Atherogenic dyslipidemia

Abstract

Atherogenic dyslipidemia (AD) refers to elevated levels of triglycerides (TG) and small-dense low-density lipoprotein and low levels of high-density lipoprotein cholesterol (HDL-C). In addition, elevated levels of large TG rich very low-density lipoproteins, apolipoprotein B and oxidised low-density lipoprotein (LDL), and reduced levels of small high-density lipoproteins plays a critical role in AD. All three elements of AD per se have been recognised as independent risk factor for cardiovascular disease. LDL-C/HDL-C ratio has shown excellent risk prediction of coronary heart disease than either of the two risk markers. Asian Indians have a higher prevalence of AD than western population due to higher physical inactivity, low exercise and diet deficient in polyunsaturated fatty acids (PUFA). The AD can be well managed by therapeutic lifestyle changes with increased physical activities, regular exercise, and diets low in carbohydrates and high in PUFA such as omega-3-fatty acids, as the primary intervention. This can be supplemented drug therapies such as statin monotherapy or combination therapy with niacin/fibrates. Rosuvastatin is the only statin, presently available, to effectively treat AD in diabetes and MS patients.

Keywords: Atherogenic dyslipidaemia; cardiovascular disease; small-dense low-density lipoprotein statins.

Figure 1

Pathophysiology of atherogenic dyslipidemia. Generation of small dense-LDL particles (pattern B) and oxidation of LDL particle are key elements in atherosclerosis develomany of the atherogenic activitiespment. HDL-C antagonizes (-) many of the atherogenic activities of ox-LDL.[2] TG rich LDL is a substrate for hepatic lipase. CE: Cholesteryl esters, CETP: Cholesteryl ester transfer protein, ET cells: Endothelial cells, HDL-C: High-density lipoprotein cholesterol, HL: Hepatic lipase, LOX: Lipoxygenase, LP: Lipoprotein lipase, MPO: Myeloperoxidase, Ox-LDL: Oxidised low-density lipoprotein, SMCs: Smooth muscle cells