Abstract

Smoking is considered a major risk factor for the development and progression of atherosclerosis. The effects of apolipoprotein E (apo E) and macrophages in the pathogenesis and progression of human atherosclerosis have not been adequately elucidated even though they are frequent components of the diseased arterial intima. Anatomically standardized samples of arteries from young people whose risk factor indices indicated them as “smokers” or “non-smokers” have been studied micromorphometrically. It was found that smokers have a greater area in which apo E is deposited in the early stages of the disease than do non-smokers. Smokers also demonstrated greater “macrophage foam cell populations” than did non-smokers. The study also demonstrates a positive correlation between the number of macrophage foam cells and the extent of apo E deposition in the developing lesions of the thoracic and abdominal aortas of white men aged 30–34 years who have evidence of recent cigarette smoking as determined by their postmortem blood thiocyanate levels.

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