Low Density Lipoprotein Cholesterol (LDL-C)
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|LDL-C variability in the general population is likely to be polygenic and also affected by environmental factors.||LDL-C variability in the general population is likely to be polygenic and also affected by environmental factors.|
|+||LDL-C levels should be used as the primary target to initiate and titrate lipid lowering therapy.|
|Causes endothelial cell injury predisposing the artery wall to inflammation that promotes the development of atherosclerotic plaque.||Causes endothelial cell injury predisposing the artery wall to inflammation that promotes the development of atherosclerotic plaque.|
Revision as of 23:46, 19 April 2012
The major cholesterol-carrying lipoprotein in plasma and is the causal agent for many forms of coronary artery disease.
Approximately 20% of men and 18% of women in the U.S. have an LDL above 160 mg/dL and age adjusted prevalence of LDL cholesterol above 130 mg/dL estimated to be 46% with higher prevalence among men.
Family and twin studies suggest that 40-80% of the population variation in levels are attributable to genetic factors.
LDL-C variability in the general population is likely to be polygenic and also affected by environmental factors.
LDL-C levels should be used as the primary target to initiate and titrate lipid lowering therapy.
Causes endothelial cell injury predisposing the artery wall to inflammation that promotes the development of atherosclerotic plaque.
It is suggested that every 10% increase in the prevalence of treatment among adults with high LDL-C could prevent approximately 8000 deaths per year in those below the age of 80 years (Farley TA et al).
All five single gene disorders that cause elevated LDL levels associated with premature coronary atherosclerosis.
Low levels increase the risk of lower respiratory tract infection.
Rare forms of hypercholesterolemia, including familial hypercholesterolemia due to mutations in the LDL receptor gene and familial defective apoliprotein B-100 due to mutations in the apolipoprotein B.
Statins inhibited LDL cholesterol biosynthesis to a greater extent than they lower apolipoprotein B levels.
Goal in primary prevention is a LDL-C target level of <70 mg/dl.
The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATPIII) primary prevention guidelines among adults aged 35-85 years could prevent 20,000 myocardial infarctions and 10,000 deaths from coronary artery disease per year (Pletcher MJ et al).
Small dense LDL with increased levels of Apo B are more atherogenic than larger more buoyant LDL even if the LS+DL-C levels is in the normal range.
Small dense LDL with increased levels of Apo B is associated with insulin resistance and increase glucose levels.
Aggressive treatment to lower levels associated with reduction in rates of cardiovascular events.
Low density lipoprotein cholesterol levels may not adequately evaluate cardiovascular risk when other apolipoprotein B containing atherogenic particles predominate-in cases such as diabetes, metabolic syndrome, or coronary heart disease.
Each low density lipoprotein, intermediate density lipoprotein, or very low density lipoprotein particle has a single Apo B molecule.
The amount of cholesterol in each LDL particle is heterogeneous and can vary in individuals.
The National Health and Nutrition Examination Survey (NHANES) data 2005 through 2008 demonstrated: the prevalence of high LDL-C increases with age 11.4%, 41.2% and 58.2% for age groups 20-39, 40-64 and 65 years or greater, respectively(MMWR).
In the above study the prevalence of high LDL-C did not change significantly from 1999-2002( 34,5%) to 2005-2008(33.3%).
Highest doses of statins offers limited additional lowering of LDL cholesterol at the expense of increased side effects.
The National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) recommends lowering of the LDL-C to 100 mg/deciliter for individuals at moderately high risk of coronary artery disease with two or more major coronary artery disease risk factors and a 10-20% 10 year coronary artery disease risk.
Up to 40% of individuals who develop coronary artery disease have LDL-C levels that are lower than the previous goal of less than 130 mg/dL.
Thyroid hormone lowers the level of serum LDL cholesterol.
Thyroid hormone analogue eprotirone utilized in a randomized, placebo controlled, double blind trial in patients with hypercholesterolemia on statins was associated with decreases in serum LDL levels and similar reductions in serm apoliprotein B, triglycerides and Lp(a) lipoprotein (Ladenson PW).
The National Health and Nutrition Examination Survey (NHANES) data 2005 through 2008 demonstrated: high LDL-C can be managed successfully wave lifestyle changes, medications or combination of these efforts.
The National Health and Nutrition Examination Survey (NHANES) data 2005 through 2008 demonstrated: Lifestyle modifications with low-fat and high fiber diets and increase physical activity and weight control can decrease LDL-C levels by up to 20 to 30%.
Meta-analysis of 14 clinical trials with statins indicated that such drugs can reduce the five-year incidence of major coronary events, coronary revascularization and stroke by each 20% for each millimole per liter (about 39 mg per deciliter) reduction in LDL-C (Baigent C et al).