Numerous factors have been implicated in the aetiology of CHD.4
Of these, the role of the classical risk blood cholesterol concentrations, blood pressure and cigarette smoking have been the best documented in both men and women. Mean levels of these risk factors increase with age, more steeply in women than in men. At younger ages, women tend to have lower mean levels of systolic blood pressure and serum cholesterol compared to men; this pattern reverses at older ages. In contrast, cigarette smoking habit appears to decline with age in both men and women. Though the prevalence of smoking is higher in older men, the most recent figures show higher prevalence of smoking in younger women compared to men.3,5
The evidence for the major importance of raised blood cholesterol for CHD in both men and women is overwhelming. Raised blood pressure, fibrinogen values, cigarette smoking habit, diabetes, inflammatory markers such as C‐reactive protein, and obesity are also well documented risk factors in women. Of these, reduction of blood pressure and cholesterol have been demonstrated to be of cardiovascular benefit in randomised trials which have included women.6
The classical risk factors—blood pressure, raised blood cholesterol and cigarette smoking—appear to confer the same relative increase in CHD risk in women and some of the sex difference in CHD can be explained by lower levels of risk factors in women, at least at younger ages. In particular, cigarette smoking habit has been substantially lower in the past in women compared to men, but trends appear to be reversing in younger cohorts. Some of the apparent protection that women seem to have from CHD may diminish as prevalence of cigarette smoking in women increases and even exceeds that in men.
While the magnitude of the relative risk of subsequent CHD associated with the major risk factors are similar in men and women, the absolute risk of CHD is higher in men compared to women at any given level of risk factor.7,8
This has implications for individual‐based preventive therapies such as pharmacologic treatment of hypertension and hypercholesterolaemia. Though trials indicate these confer similar relative benefits for CHD in men and women, the absolute benefit is likely to be lower in women. Thus, the risk‐benefit balance may be different and more finely balanced in women compared to men when individual preventive treatments are considered.
Lifestyle factors, diet, physical activity, and psychosocial factors in CHD may have effects through influencing levels of known physiological risk factors such as lipid values and blood pressure or through other mechanisms involved such as inflammation or thrombosis. Though there are few randomised trials of primary prevention of CHD using lifestyle measures in women, it may seem reasonable to assume from the consistency in the data from observational studies that similar lifestyle factors apply to women as well as men. Observational studies in women as well as men indicate lower CHD rates are associated with dietary patterns with lower saturated fat intake, higher fruit and vegetable intake and higher physical activity levels.6