DETAID EPIDEMOLOGCAL studies carried out in the last 10 years have shown conclusively that in populations where there is a high risk of ischic heart disease there is a severe degree of involvement of the systemic arterial bed by raised atherosclerotic lesions. Conversely, where there is a low incidence of occlusive coronary artery disease low levels of intimal involvement are reportedl However, severity of atherosclerosis varies greatly from person to person even withi the most homogeneous population subgrops.2 Furthermore, the extent of intimal involvement in one major arteryeg the aorta-does not, in individuals, predict the severity in another artery.' We have long been interested in the morphology of aortic atherosclerotic plaques insofar as it may reflect pathogenetic manism, with special reference to the role of mural m is n plaque grt In studies of this kind, the Coons fluorescent antibody technique3 has proved a useful adjunct to conventional histological and histch Ical methods, and several worers have used it for the d onstration of fibrin or fibrinogen in raised atherosclerotic lesions.'" The facttt these antigens could be pr t within the arterial intima in differing distribution patterns was recorded some years ago 4 and, at that time, it was suggested that these individual patterns might have some implications as to the various pathogenetic processes operating in a single lesion. Subsequently it was found that some correlation exd between the presence of fibrin within raised lesions in the form of coarse, loalzed bands of fluorescent material and the presence of immunologically identifiable platelet antigens in the same lesions. The inference drawn from these data was the presence of a banded pattern of
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