Abstract

Background and Aims: Coronary artery disease (CAD) resulting from atherosclerosis is the leading cause of death globally. GWAS of CAD-related phenotypes have identified >200 associations. However, causal variant identification via QTL studies remains limited by tissue availability and study population homogeneity. We used three complementary methods in an ancestrally diverse U.S. study population to characterize candidate causal genes affected by genetic variation in coronary artery tissue.

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