A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.
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 lesions progression. The initial (type I) 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).
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Office of Scientific Affairs, American Heart Association, Dallas, TX 75231-4596, USA.
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Dinsmore
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Fuster
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Glagov
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Insull
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D000783:Aneurysm / Q000473:pathology; D001161:Arteriosclerosis / Q000145:classification / Q000473:pathology*; D001808:Blood Vessels / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D003324:Coronary Artery Disease / Q000145:classification / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D004549:Elastin / Q000378:metabolism; D005109:Extracellular Matrix / Q000737:chemistry; D005340:Fibrinogen / Q000378:metabolism; D005487:Foam Cells / Q000473:pathology; D006801:Humans; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000378:metabolism; D008214:Lymphocytes / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D011509:Proteoglycans / Q000378:metabolism; D013927:Thrombosis / Q000473:pathology; D017539:Tunica Intima / Q000473:pathology
D008074:Lipoproteins; D011509:Proteoglycans; D005340:Fibrinogen; D003094:Collagen; D004549:Elastin; D002118:Calcium