Reflections on the Pathologic Physiology of Atherosclerosis

Abstract

HALF a century ago, when Ignatowski¹ produced experimental atheromatous lesions by feeding cholesterol products to rabbits, the etiology of human atherosclerosis promised to be simple and clear cut: man ingests an excess of lipid in his diet, the excess causes elevated levels in the blood stream, and the excess is precipitated in the arterial wall.As is often the case in medicine, this simple hypothesis was soon obscured by a mass of conflicting experimental data. There were difficulties (since overcome) in reproducing experimental results in other species. There were difficulties in correlating dietary intake with serum lipid levels, and a . . .