Abstract

About one-half of infants in the first 6 mo of life have small collections of macrophages and macrophages filled with lipid droplets (foam cells) in susceptible segments of the coronary arteries. In subsequent years, fewer children have foam cells but around puberty (12-15 y) foam cell accumulations mostly larger than those in infants occur in 69% of adolescents. Lesions that represent the previously missing link between foam cell accumulations and atheromas have now been identified in a subgroup of highly susceptible locations. Such "preatheroma" lesions contain small pools of lipid droplets and dead cell remnants (extracellular lipid) in addition to macrophage foam cells. Atheromas, which emerge in some adolescents and young adults in the same locations, have a lipid core in which increased extracellular lipid displaces structural smooth muscle cells and the normal extracellular matrix. As soon as lipid cores form, calcium granules appear in some smooth muscle cells and among the extracellular lipid of the core. The degree of calcification is variable and, in youth, generally small. In the age group of 16-19 y, 15% of persons have either preatheromas or atheromas in coronary arteries; foam cell accumulations only are present in an additional 53% of 16-19-y-olds. Because the lipid cores of atheromas may be an underlying cause of lesion rupture, hematomas, and thrombosis, and because their development begins soon after puberty, it would be prudent to attempt to lower the influx of excessive atherogenic lipoproteins into the arterial wall by that age.

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