Dyslipidemia

Key Points

• Patients undergoing screening for dyslipidemia should have a complete fasting lipid profile.

• LDL and non-HDL (total cholesterol - HDL) are atherogenic and have defined targets for therapy based on global risk factor burden.

• LDL-C is currently the primary target of therapy in patients with dyslipidemia, although non-HDL-C or apoB100 may become the next primary target of therapy.

• HDL is antiatherogenic, and when less than 40 mg/dL in men and

50 mg/dL in women, therapeutic effort should be made to raise HDL.

• Therapeutic lifestyle changes are an important component of any regimen designed to treat dyslipidemia.

Figure 27-1 Molecular and histologic pathways for reverse cholesterol transport. To deliver peripheral cholesterol back to the liver or steroidogenic organs such as the adrenal glands, placenta, or ovaries, apoA-I and nascent discoidal HDL interact with cells such as macrophages and foam cells within blood vessel walls. The HDL undergoes a series of cell receptor-dependent and serum enzyme-dependent maturation and speciation reactions (HDL speciation). HDL can interact directly with a variety of hepatocyte surface receptors, including SR-BI. The cholesterol esters in HDL can also be transported back to the liver by an indirect pathway for reverse cholesterol transport that depends on CETP and the LDL and LDL-RRP receptors. ABCA1, ATP-binding membrane cassette transporter A1; apoA-I, apoprotein A-I; ApoE, apoprotein E; CE, cholesteryl ester; CETP, cholesterol ester transfer protein; GI, gastrointestinal; HDL, high-density lipoprotein; HL, hepatic lipase; IDL, intermediate-density lipoprotein; LCAT, lecithin:cholesterol acyltransferase; LDL, low-density lipoprotein; LDL-R, low-density lipoprotein receptor; LDL-RRP, low-density lipoprotein receptor-related protein; LysoPC, lysophosphatidylcholine; PC, phosphatidylcholine; PGN, proteoglycan; PL, phospholipid; PLTP, phospholipid transfer protein; SR-BI, scavenger receptor BI; UC, unesterified cholesterol; VLDL, very-low-density lipoprotein. (Reproduced with permission from Toth PP. High-density lipoprotein as a therapeutic target: clinical evidence and treatment strategies. Am J Cardiol 2005;96:50K-58K.)

Figure 27-1 Molecular and histologic pathways for reverse cholesterol transport. To deliver peripheral cholesterol back to the liver or steroidogenic organs such as the adrenal glands, placenta, or ovaries, apoA-I and nascent discoidal HDL interact with cells such as macrophages and foam cells within blood vessel walls. The HDL undergoes a series of cell receptor-dependent and serum enzyme-dependent maturation and speciation reactions (HDL speciation). HDL can interact directly with a variety of hepatocyte surface receptors, including SR-BI. The cholesterol esters in HDL can also be transported back to the liver by an indirect pathway for reverse cholesterol transport that depends on CETP and the LDL and LDL-RRP receptors. ABCA1, ATP-binding membrane cassette transporter A1; apoA-I, apoprotein A-I; ApoE, apoprotein E; CE, cholesteryl ester; CETP, cholesterol ester transfer protein; GI, gastrointestinal; HDL, high-density lipoprotein; HL, hepatic lipase; IDL, intermediate-density lipoprotein; LCAT, lecithin:cholesterol acyltransferase; LDL, low-density lipoprotein; LDL-R, low-density lipoprotein receptor; LDL-RRP, low-density lipoprotein receptor-related protein; LysoPC, lysophosphatidylcholine; PC, phosphatidylcholine; PGN, proteoglycan; PL, phospholipid; PLTP, phospholipid transfer protein; SR-BI, scavenger receptor BI; UC, unesterified cholesterol; VLDL, very-low-density lipoprotein. (Reproduced with permission from Toth PP. High-density lipoprotein as a therapeutic target: clinical evidence and treatment strategies. Am J Cardiol 2005;96:50K-58K.)

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