Cholesterol LDL - Low Density Lipoprotein Unit Conversion

SI UNITS

mmol/L
µmol/L

CONVENTIONAL UNITS

mg/dL
mg/100mL
mg%
mg/L
µg/mL
Synonyms
LDL - Cholesterol, LDL-C
Units of measurement
mmol/L, µmol/L, mg/dL, mg/100mL, mg%, mg/L, µg/mL
Description

Low Density Lipoproteins (LDL) play a key role in causing and influencing the progression of atherosclerosis and, in particular, coronary sclerosis. The LDLs are derived from VLDLs (Very Low Density Lipoproteins) rich in triglycerides by the action of various lipolytic enzymes and are synthesized in the liver. The elimination of LDL from plasma takes place mainly by liver parenchymal cells via specific LDL receptors. Elevated LDL concentrations in blood and an increase in their residence time coupled with an increase in the biological modification rate results in the destruction of the endothelial function and a higher LDL‐cholesterol uptake in the monocyte/macrophage system as well as by smooth muscle cells in vessel walls. The majority of cholesterol stored in atherosclerotic plaques originates from LDL.

LDL-cholesterol plays a causal role in the development of coronary heart disease (CHD), with numerous clinical and epidemiological studies demonstrating its atherogenic properties. LDL-cholesterol has the strongest association with coronary mortality of all lipid and lipoprotein variables (GRIPS study), with a combination of raised LDL-cholesterol and elevated triglyceride levels constituting an especially high risk. LDL-cholesterol evaluation provides early recognition of atherosclerosis risk and may be used to determine the response to lipid-lowering drug therapy. High levels of LDL-cholesterol are associated with increased cardiovascular risk and familial hyperlipidaemia. Reduced levels of LDL-cholesterol may be found in malabsorption and malnutrition.

Therefore, therapies focusing on lipid reduction primarily target the reduction of LDL‐cholesterol which is then expressed in an improvement of the endothelial function, prevention of atherosclerosis and reducing its progression as well as preventing plaque rupture.

Reference Intervals
National Cholesterol Education Program (NCEP) guidelines

< 2.6 mmol/L     (100 mg/dL)           Optimal
2.6 – 3.3 mmol/L (100 – 129 mg/dL)     Near Optimal / Above Optimal
3.4 – 4.1 mmol/L (130 – 159 mg/dL)     Borderline High
4.1 – 4.9 mmol/L (160 – 189 mg/dL)     High
≥ 4.9 mmol/L     (190 mg/dL)           Very High
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