HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: j.jacc.2007.07.045v1 50/18/1735    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mudd, J. O. Articles by Kwiterovich, P. O. Search for Related Content PubMed Articles by Mudd, J. O. Articles by Kwiterovich, P. O., Jr

STATE-OF-THE-ART PAPER

Beyond Low-Density Lipoprotein Cholesterol

Defining the Role of Low-Density Lipoprotein Heterogeneity in Coronary Artery Disease

James O. Mudd, MD^_*, Barry A. Borlaug, MD^_*, Peter V. Johnston, MD^_*, Brian G. Kral, MD, MPH^_*, Rosanne Rouf, MD^_*, Roger S. Blumenthal, MD^_* and Peter O. Kwiterovich, Jr, MD^,_*

^_* Johns Hopkins Ciccarone Preventive Cardiology Center, Baltimore Maryland
Johns Hopkins University Lipid Clinic, Baltimore, Maryland

Manuscript received April 30, 2007; revised manuscript received July 16, 2007, accepted July 17, 2007.

^_* Reprint requests and correspondence: Dr. Peter O. Kwiterovich, Jr., University Lipid Clinic, Suite 310, 550 North Broadway Building, Baltimore, Maryland 21205. (Email: pkwitero{at}jhmi.edu).

Recent clinical trials in patients with coronary artery disease (CAD) provide evidence that low-density lipoprotein cholesterol (LDL-C) levels should be lowered even further to prevent recurrent CAD. However, despite more aggressive interventions for lowering LDL-C levels, the majority of CAD events go undeterred, perhaps related to the fact that intervention was not started earlier in life or that LDL-C levels represent an incomplete picture of atherogenic potential. Nevertheless, LDL-C remains the contemporary standard as the primary goal for aggressive LDL reduction. If triglycerides are >200 mg/dl, the measurement of non–high-density lipoprotein cholesterol (HDL-C) is recommended. Measurement of apolipoprotein (apo)B has been shown in nearly all studies to outperform LDL-C and non–HDL-C as a predictor of CAD events and as an index of residual CAD risk. This is because apoB reflects the total number of atherogenic apoB-containing lipoproteins and is a superior predictor of the number of low-density lipoprotein particles (LDL-P). Estimates of LDL-P and size can also be made by nuclear magnetic resonance spectroscopy, density gradient ultracentrifugation, and gradient gel electrophoresis. Although a number of studies show that such estimates predict CAD, LDL-P, and size often accompany low HDL-C and high triglyceride levels, and therefore such additional lipoprotein testing has not been recommended for routine screening and follow-up. Because apoB is a superior predictor of LDL-P, we recommend that apoB and the apoB/apoA-I ratio be determined after measurement of LDL-C, non–HDL-C, and the ratio of total cholesterol/HDL-C to better predict CAD and assess efficacy of treatment.

Abbreviations and Acronyms   apo = apolipoprotein   CAD = coronary artery disease   CE = cholesteryl esters   DGU = density-gradient ultracentrifugation   GGE = gradient gel electrophoresis   HDL-C = high-density lipoprotein cholesterol   LDL-C = low-density lipoprotein cholesterol   LDL-P = total number of low-density lipoprotein particles   Lp(a) = lipoprotein (a)   NMR = nuclear magnetic resonance   TC = total cholesterol   TG = triglycerides

This article has been cited by other articles:

				E. M. deGoma, R. L. deGoma, and D. J. Rader Beyond high-density lipoprotein cholesterol levels evaluating high-density lipoprotein function as influenced by novel therapeutic approaches. J. Am. Coll. Cardiol., June 10, 2008; 51(23): 2199 - 2211. [Abstract] [Full Text] [PDF]