Cholesterol is carried in the blood in the form of lipoproteins, which are dynamic particles with protein on the outside and an inner core of cholesterol and fats. Both lipoproteins and apolipoproteins are strong predictors of CHD risk. The term dyslipidemia applies to a high blood level of total cholesterol (TC), as well as other abnormalities in blood lipid levels including an elevated low density lipoprotein cholesterol level (LDL-C), a decreased high density lipoprotein cholesterol (HDL-C) level and an elevated very-low-density lipoprotein (VLDL) and triglyceride level.
Blood cholesterol and the lipoproteins that transport it have been known for a long time to be risk factors for CHD. The strength of total cholesterol as a predictor of relative risk of CHD decreases with increased age. In societies that have a mean total cholesterol level of less than 150 mg/dl, CHD is virtually unknown. A higher prevalence of heart disease is found in societies with a mean TC level above 210 mg/dl when most of the elevation of blood cholesterol is in the LDL. In the Framingham Heart Study, people with cholesterol levels between 150 and 200 mg/dl accounted for 35% of those with coronary heart disease, the disease was rarely encountered with levels < 150 mg/dl.
Elevated LDL-C is a powerful risk factor for CHD. When this lipoprotein attaches to the endothelial cells of the coronary arteries, it undergoes a chemical process called oxidation, which attracts more LDL – and this process starts again. Oxidized LDL-C is more likely to be deposited in the lining of the arterial walls leading to the development of atherosclerosis. Drs Joseph Goldstein and Michael Brown were awarded the 1985 Nobel Prize in Medicine for their landmark studies on the metabolism of LDL particles. They demonstrated that specific receptors for LDL exist on cell surfaces. The level of LDL in the blood is determined by the rate of production of LDL particles in the liver and by the number of unbound LDL receptors. An imbalance between these variables by overproduction of LDL or by lack of specific receptors results in an elevated blood level of LDL-C and an increase in CHD risk.
Low levels of HDL-C are associated with an increased risk of CHD, and low HDL-C are frequently encountered in patients with CHD. HDL-C counteracts the effects of low density cholesterol by scavenging excess cholesterol from the walls of the arteries and taking it to the liver when it is broken down and excreted. The transport of cholesterol by HDL from the peripheral tissues (including atheromatous plaque) to the liver for recycling or excretion is called reverse cholesterol transport. HDL has also been shown to carry with it enzymes that may counteract the generation of the biological effects of oxidized LDL-C. HDL-C are significantly influenced by lifestyle factors. Cigarette smoking, obesity, and postmenopausal status are associated with lower HDL-C levels, moderate alcohol consumption and aerobic exercise raise HDL-C.
VLDL particles are composed predominately of triglyceride. The cholesterol contained with VLDL is usually approximated by dividing the fasting blood triglyceride concentration by 5, as long as the triglyceride level is
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