Normal lipid metabolism, familial hyperlipidaemia, lipid intervention and their benefits.
Some recent developments in lipoprotein metabolism, familial hyperlipidaemias and lipid lowering therapies with reference to coronary artery disease (CAD) are reviewed. LDL-cholesterol (LDL-C) level and particle subclass are important determinants of the extent of cholesterol delivery to the peripheral tissues and thereby of atherogenesis and CAD. LDL modifications (eg, oxidation, adduct formation, desialylation, glycation, etc) enhance the above process. HDL particles bring cholesterol from peripheral tissues to liver (reverse cholesterol transport, RCT). ApoA1, LCAT enzyme, ABCA1 and cholesterol ester transfer protein are involved in RCT. Paraoxonase of HDL prevents oxidation of other lipoproteins and probably hinders atherogenesis. Lp(a) particles are like LDL except the presence of apo(a) that inhibits fibrinolysis and are epidemiologicaly linked to the development of CAD. Indians have high Lp(a), in comparison to whites. Familial hyperlipidaemias are due to altered metabolism of lipoproteins affecting plasma lipid profile. Majority of such patients are prone to atherosclerosis and CAD. LDL-C is the primary target of lipid lowering therapy. Statins inhibit HMG-CoA reductase and are mainly used alone or with other drugs for lowering blood lipids. 'National Cholesterol Education Program' now recommends a stringent LDL-C control ( < 100 mg/dl) for CAD and CAD risk equivalents. Therapeutic lifestyle changes and drug therapy are the main modalities to reduce blood lipids, aiming at total reduction of short-and long-term coronary risk for all (primary prevention), and of coronary mortality and morbidity in patients with CAD (secondary prevention).