Atherosclerosis (an accumulation of fatty, connective, and necrotic tissue) of the coronary arteries is the principal pathological process which causes
CHD. Cynomolgus monkeys (Macaca fascicularis) are currently the only animal model of sex differences in susceptibility to diet-induced atherogenesis. Among Caucasians in Western society, men have about twice the incidence of CHD and twice as extensive coronary artery atherosclerosis as women (2-4). The male to female ratio of coronary artery atherosclerosis extent in cynomolgus monkeys is also about 2:1. Like women, female cynomolgus monkeys are protected against atherosclerosis relative to their male counterparts (5).
Female cynomolgus monkeys have menstrual cycles that are similar to those of women in terms of length and cyclic hormone fluctuations (6,7). Following bilateral ovariectomy, extensive coronary artery atherosclerosis develops in females in amounts that are indistinguishable from those of males (8). CHD risk is also increased in oophorec-tomized and postmenopausal women (9). Subcutaneous replacement of estradiol, or estradiol and progesterone in physiological doses protects against atherosclerosis in female monkeys (10), and hormone replacement therapy (HRT) is associated with decreased CHD risk in postmenopausal women (11). Thus, ovarian function, and in particular estradiol, is implicated in the phenomenon of female protection, both in women and in female cynomolgus macaques.
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