体重，遗传 同型半胱氨酸 等
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Based on the findings of Falk, we now know the primary cause of a heart attack is the rupture of unstable plaques that are <70% stenosed and are clinically silent. Approximately 200 patients from 4 studies were studied to generate these results, which have been confirmed in other studies.1
Falk reviewed the work of other investigators regarding the severity of stenosis and its association with the risk of MI. Results showed that >86% of MIs resulted from lesions that were <70% stenosed. Most experts prior to Falk thought that patients had ages that increased in size until they blocked the blood vessel and caused a heart attack.1
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动脉粥样硬化（atherosclerosis）
一种与血脂异常及血管壁成分改变有关 的动脉疾病，主要累及弹性动脉和较多弹性 纤维的肌性动脉，病变特征是血中脂质在动 脉内膜沉积，引起内膜灶性纤维性增厚，病 灶深部为由坏死组织和细胞外脂质池形成的 粥样物质（粥样斑块=纤维帽+脂质核）。
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Atherosclerotic plaque has 2 main components: a soft, lipidrich core and a hard, collagen-rich fibrous cap. In stable plaques, a thick fibrous cap may represent >70% of plaque volume. It stabilizes the plaque and prevents it from undergoing rupture. In contrast, unstable plaque has a thin fibrous cap and is at greater risk for rupture. In unstable plaque, the lipid-rich core may represent the majority of the plaque volume.