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1
Division of Endocrinology, Diabetes, Metabolism and Molecular Medicine, New England Medical Center and Tufts University School of Medicine, 750 Washington St., Boston, MA 02111.
2
Lipid Metabolism Laboratory, Jean Mayer US Department of
Agriculture Human Nutrition Research Center on Aging at Tufts
University, Boston, MA 02111.
3
Department of Epidemiology and Biostatistics, Boston
University School of Public Health, Boston, MA 02118-2394.
4
Framingham Heart Study, National Institutes of Health,
National Heart, Lung, and Blood Institute, Framingham, MA
01702.
a Address correspondence to this author at: New England Medical Center, Box 216, 750 Washington St., Boston, MA 02111.
Background: Increased plasma lipoprotein(a) [Lp(a)] concentrations have been reported to be an independent risk factor for coronary heart disease (CHD) in some prospective studies, but not in others. These inconsistencies may relate to a lack of standardization and the failure of some immunoassays to measure all apolipoprotein(a) isoforms equally.
Methods: We measured plasma Lp(a)-cholesterol [Lp(a)-C] in a Caucasian population of offspring and spouses of the Framingham Heart Study participants, using a lectin-based assay (LipoproTM). We compared the prevalence of increased Lp(a)-C to the presence of sinking pre-ß-lipoprotein (SPB). We also related Lp(a)-C concentrations to the prevalence of CHD risk in the entire population.
Results: The mean (± SD) Lp(a)-C concentration in the Framingham
population (n = 3121) was 0.186 ± 0.160 mmol/L, with no
significant gender or age differences. The mean Lp(a)-C concentrations
in the absence or presence of SPB were 0.158 ± 0.132 mmol/L and
0.453 ± 0.220 mmol/L, respectively (P <0.0001).
The mean Lp(a)-C concentration in men with CHD (n = 156) was
0.241 ± 0.204 mmol/L, which was significantly (P
<0.001) higher, by 34%, than in controls. The odds ratio for CHD risk
in men with Lp(a)-C 
0.259 mmol/L (10 mg/dL), after adjusting for
age, HDL-cholesterol, LDL-cholesterol, smoking, diabetes, blood
pressure, and body mass index, was 2.293 (confidence interval,
1.55–3.94; P <0.0005). Lp(a)-C values correlated
highly with a Lp(a)-mass immunoassay [ApotekTM
Lp(a); r = 0.832; P <0.0001; n
= 1000].
Conclusions: An increased Lp(a)-C value 0.259 mmol/L (10
mg/dL) is an independent CHD risk factor in men with a relative risk of
more than 2, but was inconclusive in women. Lp(a)-C measurements offer
an alternative to Lp(a)-mass immunoassays and can be performed on
automated analyzers.© 1999 American Association for Clinical
Chemistry
The following articles in journals at HighWire Press have cited this article:
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  M Sawabe, N Tanaka, K Nakahara, A Hamamatsu, K Chida, T Arai, K Harada, T Inamatsu, T Ozawa, M M Naka, et al. High lipoprotein(a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autopsy cases Heart, December 15, 2009; 95(24): 1997 - 2002. [Abstract] [Full Text] [PDF]
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J. Suk Danik, N. Rifai, J. E. Buring, and P. M Ridker Lipoprotein(a), measured with an assay independent of apolipoprotein(a) isoform size, and risk of future cardiovascular events among initially healthy women. JAMA, September 20, 2006; 296(11): 1363 - 1370. [Abstract] [Full Text] [PDF]
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S. S. AbuMweis, C. A. Vanstone, N. Ebine, A. Kassis, L. M. Ausman, P. J. H. Jones, and A. H. Lichtenstein Intake of a Single Morning Dose of Standard and Novel Plant Sterol Preparations for 4 Weeks Does Not Dramatically Affect Plasma Lipid Concentrations in Humans J. Nutr., April 1, 2006; 136(4): 1012 - 1016. [Abstract] [Full Text] [PDF]
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 I. J. Kullo and C. M. Ballantyne Conditional Risk Factors for Atherosclerosis Mayo Clin. Proc., February 1, 2005; 80(2): 219 - 230. [Abstract] [PDF]
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R. J. Sharp, M. A. Perugini, S. M. Marcovina, and S. P. A. McCormick Structural features of apolipoprotein B synthetic peptides that inhibit lipoprotein(a) assembly J. Lipid Res., December 1, 2004; 45(12): 2227 - 2234. [Abstract] [Full Text] [PDF]
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J. McKenney New Perspectives on the Use of Niacin in the Treatment of Lipid Disorders Arch Intern Med, April 12, 2004; 164(7): 697 - 705. [Abstract] [Full Text] [PDF]
