• Lipids
• apoproteins
• lipoproteins
• risk stratification
• coronary artery disease (CAD)

“Without cholesterol there can be no atherosclerosis” stated Anitchkov in 1915 and the causal role of lipids in this ubiquitous disorder is now indisputable. The likelihood of developing its cardiovascular consequences, especially coronary heart disease (CHD), is enhanced by dyslipidaemia, which manifests itself either as an increase in low-density lipoprotein (LDL), resulting in hypercholesterolaemia, or in very-low-density lipoprotein (VLDL), resulting in either hypertriglyceridaemia or, if VLDL remnants accumulate, mixed hyperlipidaemia. In contrast, high-density lipoprotein (HDL) is usually decreased, especially when triglycerides are raised.

The concept of ‘risk factors’, inherent or acquired traits that increase the likelihood that the bearer will develop CHD, originated in Framingham. The prospective study which started there in 1948 measured a range of putative risk factors in a representative sample of adults who were then followed up to determine which of them developed CHD. The role of lipids was established by Kannel et al,1 who demonstrated correlations between the concentrations of serum cholesterol and the major lipoprotein classes at entry to the study and the development of CHD during the subsequent 14 years. The incidence of CHD during follow-up was found to be threefold greater in subjects with serum cholesterol and VLDL and LDL concentrations in the top versus the bottom quartile, but apart from a raised VLDL in postmenopausal women, measurement of lipoprotein fractions was no more predictive than serum cholesterol alone. The main exception was HDL cholesterol, which was shown in a subsequent analysis of Framingham data to correlate even more strongly than LDL cholesterol with risk of CHD, but inversely.2