C ardiovascular disease (CVD) results in substantial morbidity and mortality in most western countries in the world. The mortality burden of CVD in the UK in 2002 appears to be similar in men and women and CVD accounts for approximately 39.1% of deaths in men and 39.2% in women (http://www.heartstats.org/). Rates for coronary heart disease (CHD) mortality in the UK have been falling since 1970. CHD is a multifactorial disease, but certain major risk factors can account for the vast majority of acute myocardial infarction (MI). A recently published study (INTERHEART) of nearly 30 000 men and women from different communities and ethnic groups worldwide showed that such risk factors are common to all groups and can predict over 90% of the CHD risk. Lifestyle factors, including cigarette smoking, poor diet high in saturated fats and low in fruit and vegetables, physical inactivity, and stress have an important causal role in the incidence of CHD in all populations, while moderate alcohol consumption is protective.1 Genetic and environmental factors are also significant. Metabolic diseases and risk factors, including diabetes mellitus, obesity, dyslipidaemia, hypertension, and insulin resistance, have a substantial impact on the development of CHD. These risk factors contribute to the development of atherosclerosis and thrombotic complications. Reducing these risk factors can slow the progression of CHD and its clinical complications before, and even after, the occurrence of a cardiovascular event.Loss of ovarian hormones at the menopause has a widespread adverse impact on many of these risk factors. However, recent large clinical trials of essentially one form of hormone therapy (HT) have not shown a benefit on cardiovascular risk and therefore, at the present time, HT is not recommended in postmenopausal women solely for cardioprotection. The failure of the clinical trials to show a benefit may be, in part, due to the selection of the wrong population in terms of age, but may additionally be due to inappropriate HT regimens, in terms of dose and possibly type of steroids, being employed. A pattern of early harm followed by later benefit has emerged from these trials. It is plausible that transient adverse effects on thrombogenesis and vascular remodelling are responsible for the early harm, while beneficial effects on metabolic risk factors and arterial function are responsible for the later benefit. HT regimens vary considerably in their metabolic effects, and hence in their cardiovascular effects. Further research is required to define the ideal dose, type, route of administration, and duration of HT for maximum potential cardiovascular benefit. These aspects will be discussed further.
RISK FACTORS FOR CHDRisk factors can be modifiable, potentially modifiable, or fixed. Definitely modifiable factors include; blood lipids, blood pressure, cigarette smoking, lifestyle and behavioural factors. Potentially modifiable risk factors include newer parameters such as homocysteine and hs C-reactive protein (CRP). The scien...