Since CHDL level is inversely associated with coronary heart disease in adults, it is important to quantitate C-HDL and low-density lipoprotein cholesterol (C-LDL) in hypercholesterolemic children and to identify those with putatively reduced risk (elevated C-HDL level) or increased risk (elevated C-LDL level).
Evidently, apolipoprotein E polymorphism can contribute to total and LDL-cholesterol concentrations in serum, thereby affecting risk of coronary heart disease and myocardial infarction.
Using cloned apolipoprotein A-I and insulin gene probes, we determined the genotypes of 39 subjects from six different kindreds with familial clustering of hypertriglyceridemia, 20 additional unrelated subjects with hypertriglyceridemia, 39 patients with angiographically confirmed coronary heart disease (CHD) and 61 normolipemic control subjects.
These findings suggest that low levels of HDL2-C in children may identify families in which there is an increased risk of coronary heart disease and that parental smoking may contribute to changes in this risk factor in the children of smokers as well as in the smokers themselves.
A mutant form of apolipoprotein E that is defective in binding to low density lipoprotein receptors is associated with familial type III hyperlipoproteinemia, a genetic disorder characterized by elevated plasma cholesterol levels and accelerated coronary artery disease.
Coronary heart disease risk correlates directly with plasma concentrations of lipoprotein(a) (Lp(a)), a low-density lipoprotein-like particle distinguished by the presence of the glycoprotein apolipoprotein(a) (apo(a)), which is bound to apolipoprotein B-100 (apoB-100) by disulfide bridges.
Coronary heart disease risk correlates directly with plasma concentrations of lipoprotein(a) (Lp(a)), a low-density lipoprotein-like particle distinguished by the presence of the glycoprotein apolipoprotein(a) (apo(a)), which is bound to apolipoprotein B-100 (apoB-100) by disulfide bridges.
Immunologically defined alleles of the pig apolipoprotein B (ApoB) locus (apoB) are correlated with different blood cholesterol levels and predisposition towards premature coronary heart disease.
The family at increased risk for future coronary heart disease is the family with a member who has 1) had one or more myocardial infarctions before age 55 years; 2) has levels of LDL cholesterol greater than 75th percentile for age; 3) has excessively low levels of HDL2 cholesterol; 4) has hypertension or has had a stroke, or both; 5) has excessive weight at any age and excessive weight gain during adulthood, or 6) smokes in the household.
Together these results suggest that inherited variations of the apolipoprotein-B gene, probably in the form of charged aminoacid substitutions, influence circulating cholesterol concentration, and that these and other functional variants of the apolipoprotein-B gene affect susceptibility to coronary heart disease and obesity.
Lipoprotein(a) [Lp(a)] is a macromolecular complex found in human plasma that combines structural elements from the lipoprotein and blood clotting systems and that is associated with premature coronary heart disease and stroke.
Homozygotes and compound heterozygotes (i.e., those who carry two different FH genes) are very rare (one in 1,000,000) have severe hypercholesterolemia with xanthomas, and develop coronary heart disease early in life.
Variation in the concentrations of both plasma and low density lipoprotein cholesterol, as well as apolipoprotein B, were related neither to age at death from CHD nor to the clinical course of CHD.