This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Desai, M. Y. Articles by Lima, J. A.C. Search for Related Content PubMed PubMed Citation Articles by Desai, M. Y. Articles by Lima, J. A.C.

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e110.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Association of Cholesterol Subfractions and Carotid Lipid Core Measured by MRI

Milind Y. Desai; Annabelle Rodriguez; Bruce A. Wasserman; Gary Gerstenblith; Sachin Agarwal; Margene Kennedy; David A Bluemke; João A.C. Lima

Divisions of Cardiology (M.Y.D., G.G., S.A., M.K., J.A.C.L.) and Endocrinology (A.R.), Department of Medicine and Department of Radiology (R.A.W., D.A.B., J.A.C.L.), Johns Hopkins University, Baltimore, Md

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

To the Editor:

A strong relationship exists between cholesterol and atherosclerosis,¹ with low density lipoprotein (LDL) being a major risk factor.² However, 50% of patients with acute coronary events have "normal" cholesterol, and 75% patients with premature coronary heart disease (CHD) have normal LDL.³ Thus, contribution of other lipoproteins has been explored. High density lipoprotein (HDL), comprised primarily of 2 subfractions, HDL₂ (large buoyant) and HDL₃ (small dense), has a protective role in CHD.^4,5 LDL can be dense or buoyant, and dense LDL is highly atherogenic, associated with 4-fold increased CHD risk.⁶ Lipoprotein_a [Lp(a)], is a strong risk factor for CHD and stroke.⁷

MRI can noninvasively visualize arterial wall remodelling and atherosclerotic plaque components (lipid core, fibrous cap, and calcium).^8,9 However, in vivo relationships between plaque components and cholesterol subfractions have not been demonstrated in humans. We examined in vivo relationship between cholesterol subfractions and atherosclerotic plaque, measured by MRI, in internal carotid arteries (ICA) of atherosclerotic patients.

This was an exploratory cross-sectional study of consecutively enrolled initial 28 patients who were part of an ongoing randomized trial testing the effects of extended release Niacin versus placebo station top of baseline therapy on carotid plaque regression, analyzed at baseline. All patients signed written informed consent and had documented atherosclerosis in at least one vascular territory: >3.9 mm aortic atherosclerosis on transesophageal echocardiography, >50% lesion in one coronary artery at cardiac catheterization, >50% carotid lesion on ultrasound or peripheral arterial disease (PAD). We excluded patients with pacemakers, defibrillators, aneurysm clips, elevated . . . [Full Text of this Article]

This article has been cited by other articles:

				N. M. Rajamannan Calcific Aortic Stenosis: Lessons Learned From Experimental and Clinical Studies Arterioscler Thromb Vasc Biol, February 1, 2009; 29(2): 162 - 168. [Abstract] [Full Text] [PDF]

				A. Kontush and M. J. Chapman Functionally Defective High-Density Lipoprotein: A New Therapeutic Target at the Crossroads of Dyslipidemia, Inflammation, and Atherosclerosis Pharmacol. Rev., September 1, 2006; 58(3): 342 - 374. [Abstract] [Full Text] [PDF]