ABSTRACT
Cholesterol was recognized as the lipid present in atheromatous plaques in the 19th century soon after its discovery.1 The epidemiological association between serum cholesterol or, more precisely, serum low-density lipoprotein (LDL) and coronary heart disease (CHD) was well established by the 1960s,2 and the confirmation in the 1970s that familial hypercholesterolaemia was a monogenic disorder due to mutations of the LDL receptor3 demonstrated that raised circulating LDL without the need for other CHD risk factors could cause accelerated atherosclerosis. It was also demonstrated that the cholesterol in atheromatous lesions was derived from LDL cholesterol.4 Also in the 1970s it was recognized that low high-density lipoprotein (HDL) levels were a potent risk factor for atherosclerosis,5 often more important even than LDL in women and older patients.6-9 Raised serum triglyceride levels have only recently become recognized as risk factors for CHD. Earlier controversy about triglycerides and CHD risk may have been the consequence of the greater biological variation in the serum triglyceride concentration compared to HDL cholesterol with which they are relatively strongly correlated, which meant that triglycerides were rejected in multivariate analysis of CHD risk on mathematical grounds.10
