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Cholesterol  2013 

Discordance of Non-HDL and Directly Measured LDL Cholesterol: Which Lipid Measure is Preferred When Calculated LDL Is Inaccurate?

DOI: 10.1155/2013/502948

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Objective. To determine if non-HDL cholesterol (N-HDL) and directly measured LDL cholesterol (D-LDL) are clinically equivalent measurements. Patients and Methods. Eighty-one subjects recruited for 2 cholesterol treatment studies had at least 1 complete fasting lipid panel and D-LDL performed simultaneously; 64 had a second assessment after 4 to 6 weeks, resulting in 145 triads of C-LDL, D-LDL, and N-HDL. To directly compare N-HDL to D-LDL and C-LDL, we normalized the N-HDL by subtracting 30 from the N-HDL (N-HDLA). Results. There was significant correlation between N-HDLA, D-LDL, and C-LDL. Correlation was significantly greater between N-HDLA and C-LDL than between N-HDLA and D-LDL. A greater than 20?mg/dL difference between measures was observed more commonly between N-HDLA and D-LDL, 29%, than between C-LDL and N-HDLA, 11% ( ), and C-LDL and D-LDL, 17% ( ). Clinical discordance was most common, and concordance was least common between N-HDL and D-LDL. Conclusions. Our findings suggest that N-HDL cholesterol and D-LDL cholesterol are not clinically equivalent and frequently discordant. As N-HDL may be superior to even C-LDL for predicting events in statin-treated patients, utilizing N-HDL to guide therapy would appear to be preferable to D-LDL when C-LDL is inaccurate. 1. Introduction Calculated low density lipoprotein cholesterol (LDL) is the cornerstone of lipid lowering therapy [1–3]. In certain clinical situations, namely, the fed state or when triglycerides are greater than 400?mg/dL, calculated LDL is inaccurate and the guidelines recommend the use of directly measured LDL cholesterol [1]. We previously reported that calculated and directly measured LDL are not clinically equivalent when targeting ATP III goals with lipid lowering therapy in a significant number of patients [4]. Based on this finding, we recommended that non-HDL cholesterol (N-HDL), an accepted, inexpensive, and guideline-based measure of atherogenic particles, available from the routine lipid panel, replace directly measured LDL (D-LDL) when the calculated LDL (C-LDL) is inaccurate [4]. However, few studies are available comparing the clinical equivalence of calculated LDL, directly measured LDL, and non-HDL cholesterol measurements. Therefore, we evaluated the clinical equivalence of N-HDL and D-LDL which would allow us to determine which lipid measure is more appropriate when C-LDL is inaccurate. 2. Methods Our population consisted of 81 subjects from the Bronx Veterans Affairs Medical Center recruited for 2 research studies from January 2007 through March 2009. The studies


[1]  J. I. Cleeman, “Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III),” Journal of the American Medical Association, vol. 285, no. 19, pp. 2486–2497, 2001.
[2]  R. McPherson, J. Frohlich, G. Fodor, and J. Genest, “Canadian Cardiovascular Society position statement—recommendations for the diagnosis and treatment of dyslipidemia and prevention of cardiovascular disease,” Canadian Journal of Cardiology, vol. 22, no. 11, pp. 913–927, 2006.
[3]  S. M. Grundy, J. I. Cleeman, C. N. Merz, et al., “National Heart, Lung, and Blood Institute, American College of Cardiology Foundation, American Heart Association. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines,” Circulation, vol. 110, pp. 227–239, 2004.
[4]  L. Baruch, S. Agarwal, B. Gupta et al., “Is directly measured low-density lipoprotein clinically equivalent to calculated low-density lipoprotein?” Journal of clinical lipidology, vol. 4, no. 4, pp. 259–264, 2010.
[5]  K. A. Foley, R. J. Simpson, J. R. Crouse, T. W. Weiss, L. E. Markson, and C. M. Alexander, “Effectiveness of statin titration on low-density lipoprotein cholesterol goal attainment in patients at high risk of atherogenic events,” American Journal of Cardiology, vol. 92, no. 1, pp. 79–81, 2003.
[6]  J. J. Kastelein, W. A. van der Steeg, I. Holme, et al., “Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment,” Circulation, vol. 117, pp. 3002–3009, 2008.
[7]  P. M. Ridker, N. Rifai, N. R. Cook, G. Bradwin, and J. E. Buring, “Non-HDL cholesterol, apolipoproteins A-I and B100, standard lipid measures, lipid ratios, and CRP as risk factors for cardiovascular disease in women,” Journal of the American Medical Association, vol. 294, no. 3, pp. 326–333, 2005.
[8]  T. Pischon, C. J. Girman, F. M. Sacks, N. Rifai, M. J. Stampfer, and E. B. Rimm, “Non-high-density lipoprotein cholesterol and apolipoprotein B in the prediction of coronary heart disease in men,” Circulation, vol. 112, no. 22, pp. 3375–3383, 2005.
[9]  Y. Cui, R. S. Blumenthal, J. A. Flaws, et al., “Non-high-density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality,” Archives of Internal Medicine, vol. 161, pp. 1413–1419, 2001.
[10]  B. J. Arsenault, J. S. Rana, E. S. G. Stroes et al., “Beyond low-density lipoprotein cholesterol. Respective contributions of non-high-density lipoprotein cholesterol levels, triglycerides, and the total cholesterol/high-density lipoprotein cholesterol ratio to coronary heart disease risk in apparently healthy men and women,” Journal of the American College of Cardiology, vol. 55, no. 1, pp. 35–41, 2009.
[11]  J. G. Robinson, S. Wang, B. J. Smith, and T. A. Jacobson, “Meta-analysis of the relationship between non-high-density lipoprotein cholesterol reduction and coronary heart disease risk,” Journal of the American College of Cardiology, vol. 53, no. 4, pp. 316–322, 2009.
[12]  M. J. Blaha, R. S. Blumenthal, E. A. Brinton, and T. A. Jacobson, “The importance of non-HDL cholesterol reporting in lipid management,” Journal of Clinical Lipidology, vol. 2, no. 4, pp. 267–273, 2008.
[13]  J. D. Brunzell, M. Davidson, C. D. Furberg et al., “Lipoprotein management in patients with cardiometabolic risk. Consensus conference report from the american diabetes association and the american college of cardiology foundation,” Journal of the American College of Cardiology, vol. 51, no. 15, pp. 1512–1524, 2008.
[14]  J. H. Contois, J. P. McConnell, A. A. Sethi et al., “Apolipoprotein B and cardiovascular disease risk: position statement from the AACC lipoproteins and vascular diseases division working group on best practices,” Clinical Chemistry, vol. 55, no. 3, pp. 407–419, 2009.
[15]  M. H. Davidson, C. M. Ballantyne, T. A. Jacobson, et al., “Clinical utility of inflammatory markers and advanced lipoprotein testing: advice from an expert panel of lipid specialists,” Journal of Clinical Lipidology, vol. 5, pp. 338–567, 2011.
[16]  S. M. Boekholdt, B. J. Arsenault, S. Mora, et al., “Association of LDL cholesterol, non-HDL cholesterol, and apolipoprotein B levels with risk of cardiovascular events among patients treated with statins: a meta-analysis,” The Journal of the American Medical Association, vol. 307, pp. 1302–1309, 2012.


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