Extract

The oxidative modification of low‐density lipoprotein (LDL) is an important pre‐requisite for macrophage uptake and accumulation of cellular cholesterol ester in the arterial wall. This is a key component to the development of the atherosclerotic lesion.

Patients with coronary artery disease (CHD), i.e. stable and unstable angina and acute myocardial infarction, have significantly elevated levels of oxidized LDL when compared with age‐matched controls; however, at any given concentration of plasma cholesterol, there is considerable variability in the clinical expression of CHD. This reflects the diversity in the reaction of the arterial wall to hypercholesterolaemia and the associated changes in endothelial function, immunological effects, smooth muscle cell proliferation and coagulation. Despite the complexity of these responses, opinion is generally united that LDL‐cholesterol lowering is essential to achieve a reduction in CHD mortality and clinical event rates.

The strong positive relationship between cholesterol and CHD and the role of other risk factors can be derived from several lines of evidence. The large cohort studies carried out between populations1,2 and within single and migrating populations,3,4 have helped us to understand the association of low‐ and high‐density lipoprotein, and the correlation between CHD and all the primary risk factors. Although total cholesterol does not appear to differ greatly among ethnic groups, high‐density lipoprotein (HDL) cholesterol is lowest, and serum triglycerides highest, among South Asians.

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