动脉粥样斑块发展的过程

     美国心脏病学学会根据其病变发展过程将其细分为6型：

    Ⅰ型脂质点。动脉内膜出现小黄点，为小范围的巨噬细胞含脂滴形成泡沫细胞积聚。

    Ⅱ型脂质条纹。动脉内膜见黄色条纹，为巨噬细胞成层并含脂滴，内膜有平滑肌细胞也含脂滴，有T淋巴细胞浸润。

    Ⅲ型斑块前期。细胞外出现较多脂滴，在内膜和中膜平滑肌层之间形成脂核，但尚未形成脂质池。

    Ⅳ型粥样斑块。脂质积聚多，形成脂质池，内膜结构破坏，动脉壁变形。

    Ⅴ型纤维粥样斑块。为动脉粥样硬化最具特征性的病变，呈白色斑块突入动脉腔内引起管腔狭窄。斑块表面内膜被破坏而由增生的纤维膜（纤维帽）覆盖于脂质池之上。病变并可向中膜扩展，破坏管壁，并同时可有纤维结缔组织增生，变性坏死等继发病变。

    Ⅵ型复合病变。为严重病变。由纤维斑块发生出血、坏死、溃疡、钙化和附壁血栓所形成。粥样斑块可因内膜表面破溃而形成所谓粥样溃疡。破溃后粥样物质进入血流成为栓子。

Progression of atherosclerosis 

Macrophages augment the expression of scavenger receptors in response to inflammatory mediators, transforming them into lipid-laden foam cells following the endocytosis of modified lipoprotein particles. Macrophage-derived foam cells drive lesion progression by secreting proinflammatory cytokines. T lymphocytes join macrophages in the intima and direct adaptive immune responses. These leukocytes, as well as endothelial cells, secrete additional cytokines and growth factors that promote the migration and proliferation of SMCs. In response to inflammatory stimulation, vascular SMCs express specialized enzymes that can degrade elastin and collagen, allowing their penetration into the expanding lesion.