SERMs are nonsteroidal estrogenic compounds with both estrogenic agonist (on bone and lipoproteins) and estrogenic-antagonist (on breast and endometrium) effects in use for the treatment of osteoporosis. Although SERMs have shown beneficial effects on some surrogate markers of CVD it is not known whether this will translate into clinical benefit. The recent secondary analysis of the osteoporosis prevention study, the Multiple Outcomes of Raloxifene Evaluation (MORE) trial, suggested that there were no significant differences between raloxifene and placebo group regarding combined CHD and CVD events. Interestingly, however, in the subset with increased cardiovascular risk, the raloxifene group had a significantly lower risk of CVD events compared with placebo (99). The Raloxifene Use for the Heart Studyis currently testing the impact of raloxifene on cardiovascular endpoints in postmenopausal women. The results of this trial will provide information on the net clinical cardiovascular benefits of SERMs.
Phytoestrogens are a group of natural compounds that have both estrogen agonist and antagonist properties and could be considered as natural SERMs. There is growing evidence from epidemiological and experimental studies that consumption of phytoestrogens has beneficial effects on the risk of CHD (100,101). Soy phytoestrogens have shown beneficial effects on endothelium-dependent vasodilation and the development of atherosclerosis in nonhuman primates (102,103). Some studies in postmenopausal women, but not all, have shown improvements on lipid profiles and endothelial function (104). Clinical end-point data from randomized trials are not available to make recommendations regarding use of soy phytoestrogens for prevention of CVD.
Tibolone is a steroid hormone with a progestogen-like structure that is converted to estrogenic and androgenic derivatives in vivo. It improves menopausal symptoms and bone density and potentially has fewer side effects than conventional HRT. Limited human observational data on the cardiovascular effects of tibolone indicate that it reduces triglycerides and Lp(a) levels but also HDL and there is a suggestion that tibolone may not increase thrombotic risk (105). We must await data from clinical trials on definite clinical end-points to establish the vascular effects of tibolone.
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