Atherosclerotic lesions from the reduction of pulmonary emboli.
Seventy-five intimal arterial thickenings (from 58 subjects) related to pulmonary emboli were examined. Many showed residua derived from the emboli (fibrin, platelets, haemosiderin) and proliferation of elastica and smooth muscle cells. Features resembling those of atherosclerosis were the frequent presence of extracellular lipid and apolipoprotein-B containing lipoproteins (LpB) which corresponded closely in distribution; and (in about 40% of the thickenings) collections of fat-filled (foam) cells. Platelet antigens were often detected within foam cells in some cases, in company with LpB. The results indicate that at least some intimal thickenings originating from pulmonary emboli undergo transformation to atherosclerotic plaques. The role of pulmonary hypertension in the process was investigated. Mechanisms relevant to this transformation and to theories of atherogenesis are discussed.
D000293:Adolescent; D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000378:metabolism; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D001792:Blood Platelets / Q000502:physiology; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D005487:Foam Cells / Q000473:pathology; D006801:Humans; D006976:Hypertension, Pulmonary / Q000150:complications; D050356:Lipid Metabolism; D008171:Lung Diseases / Q000150:complications; D008297:Male; D008875:Middle Aged; D011655:Pulmonary Embolism / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors
D001055:Apolipoproteins B; D005337:Fibrin; D005340:Fibrinogen