An experimental model of atherosclerosis sheep veins identical to the human disease indicates (i) that ingestion of an atherogenic diet is not a prerequistie in atherosclerosis and (ii) that haemodynamic stress must be the dominant aetiological factor in atherosclerosis. Ultrastructural studies reveal that the early lipid deposition in spontaneous human atherosclerosis and in haemodynamically induced atherosclerosis is related to the trasnformation of extracellular vesicular debris into closely packed membranous profiles with electron-translucent centres. It is postulated that the vesicular dtsintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular disintegration of mural cells is due to the same haemodynamic stresses which induce degenerative changes in the vascular connective tissues, and that the lipid accumulation within the vesicular debris is a cellular debris which have not undergone resolution or phagocytosis.
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