Familial hypercholesterolemia (FH) is one of the most common genetic disorders of cholesterol metabolism [6], and the mutations in FH-associated genes, such as low-density lipoprotein receptor (LDLR), apolipoprotein B (APOB), proprotein convertase subtilisin/kexin type 9 (PCSK9) and low-density lipoprotein receptor adaptor protein 1 (LDLRAP1), can increase the plasma levels of low-density lipoprotein cholesterol (LDL-C) and lead to PMI. This evidence concerns the gene LDLR and familial hypercholesterolemia.