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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:474.)
© 2005 American Heart Association, Inc.

Editorials

Increased ApoB in Small Dense LDL Particles Predicts Premature Coronary Artery Disease

John D. Brunzell

From the Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington, Seattle.

Correspondence to John D. Brunzell, University of Washington, Division of Metabolism, Endocrinology, and Nutrition, Seattle, WA 98195-6426. E-mail brunzell@u.washington.edu

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

The relation between plasma lipoproteins and atherosclerosis has evolved over the past fifty years. Serum cholesterol levels were shown to be associated with coronary artery disease (CAD) in familial hypercholesterolemia in the early 20^th century (see Frederickson¹). This cholesterol was determined to be in a particular lipoprotein class² now termed low-density lipoprotein (LDL) cholesterol.³ LDL cholesterol has been shown to predict premature CAD in many studies,⁴ and a reduction in LDL cholesterol with statin therapy has been shown to decrease CAD events by up to 50% in primary⁵ and in secondary⁶ intervention trials. The National Cholesterol Education Program Adult Treatment Panel⁷ initially based recommendations for therapy to prevent CAD on LDL cholesterol levels. Later the measurement of HDL cholesterol was added to estimate risk.⁸

See page 553

Because treatment for LDL cholesterol levels only decreases the risk for premature CAD by about half, other lipoprotein factors have been sought to explain the additional risk. Plasma triglyceride levels are associated with CAD, independently of LDL and HDL cholesterol levels.⁹ Hypertriglyceridemia also has been associated with small dense LDL particles.^1,10

Studies of the heterogeneity of LDL particles and their number have suggested that small dense LDL and increased number of LDL particles, as reflected by increased apoB, are specific components of LDL important in the risk for premature CAD. Several studies noted heterogeneity of LDL particles with apoB enrichment of LDL in hypertriglyceridemic individuals.^11–13 Total apoB levels were then noted to be elevated in individuals with atherosclerosis.^14,15 Hyperapobetalipoproteinemia, an elevated LDL . . . [Full Text of this Article]

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