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<70 <1.8 Optimal LDL cholesterol, corresponding to lower rates of progression, promoted as a target option for those known to clearly have advanced symptomatic cardiovascular disease <100 <2.6 Optimal LDL cholesterol, corresponding to lower, but not zero, rates for symptomatic cardiovascular disease events 100 to 129 2.6 to 3.3
Guidelines by the American College of Cardiology and the American Heart Association recommend statin treatment for primary prevention of cardiovascular disease in adults with LDL cholesterol ≥ 190 mg/dL (4.9 mmol/L) or those with diabetes, age 40–75 with LDL-C 70–190 mg/dL (1.8–4.9 mmol/dL); or in those with a 10-year risk of developing ...
[2] [5] Remnant cholesterol is primarily chylomicron and VLDL, and each remnant particle contains about 40 times more cholesterol than LDL. [6] Remnant cholesterol corresponds to all cholesterol not found in high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C). It is calculated as total cholesterol minus HDL-C and LDL-C. [7]
Cholesterol is tested to determine for "normal" or "desirable" levels if a person has a total cholesterol of 5.2 mmol/L or less (200 mg/dL), an HDL value of more than 1 mmol/L (40 mg/dL, "the higher, the better"), an LDL value of less than 2.6 mmol/L (100 mg/dL), and a triglycerides level of less than 1.7 mmol/L (150 mg/dL).
After six weeks, The National Cholesterol Education Program recommends checking the LDL cholesterol response to the changes; if the LDL cholesterol goal has not been achieved, other therapeutic options for LDL lowering can be implemented. These include: 2 grams per day of plant stanols or sterols and 10–25 grams per day of soluble fiber.
Hyperlipidemia is abnormally high levels of any or all lipids (e.g. fats, triglycerides, cholesterol, phospholipids) or lipoproteins in the blood. [2] The term hyperlipidemia refers to the laboratory finding itself and is also used as an umbrella term covering any of various acquired or genetic disorders that result in that finding. [3]
Levels of LDL or non-HDL cholesterol both predict future coronary heart disease; which is the better predictor is disputed. [39] High levels of small dense LDL may be particularly adverse, although measurement of small dense LDL is not advocated for risk prediction. [39] In the past, LDL and VLDL levels were rarely measured directly due to cost.
In familial hypercholesterolemia, a mutation in the LDLR, PCSK9, or APOB is usually the reason for this and these mutations result in high LDL cholesterol. [8] In combined hyperlipidemia, there is an overproduction of apoB-100 in the liver. [9] This causes high amounts of LDL and VLDL molecules to form. [9]