Abstract
Background and Aims: A pathogenic variant in the LDLR, APOB, or PCSK9 genes can be identified in 30 – 80% of patients with clinically-diagnosed familial hypercholesterolemia (FH). Alternatively, ∼20% of clinical FH is thought to have a polygenic cause. The cardiovascular disease (CVD) risk associated with polygenic versus monogenic FH has not been previously determined. We evaluated the impact of monogenic and polygenic causes of FH on premature (age<55 years) CVD events in patients with clinically-diagnosed FH.
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