KNOWLEDGE ABOUT the role of blood lipids has evolved rapidly since the 1950s when there was preoccupation with neutral fat (triglycerides) and the serum total cholesterol.1 With the advent of ultracentrifugation, the emphasis shifted to the lipoproteins that transport cholesterol and triglycerides.2 Electrophoretic analysis spawned a phenotypic classification system,3 leading to β-and pre-β-lipoproteins becoming the focus of research. Soon it became evident that there was a 2-way traffic of cholesterol entering the arterial intima in the atherogenic low density lipoproteins (LDLs), with removal by other particles, apparently high density lipoproteins (HDLs).4 The total-HDL cholesterol ratio was proposed to assess the joint effect of the influences of LDL and HDL. More recently, interest has focused on oxidized LDL, small, dense LDL particles, and triglycerides.5
Although not the latest entry, one with an intriguing role in the field of dyslipidemic atherogenesis research is lipoprotein Lp(a). Bearing these
Wilson PWF, Kannel WB. Should We Measure Lipoprotein Lp(a)? Arch Intern Med. 1997;157(11):1161–1162. doi:10.1001/archinte.1997.00440320023003
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