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Clin Chem. 2017 Nov;63(11):1705-1713. doi: 10.1373/clinchem.2016.270751. Epub 2017 Sep 13.

Evaluation of Lipoprotein(a) Electrophoretic and Immunoassay Methods in Discriminating Risk of Calcific Aortic Valve Disease and Incident Coronary Heart Disease: The Multi-Ethnic Study of Atherosclerosis.

Author information

1
Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX.
2
Department of Pathology, Texas Children's Hospital, Houston, TX.
3
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN.
4
Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN.
5
Department of Medicine, University of California, Los Angeles, CA.
6
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, MD.
7
Department of Medicine and Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY.
8
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN; tsaix001@umn.edu.

Abstract

BACKGROUND:

A number of lipoprotein(a) [Lp(a)] analytical techniques are available that quantify distinct particle components, yet their clinical efficacy has not been comprehensively evaluated. This study determined whether Lp(a) mass [Lp(a)-M], Lp(a) cholesterol content [Lp(a)-C], and particle concentration [Lp(a)-P] differentially discriminated risk of calcific aortic valve disease (CAVD) or incident coronary heart disease (CHD) among 4679 participants of the Multi-Ethnic Study of Atherosclerosis (MESA).

METHODS:

Lp(a)-M, Lp(a)-C, and Lp(a)-P were measured in individuals without clinical evidence of CHD at baseline. Relative risk regression and Cox proportional analysis determined associations between Lp(a) and the presence of CAVD or 12-year risk of CHD, respectively. To control for the relatively high lower limits of quantification for Lp(a)-C and Lp(a)-P assays, the upper 25th and 15th percentiles were selected as analytical cutoff points.

RESULTS:

Regardless of method or analytical cutoff, high Lp(a) concentrations were significantly associated with CAVD and CHD in MESA participants following adjustment for typical cardiovascular risk factors. Stratifying by race/ethnicity rendered most associations nonsignificant after correction for multiple comparisons, but Lp(a) remained associated with CAVD in whites irrespective of method (all P < 0.0001).

CONCLUSIONS:

Associations of Lp(a)-C, Lp(a)-P, and Lp(a)-M with CAVD or incident CHD were similar in this entire MESA sample using a dichotomized statistical approach. However, the high lower limits of quantification and imprecision of the Lp(a)-C and Lp(a)-P assays limited their usefulness in our analyses and would likely do so in research and clinical settings.

PMID:
28904058
DOI:
10.1373/clinchem.2016.270751
[Indexed for MEDLINE]
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