ABSTRACT
Incontrovertible evidence indicates that dyslipidaemia is intimately involved in atherogenesis and that correcting disordered lipid metabolism slows progression of lesions, stabilizes them and reduces coronary morbidity and mortality.1,2 The mechanisms of lipid-induced atherogenesis are now better understood, involving oxidative modification of low-density lipoprotein (LDL) cholesterol, small-dense LDL, reverse cholesterol transport in high-density lipoprotein (HDL) and platelet activation.3-6 Modification of diet, weight control, exercise and a number of pharmaceutical agents can interfere with various elements of this atherogenic process. Currently available agents include statins, fibric acid derivatives, resins that sequester cholesterol in the bowel, antioxidants and niacin. Rapid, convenient and economical techniques are currently available for measuring blood lipids, and guidelines have been promulgated for the evaluation and treatment of dyslipidaemia.1 However, it is still not determined whether therapy tailored to the pattern of dyslipidaemia is more efficacious than therapy focused primarily on lowering LDL cholesterol.
