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Genetics of coronary artery calcification among African Americans, a meta-analysis. 2013
Mary K Wojczynski, and
Mingyao Li, and
Lawrence F Bielak, and
Kathleen F Kerr, and
Alex P Reiner, and
Nathan D Wong, and
Lisa R Yanek, and
Liming Qu, and
Charles C White, and
Leslie A Lange, and
Jane F Ferguson, and
Jing He, and
Taylor Young, and
Thomas H Mosley, and
Jennifer A Smith, and
Brian G Kral, and
Xiuqing Guo, and
Quenna Wong, and
Santhi K Ganesh, and
Susan R Heckbert, and
Michael E Griswold, and
Daniel H O'Leary, and
Matthew Budoff, and
J Jeffrey Carr, and
Herman A Taylor, and
David A Bluemke, and
Serkalem Demissie, and
Shih-Jen Hwang, and
Dina N Paltoo, and
Joseph F Polak, and
Bruce M Psaty, and
Diane M Becker, and
Michael A Province, and
Wendy S Post, and
Christopher J O'Donnell, and
James G Wilson, and
Tamara B Harris, and
Maryam Kavousi, and
L Adrienne Cupples, and
Jerome I Rotter, and
Myriam Fornage, and
Lewis C Becker, and
Patricia A Peyser, and
Ingrid B Borecki, and
Muredach P Reilly
Department of Genetics, Division of Statistical Genomics, Washington University School of Medicine, St. Louis, MO, USA. mwojczynski@wustl.edu
BACKGROUND Coronary heart disease (CHD) is the major cause of death in the United States. Coronary artery calcification (CAC) scores are independent predictors of CHD. African Americans (AA) have higher rates of CHD but are less well-studied in genomic studies. We assembled the largest AA data resource currently available with measured CAC to identify associated genetic variants. METHODS We analyzed log transformed CAC quantity (ln(CAC + 1)), for association with ~2.5 million single nucleotide polymorphisms (SNPs) and performed an inverse-variance weighted meta-analysis on results for 5,823 AA from 8 studies. Heritability was calculated using family studies. The most significant SNPs among AAs were evaluated in European Ancestry (EA) CAC data; conversely, the significance of published SNPs for CAC/CHD in EA was queried within our AA meta-analysis. RESULTS Heritability of CAC was lower in AA (~30%) than previously reported for EA (~50%). No SNP reached genome wide significance (p < 5E-08). Of 67 SNPs with p < 1E-05 in AA there was no evidence of association in EA CAC data. Four SNPs in regions previously implicated in CAC/CHD (at 9p21 and PHACTR1) in EA reached nominal significance for CAC in AA, with concordant direction. Among AA, rs16905644 (p = 4.08E-05) had the strongest association in the 9p21 region. CONCLUSIONS While we observed substantial heritability for CAC in AA, we failed to identify loci for CAC at genome-wide significant levels despite having adequate power to detect alleles with moderate to large effects. Although suggestive signals in AA were apparent at 9p21 and additional CAC and CAD EA loci, overall the data suggest that even larger samples and an ethnic specific focus will be required for GWAS discoveries for CAC in AA populations.
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