The evidence that plasma levels of apolipoprotein B and apolipoprotein AI are important determinants of the risk of premature coronary artery disease (CAD) are reviewed and a metabolic framework for these relations presented.
The children with heFH with a family history of pCAD had higher LDL cholesterol and apolipoprotein B levels and greater aIMT and cIMT than those with negative family history.
In adults, a low density lipoprotein cholesterol (LDL-C)/apolipoprotein B-100 (ApoB) ratio is an indicator of ApoB-enriched small dense LDL, which is associated with premature coronary artery disease (CAD).
This employs the personal and family history of premature coronary artery disease and hypercholesterolemia and the presence of a pathogenic mutation in the low-density lipoprotein receptor (LDLR) and apolipoprotein B (APOB) genes.
In a family with premature coronary artery disease and hyperapo-beta-lipoproteinaemia, a mutation in codon 4046 in exon 29 of the apolipoprotein B gene, a CGG to TGG transition produced a change from arginine, a positively charged amino acid, to tryptophan, a hydrophobic amino acid, at position 4,019 of the mature apolipoprotein B protein.