Tracy R E, Kissling G E, Malcom G T, Devaney K
LSUMC, Department of Pathology, New Orleans 70112-1393.
Virchows Arch A Pathol Anat Histopathol. 1987;411(5):425-34. doi: 10.1007/BF00735223.
Atherosclerosis of the human aorta has been studied by morphometric, chemical, and histochemical methods. Results of these separate approaches are converging upon a theory of pathogenesis. This theory begins with the standard view of a two stage process, intimal fibroplasia followed by atheronecrosis in the most thickened and aged places. The first stage, fibroplasia, can be described in terms of a stochastic process wherein smooth muscle cells, scattered in accordance with a Poison distribution, elaborate matrix materials over time, causing the realms of the cells to expand and to aggregate. The fusion of the expanded smooth muscle cell realms seems to mark the advent of necrosis. The second stage, atheronecrosis, can be described such that the probability of a necrotic core emerging at a site in a vessel is governed by the amount and the age of interstitial matrix materials at the site. Further evidence shows that the matrix materials tend to sequester lipids in greater than proportionate amounts as the intimal bulk increases. The sequestered perifibrous lipid is histochemically different from the lipids of the necrotic core, in that only the latter can be fixed with chromic acid. These results suggest that lipids undergo a qualitative change as well as a quantitative increase at the stage of impending necrosis. This qualitative change is governed by age, which raises the possibility that necrotizing toxicity accumulates in the sequestered lipid as it ages.
