(Stroke. 2002;33:1174.)
© 2002 American Heart Association, Inc.
Editorials |
From the Department of Neurology (F.M.Y.), University of Texas-Houston Medical School, and the Department of Internal Medicine (J.D.M.), Baylor College of Medicine, Houston, Tex.
Correspondence to Frank M. Yatsu, Department of Neurology, University of Texas-Houston Medical School, Houston, TX 77030. E-mail Frank.M.Yatsu@uth.tmc.edu
Key Words: carotid arteries hyperlipoproteinemia, familial combined lipoproteins, LDL cholesterol oxygen radical ultrasonography
In the article by Liu et al, as part of the European Multicenter Study on Familial Dyslipidemia (EUFAM),1 148 asymptomatic familial combined hyperlipidemia members from 38 Finnish families were investigated for low-density lipoprotein (LDL) particle size, LDL susceptibility to oxidation, and the association of these LDL properties with carotid intima-media thickness (IMT) determined by ultrasound and B-mode scanning of 28 sites involving the common carotid artery, carotid bulb, and internal carotid artery. The authors found a statistically significant inverse relationship between LDL size (but not with LDL oxidation) and IMT. Using several multivariate analyses, the most rigorous also showed a correlation of IMT with pulse pressure and gender, but not with many of the other customary vascular risk factors such as hypertension, smoking, and total cholesterol.
This study is important in showing a potentially critical role for small, dense LDL particles in IMT expansion, a prelude to overt atherosclerosis. However, the precise role of small, dense LDL particles in this process still remains uncertain because no consensus exists. Some studies show no relationship of LDL size to atherogenesis,24 while others show a strong correlation. This association is evident in the following: (1) subjects with the so-called metabolic syndrome or "syndrome X," a complex disorder including diabetes mellitus or insulin resistance plus hypercholesterolemia and hypertriglyceridemia5; (2) when more accurate separation of small LDL is undertaken (22.5 to 23.5 nm)6; and (3) in longitudinal follow-up of asymptomatic subjects who subsequently develop ischemic heart disease.7 Persuasive support for the role of
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