This review summarises current evidence for therapeutic options for hyperlipidaemia in post menopausal women. The two situations in which treatment is recommended are: 1. Primary prevention, which requires assessment of total risk factors for coronary heart disease. a) Statins. AFCAPS/TEXCAPS is the only randomised controlled trial (RCT) to include women. Fewer coronary heart disease (CHD) events, but no difference in mortality was found. b) Hormone replacement therapy (HRT). While there are numerous reports of positive observational epidemiological studies for HRT, there are no completed RCTs. There is little evidence for statin use in women except for familial hypercholesterolaemia. HRT is therefore not only appropriate for its multiple effects on lipoproteins, vascular function and insulin sensitivity but also for prevention of osteoporosis. 2. Secondary prevention, to achieve target total and low density lipoprotein (LDL) cholesterol. a) Statins. The major measurable effect of these drugs is to reduce total and LDL cholesterol. In the RCTs 4S, CARE and LIPID, where 20% of subjects were female, CHD events, but neither CHD mortality nor total mortality were significantly reduced in women. b) HRT. Data available from two RCTs using conjugated equine oestrogens and medroxyprogesterone acetate show no benefit. Other studies of HRT have been observational and positive. The effects of treatment on lipoproteins with statins, HRT and the combination have been investigated. In secondary prevention for hyperlipidaemic women to achieve cholesterol <5 and LDL<3 mmol/L statins will be first choice, with HRT a possible addition for its other benefits on cardiovascular risk factors. Choice of HRT medication. The route of administration will affect specific risk factors, eg, oral oestrogen reduces Lp(a) and LDL, increases HDL, while the transdermal route is less effective at reducing Lp(a) and LDL but does not increase triglyceride. Both routes reduce fibrinogen, factor VII and adhesion molecules and improve blood flow. The choice of progestogen will also affect cardiovascular risk factors. The most important lipid risk factors in women are HDL, triglyceride and Lp(a). The risk associated with raised triglyceride and LDL is offset by high HDL. Thus, in women with risk factors in primary prevention, theoretically oral HRT with a non-androgenic progestogen is likely to be of most benefit. However, since long-term adherence to therapy is important in reducing cardiovascular risk, the individual's choice of route and type of HRT is paramount.
Genetic variation in the renin–angiotensin–aldosterone system is associated with cardiovascular risk factors and early mortality in established coronary heart disease
