ABSTRACT
Animals are extensively used as in vivo models of human atherosclerosis since it was first demonstrated by Anitschkow more than eight decades ago that atheroma lesions can be induced in rabbits by a cholesterol-rich diet.1 At present, many species besides rabbits are used in atherosclerosis research, such as rodents, dogs, and monkeys. Data from the non-primate cynomolgus monkey model are sometimes extrapolated to the human situation (because the monkey has a 28-day menstrual cycle, undergoes menopause, has changes in plasma lipoprotein concentrations at menopause, and has responses to estrogen/progestogen replacement therapy (HRT) similar to those observed in postmenopausal women, etc.) but in fact in terms of hard endpoints there are no data to indicate that these changes reflect what takes place in humans. Accumulating evidence suggests, however, that the monkey and the rabbit produce very similar and consistent results, at least regarding the effect of HRT on atherosclerosis. The rabbit model, however, has certain drawbacks, particularly with respect to the lipid and lipoprotein profile during cholesterol feeding and HRT, which differ from the human situation. Another drawback is the degree of heterogeneity in plaque size (or accumulation of cholesterol) among rabbits as a result of a fat-rich diet, increasing the number of animals needed in a study to obtain statistical differences between treatment groups.
