Stary H C, Chandler A B, Dinsmore R E, Fuster V, Glagov S, Insull W, Rosenfeld M E, Schwartz C J, Wagner W D, Wissler R W
Office of Scientific Affairs, American Heart Association, Dallas, TX 75231-4596, USA.
Arterioscler Thromb Vasc Biol. 1995 Sep;15(9):1512-31. doi: 10.1161/01.atv.15.9.1512.
This report is the continuation of two earlier reports that defined human arterial intima and precursors of advanced atherosclerotic lesions in humans. This report describes the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions. These, with the earlier definitions of precursor lesions, led to the histological classification of human atherosclerotic lesions found in the second part of this report. The Committee on Vascular Lesions also attempted to correlate the appearance of lesions noted in clinical imaging studies with histological lesion types and corresponding clinical syndromes. In the histological classification, lesions are designated by Roman numerals, which indicate the usual sequence of lesion progression. The initial (type 1) lesion contains enough atherogenic lipoprotein to elicit an increase in macrophages and formation of scattered macrophage foam cells. As in subsequent lesion types, the changes are more marked in locations of arteries with adaptive intimal thickening. (Adaptive thickenings, which are present at constant locations in everyone from birth, do not obstruct the lumen and represent adaptations to local mechanical forces). Type II lesions consist primarily of layers of macrophage foam cells and lipid-laden smooth muscle cells and include lesions grossly designated as fatty streaks. Type III is the intermediate stage between type II and type IV (atheroma, a lesion that is potentially symptom-producing). In addition to the lipid-laden cells of type II, type III lesions contain scattered collections of extracellular lipid droplets and particles that disrupt the coherence of some intimal smooth muscle cells. This extracellular lipid is the immediate precursor of the larger, confluent, and more disruptive core of extracellular lipid that characterizes type IV lesions. Beginning around the fourth decade of life, lesions that usually have a lipid core may also contain thick layers of fibrous connective tissue (type V lesion) and/or fissure, hematoma, and thrombus (type VI lesion). Some type V lesions are largely calcified (type Vb), and some consist mainly of fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).
本报告是之前两份报告的延续，那两份报告定义了人类动脉内膜以及人类晚期动脉粥样硬化病变的前驱病变。本报告描述了各种晚期动脉粥样硬化病变的特征性成分和致病机制。这些内容，连同之前对前驱病变的定义，促成了本报告第二部分中人类动脉粥样硬化病变的组织学分类。血管病变委员会还试图将临床影像学研究中观察到的病变表现与组织学病变类型及相应的临床综合征联系起来。在组织学分类中，病变用罗马数字表示，这些数字表明病变进展的通常顺序。初始（I 型）病变含有足够的致动脉粥样硬化脂蛋白，可引起巨噬细胞增多并形成散在的巨噬细胞泡沫细胞。与后续病变类型一样，这些变化在具有适应性内膜增厚的动脉部位更为明显。（适应性增厚从出生起就存在于每个人的固定位置，不会阻塞管腔，代表对局部机械力的适应）。II 型病变主要由巨噬细胞泡沫细胞层和富含脂质的平滑肌细胞组成，包括大体上称为脂纹的病变。III 型是 II 型和 IV 型（动脉粥样瘤，一种可能产生症状的病变）之间的中间阶段。除了 II 型富含脂质的细胞外，III 型病变还含有散在的细胞外脂质滴和颗粒聚集体，这些会破坏一些内膜平滑肌细胞的连贯性。这种细胞外脂质是 IV 型病变特征性的更大、融合且更具破坏性的细胞外脂质核心的直接前体。大约从生命的第四个十年开始，通常具有脂质核心的病变也可能含有厚层纤维结缔组织（V 型病变）和/或裂隙、血肿和血栓（VI 型病变）。一些 V 型病变大部分钙化（Vb 型），一些主要由纤维结缔组织组成，几乎没有或没有积累的脂质或钙（Vc 型）。
