Lipoprotein(a) (Lp(a)) consists of LDL-like particle covalently banded with apolipoprotein (a) [apo(a)]. Apo(a) is encoded by LPA gene localized on chromosome 6q27 and consists of loop-like structures called cringles. KIV-2 copy number variation (from 1 to 40 repeat sequences) polymorphism is the most important predictor of variations in Lp(a) concentration. Small isoforms (≤22 KIV repeats) are related to 4 to 5-fold higher Lp(a) concentrations than large isoforms (>22 KIV). Roeseler at al. reported that 95% patients with CVD undergoing lipoprotein apheresis (LA) therapy expressed at least one small apo(a) isoform.

Familial Hypercholesterolemia (FH) is one of the most common genetic disorders in humans with a prevalence of 1:311.1 It is an autosomal dominant trait, affecting males and females equally. Loss-of-function variants in the low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), or gain-of-function in protein convertase subtilisin/kesin-9 (PCSK9) genes are most commonly responsible for the FH phenotype, which is characterized by an excessive accumulation of low-density lipoprotein cholesterol (LDL-C) in the blood, leading to elevated lifetime risk of atherosclerotic cardiovascular disease (ASCVD) and premature ASCVD (defined as <55 years in men and <65 years in women).