IntroductionThe clinical presentations of atherosclerosis mainly involve the coronary and carotid arteries, which remain the leading causes of morbidity and mortality in both men and women of all racial groups with Coronary Heart Disease (CHD) the leading cause of death worldwide. 1 The presence of CHD is considered to be a reliable index for more widespread of atherosclerosis. The disease develops slowly over many years in the intima layer of large and medium sized arteries, with devastating manifestations usually after the fourth or fifth decade. 2 Many factors have been attributed to the aetiology of atherosclerosis; inherited and lifestyle factors contribute to the progression and clinical manifestations. A major contributor to this progression is abnormalities in lipid and lipoprotein metabolism. The association of high concentrations of plasma cholesterol, particularly Low Density Lipoprotein (LDL) cholesterol, and CHD is emphasised by the findings of cholesterol-lowering drug intervention trials. [3][4][5][6] Numerous epidemiological studies have demonstrated an inverse relation between HDL cholesterol levels and the incidence of atherosclerotic CHD.7 High-Density Lipoprotein (HDL) has both anti-oxidative and anti-inflammatory activities, in addition to their known cardioprotective role in reverse cholesterol transport.8, 9 HDL is considered to be an important marker of CHD risk. 10 Patients with low levels of HDL cholesterol have a significantly increased risk of developing atherosclerotic coronary events.11-13 Increased HDL cholesterol levels were identified as the most important predictor of a favourable outcome with respect to a reduction in myocardial infarction rates after lipid-lowering therapy.14 The association of elevated HDL cholesterol levels with protection against CHD has been attributed to indicate the efficiency of reverse cholesterol transport involved in removing cholesterol from the atheroma.
15Several studies assessed the relationships between TriGlyceride (TG), TG-Rich Lipoproteins (TG-RL) and the development of atherosclerosis. The link between TG and CHD was established in the1950s; Albrink and Man reported that fasting TG levels were increased among patients with CHD. 16 In addition, Hokanson Effectively, the close relationship linking high TG concentrations with potentially atherogenic factors such as Intermediate Density Lipoprotein (IDL), small dense LDL and increased cholesteryl ester exchange may affect its predictive power in CHD risk. 28 In the context of 24-hour TG metabolism, the fasting TG concentration could be considered spurious as it is considered an unstressed, equilibrated state that is not representative of the dynamic metabolic state present for most of the day. As human beings consume meals regularly during the waking hours, plasma TG concentrations are above fasting levels for perhaps three-quarters of the day.
29Furthermore, these postprandial TG concentrations are not necessarily reflected by fasting TG concentrations. Individuals with
Review Article
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