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...