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In this study, Lp(a) was estimated from exome data by quantifying Kringle IV subtype 2 repeats alongside a single-nucleotide variant-based genetic risk score. This method was applied to a diverse cohort (N = 76,147) from the Helix Research Network. The method better identified individuals with high Lp(a) levels, especially among individuals not genetically similar to Europeans. High genetic risk for high Lp(a) level was correlated with earlier and more frequent ASCVD diagnoses. 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