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(Circulation. 2002;106:2526.)
© 2002 American Heart Association, Inc.

Low-Density Lipoprotein, Non-High-Density Lipoprotein, and Apolipoprotein B as Targets of Lipid-Lowering Therapy

Scott M. Grundy, MD, PhD

From the Center for Human Nutrition and the Departments of Internal Medicine and Clinical Nutrition, University of Texas Southwestern Medical Center at Dallas.

Correspondence to Scott M. Grundy, the Center for Human Nutrition and the Departments of Internal Medicine and Clinical Nutrition, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Y3.206, Dallas, TX 75390-9052. E-mail scott.grundy@utsouthwestern.edu

Key Words: Editorials • lipids • lipoproteins • apolipoproteins

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Although low-density lipoprotein (LDL) is widely recognized as the major atherogenic lipoprotein and the primary target of lipid-lowering therapy,¹ other lipoprotein species nonetheless appear to be involved in atherogenesis. These include very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), and high-density lipoproteins (HDL). Both VLDL and IDL are triglyceride-rich lipoproteins (TGRLP). Thus, in the aftermath of unequivocal evidence that LDL lowering reduces risk for major coronary events and stroke,² the field of lipid study is turning more of its attention to the other lipoproteins that appear to be involved in atherosclerosis. The recent Adult Treatment Panel III (ATP III) report¹ of the National Cholesterol Education Program has summarized our current understanding of the relationship between other lipoprotein species and risk for coronary heart disease (CHD).

See p 2537

ATP III¹ placed more emphasis on TGRLP and HDL as secondary targets of lipid-modifying therapy than did previous ATP reports.³ There is an emerging consensus that among TGRLP, cholesterol-rich remnant lipoproteins carry atherogenic potential. This view led ATP III to designate LDL+IDL+VLDL cholesterol (called non-HDL cholesterol) as "atherogenic cholesterol" and to identify it as a secondary target of therapy, after LDL cholesterol. In the ATP III report, however, non-HDL cholesterol as a secondary target is limited to persons who have elevated serum triglyceride levels (200 mg/dL). In the majority of people who have lower triglyceride levels, LDL cholesterol contains the bulk of "atherogenic cholesterol" and thus is a sufficient target alone.

The designation of elevated non-HDL cholesterol as a treatment target depended . . . [Full Text of this Article]

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