Misinterpretation of Coronary Cholesterol Atheromata in Cholesterol-Fed Rabbits as Suitable Model for Conventional Human Coronary Plaques

Abstract

Occlusion of coronary arteries following arteriosclerotic plaque formation with thrombotic complications is the main etiological factor in the development of myocardial ischemia with subsequent infarction and cell necrosis. Originally, in the 16th century, arteriosclerosis was considered to be an “ossification” of arteries¹. Hodgson² was the first to report in 1815 chemical analyses of arterial plaques, which contained 65% calcium (Ca) salts and 35% organic matter. However, current concepts of the development of arteriosclerosis are overshadowed by the assumption, that the main etiological factor is an enormous accumulation of lipids, particularly cholesterol, in the arterial walls brought about by an increase in serum cholesterol³. Consequently, arterial cholesterol atheromata of cholesterol-fed rabbits are widely considered to be suitable experimental models for conventional human arteriosclerosis⁴. Moreover, standard anti-arteriosclerotic therapy particularly aims at the so-called “normalization” of serum lipids. Our present data, obtained from microchemical analyses of coronary artery plaques of cholesterol-fed rabbits, and humans respectively, enhance the doubts about an exclusive cholesterol hypothesis of conventional atherogenesis.