Abstract
Background and Aims: Background: A polygenic background can be recognized in part of patients with clinically diagnosed familial hypercholesterolemia (FH). The phenotypical distinction between monogenic (due to causative mutations in major LDLR, APOB or PCSK9 genes) and polygenic FH is not completely clarified. Aims: We aimed to compare the clinical phenotype and response to treatment in monogenic vs. polygenic FH
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