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Normal lipid metabolism, familial hyperlipidaemia, lipid intervention and their benefits
B C Koner1, K Goswami, S Kavitha
1Department of Biochemistry, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006.
Insights
This review covers lipoprotein metabolism, high cholesterol, and therapies for coronary artery disease (CAD). Effective lipid lowering, particularly LDL-cholesterol, is crucial for preventing and managing CAD.
Area of Science:
- Cardiovascular Medicine
- Lipidology
- Metabolic Disorders
Background:
- Lipoprotein metabolism, including LDL-cholesterol (LDL-C) and HDL particles, is central to atherogenesis and coronary artery disease (CAD).
- Modified LDL particles and elevated Lp(a) levels, particularly in certain populations like Indians, are linked to increased CAD risk.
- Familial hyperlipidemias significantly elevate atherosclerosis and CAD susceptibility due to altered lipoprotein metabolism.
Purpose of the Study:
- To review recent advancements in lipoprotein metabolism, familial hyperlipidemias, and lipid-lowering therapies concerning coronary artery disease (CAD).
- To highlight the significance of LDL-cholesterol levels and particle subclasses in atherogenesis.
- To discuss the role of HDL particles in reverse cholesterol transport and the impact of Lp(a) on CAD.
Main Methods:
- Literature review of recent developments in lipoprotein metabolism.
- Analysis of the role of LDL-cholesterol, LDL modifications, HDL function, and Lp(a) in CAD.
- Examination of lipid-lowering therapies, including statins, and current NCEP guidelines for LDL-C control.
Main Results:
- LDL-C levels and particle subclasses are key determinants of cholesterol delivery and atherogenesis.
- HDL particles facilitate reverse cholesterol transport, with components like Paraoxonase-1 playing a protective role.
- High Lp(a) levels, prevalent in Indians, are epidemiologically linked to CAD development.
Conclusions:
- Stringent LDL-C control (< 100 mg/dl) is recommended for CAD and its risk equivalents.
- Therapeutic lifestyle changes and pharmacotherapy, primarily statins, are essential for reducing blood lipids.
- Comprehensive lipid management is vital for both primary prevention and secondary prevention of coronary events.
Abstract:
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).