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 V. Tsimihodimos, A. Kostoula, A. Kakafika, E. Bairaktari, A. D. Tselepis, D. P. Mikhailidis, and M. Elisaf Effect of Fenofibrate on Serum Inflammatory Markers in Patients With High Triglyceride Values Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2004; 9(1): 27 - 33. [Abstract] [PDF]
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 N. S. Haque, J. T. Fallon, J. J. Pan, M. B. Taubman, and P. C. Harpel Chemokine receptor-8 (CCR8) mediates human vascular smooth muscle cell chemotaxis and metalloproteinase-2 secretion Blood, February 15, 2004; 103(4): 1296 - 1304. [Abstract] [Full Text] [PDF]
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C. Y. Y. Liu, R. Broadhurst, S. M. Marcovina, and S. P. A. McCormick Mutation of lysine residues in apolipoprotein B-100 causes defective lipoprotein[a] formation J. Lipid Res., January 1, 2004; 45(1): 63 - 70. [Abstract] [Full Text] [PDF]
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 R. J. Sharp, M. A. Perugini, S. M. Marcovina, and S. P.A. McCormick A Synthetic Peptide That Inhibits Lipoprotein(a) Assembly Arterioscler Thromb Vasc Biol, March 1, 2003; 23(3): 502 - 507. [Abstract] [Full Text] [PDF]
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References Circulation, December 17, 2002; 106(25): 3373 - 3421. [Full Text]
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 O. I Bermudez, W. Velez-Carrasco, E. J Schaefer, and K. L Tucker Dietary and plasma lipid, lipoprotein, and apolipoprotein profiles among elderly Hispanics and non-Hispanics and their association with diabetes Am. J. Clinical Nutrition, December 1, 2002; 76(6): 1214 - 1221. [Abstract] [Full Text] [PDF]
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 M.B. Andresdottir, G. Sigurdsson, H. Sigvaldason, and V. Gudnason Fifteen percent of myocardial infarctions and coronary revascularizations explained by family history unrelated to conventional risk factors. The Reykjavik Cohort Study Eur. Heart J., November 1, 2002; 23(21): 1655 - 1663. [Abstract] [Full Text] [PDF]
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E. J Schaefer Lipoproteins, nutrition, and heart disease Am. J. Clinical Nutrition, February 1, 2002; 75(2): 191 - 212. [Abstract] [Full Text] [PDF]
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A. R. Sharrett, C. M. Ballantyne, S. A. Coady, G. Heiss, P. D. Sorlie, D. Catellier, and W. Patsch Coronary Heart Disease Prediction From Lipoprotein Cholesterol Levels, Triglycerides, Lipoprotein(a), Apolipoproteins A-I and B, and HDL Density Subfractions: The Atherosclerosis Risk in Communities (ARIC) Study Circulation, September 4, 2001; 104(10): 1108 - 1113. [Abstract] [Full Text] [PDF]
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Y. Cui, R. S. Blumenthal, J. A. Flaws, M. K. Whiteman, P. Langenberg, P. S. Bachorik, and T. L. Bush Non-High-Density Lipoprotein Cholesterol Level as a Predictor of Cardiovascular Disease Mortality Arch Intern Med, June 11, 2001; 161(11): 1413 - 1419. [Abstract] [Full Text] [PDF]
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J. Ordonez-Llanos, A. M. Wagner, R. Bonet-Marques, J. L. Sanchez-Quesada, F. Blanco-Vaca, and F. Gonzalez-Sastre Which Cholesterol Are We Measuring with the Roche Direct, Homogeneous LDL-C Plus Assay? Clin. Chem., January 1, 2001; 47(1): 124 - 126. [Full Text] [PDF]
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N. S. Haque, J. T. Fallon, M. B. Taubman, and P. C. Harpel The chemokine receptor CCR8 mediates human endothelial cell chemotaxis induced by I-309 and Kaposi sarcoma herpesvirus-encoded vMIP-I and by lipoprotein(a)-stimulated endothelial cell conditioned medium Blood, January 1, 2001; 97(1): 39 - 45. [Abstract] [Full Text] [PDF]
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M. von Depka, U. Nowak-Gottl, R. Eisert, C. Dieterich, M. Barthels, I. Scharrer, A. Ganser, and S. Ehrenforth Increased lipoprotein (a) levels as an independent risk factor for venous thromboembolism Blood, November 15, 2000; 96(10): 3364 - 3368. [Abstract] [Full Text] [PDF]
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N. S. Haque, X. Zhang, D. L. French, J. Li, M. Poon, J. T. Fallon, B. R. Gabel, M. B. Taubman, M. Koschinsky, and P. C. Harpel CC Chemokine I-309 Is the Principal Monocyte Chemoattractant Induced by Apolipoprotein(a) in Human Vascular Endothelial Cells Circulation, August 15, 2000; 102(7): 786 - 792. [Abstract] [Full Text] [PDF]
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M. Nauck, W. Marz, and H. Wieland Is Lipoprotein(a) Cholesterol a Significant Indicator of Cardiovascular Risk? Clin. Chem., March 1, 2000; 46(3): 436 - 437. [Full Text] [PDF]
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