Children have both macrophages and macrophages that are filled
with lipid droplets (foam cells) at susceptible sites of arteries. Such changes
are minimal and may not develop further. However, in some adolescents, small
pools of dead foam cell remnants and lipid droplets (extracellular lipid) are
added to the foam-cell accumulations at the susceptible sites. The pools are the
precursor of a much larger confluent accumulation of extracellular lipids (the
lipid core)-the hallmark of the atheromas of young adults.
As soon as a lesion with a lipid
core is present, calcium granules of microscopic size are found
among the packed extracellular particles and droplets and in smooth-muscle
cells isolated among them. Disintegration of arterial structure at the core
facilitates tears at the surface, hematoma, and thrombosis. As a response,
layers of reparative fibromuscular tissue are added and may predominate in a
lesion. Over time, calcium lumps and plates form through accretion of adjacent
extracellular calcium granules.
In adults past the fourth decade
of life, the greater part of
the former lipid core of a lesion may be calcified and there may be
osseous metaplasia (development of bony structure in soft structure). The
effect of therapeutic reduction of high levels of blood cholesterol on lesions
was studied in rhesus monkeys.
Drastic reduction of blood
cholesterol levels for 3.12 years
resulted in the disappearance of macrophages, macrophage foam cells and
lymphocytes, and reduction of extracellular lipid from advanced lesions.
