It is suggested that the stenosing effects of atherosclerosis may be
offset by regression of the lesion, senescent dilatation of the arterial
wall and by enlargement of anastomotic channels. Regression is slow and
such inertia is attributed to: absence of cholesterol catabolic enzymes;
disproportion of the ratio of LDLlHDL; physical inaccessibility of
crystalline cholesterol; and relative absence of reticuloendothelial
phagocytes. Moderate dilatation of the human coronary arterial wall with
advancing age seems to compen- sate for the inward encroachment of
atherosclerosis on the lumen, hence the status quo ante may be
preserved. Severe atrophy with gross dilatation (ectasia) leads to
haemodynamic difficulties with slow circulation as a result of marked
fall in perfusion pressure. Such overdilated ectatic coronary arteries
are particularly liable to undergo thrombosis. References Adams, C. W.
M., and Bayliss, O. B. (1976a): Detection of macrophages in
atherosclerotic lesions with cytoduome oxidase. Brit. J. Exp. Pathol.
57, 30 to 36. Adams, C. W. M., and Bayliss, O. B. (1976b): Succinic
dehydrogenase and cytochrome oxidase in arterial, venous and other
smooth muscle. Atherosclerosis 23, 367 to 370. Adams, C. W. M., Knox,
J., and Morgan, R. S. (1975a): The resorption rate of atheroma lipids in
situ and implanted subcutaneously. Atherosclerosis 22, 79 to 90. Adams,
C. W. M., Morgan, R. S., and Bayliss, o. B. (1973): No regression of
atheroma over one year in rabbits previously fed a cholesterol or
enriched diet. Atherosclerosis 18, 429 to 444.