Increased rates of coronary heart disease (CHD) occur with advancing age in both sexes, although CHD rates in women lag behind those of men by about 10 years. There is a sharp increase in CHD rate among women after approximately 50 years of age. The reasons for this are not completely understood and are undoubtedly multifactorial. Cross-sectional data from large-scale population studies suggest that around the time of the menopause, low-density lipoprotein (LDL)-cholesterol levels increase by approximately 15 to 25%. Because this increase is larger than that observed in men over the same age span and closely approximates that observed in women after oophorectomy, it is likely that reduced circulating estrogen levels associated with menopause play a role in the adverse changes in both blood lipid levels and CHD incidence. There is clear evidence that treating hypercholesterolemia reduces cardiovascular risk in women, as well as in men. In the US National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) guidelines, diet and other lifestyle changes are recommended as first-line therapy. If the treatment goals cannot be achieved through non-pharmacological measures, drug therapy should be added. Of the available lipid-lowering agents, HMG CoA reductase inhibitors (statins) are the clear choice to decrease LDL-cholesterol levels. However the favourable effects of statins on high-density lipoprotein (HDL)-cholesterol and triglyceride levels are more modest, and statins are not known to decrease lipoprotein (a) [Lp(a)] levels. Estrogen or hormone replacement therapy (ERT/HRT) and nicotinic acid improve LDL- and HDL-cholesterol levels and also decrease Lp(a) levels. However, ERT/HRT is no longer recommended as first-line therapy for decreasing CHD risk. Nicotinic acid is particularly useful for decreasing triglyceride levels (as are fibrates) and raising HDL-cholesterol levels. Bile-acid sequestrants reduce LDL-cholesterol and slightly increase HDL-cholesterol levels. Both bile acid sequestrants and ERT/HRT tend to raise triglyceride levels, therefore they should be used cautiously in women with hypertriglyceridaemia. Treatment should be individualised for each patient. It is important to evaluate the primary form of dyslipidaemia, other CHD risk factors, comorbidities, and the extent of lipid improvement needed in order to reach treatment goals. The effects of each type of therapy and potential adverse effects should also be considered.