A unique construct of low-density lipoprotein (LDL), lipoprotein[a] has been shown to be a valuable independent risk factor for coronary artery disease.
Lipoprotein(a) interactions with lipid and non-lipid risk factors in patients with early onset coronary artery disease: results from the NHLBI Family Heart Study.
High plasma concentrations of lipoprotein(a) [Lp(a)], a covalent low-density lipoprotein-apolipoprotein(a) [apo(a)] complex, are associated with coronary heart disease and stroke.
The purpose of this study was to investigate lipoprotein(a) [Lp(a)] levels and apolipoprotein(a) [apo(a)] phenotypes in relation to age of onset of coronary heart disease (CHD).
High plasma concentrations of lipoprotein(a) [Lp(a)], a covalent low-density lipoprotein-apolipoprotein(a) [apo(a)] complex, are associated with coronary heart disease and stroke.
Since up to 90% of the variance in Lp(a) levels has been suggested to be attributable to the apo(a) locus, the hypothesis that polymorphisms of the apo(a) gene other than size could contribute to the increase of Lp(a) levels in CHD patients must be considered.
To examine the association between the Family Risk Score (FRS) for coronary heart disease (CHD) and body mass index (BMI), waist-to-hip ratio (WHR), high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol, triglycerides, and lipoprotein(a) protein [Lp(a)].
High plasma lipoprotein(a) [Lp(a)] levels have been implicated as an independent risk factor for coronary artery disease in Caucasians, Chinese, Africans, and Indians.
Single effects of apolipoprotein B, (a), and E polymorphisms and interaction between plasminogen activator inhibitor-1 and apolipoprotein(a) genotypes and the risk of coronary artery disease in Czech male caucasians.
Polymorphisms in human apolipoprotein(a) kringle IV-10 and coronary artery disease: relationship to allele size, plasma lipoprotein(a) concentration, and lysine binding site activity.
Variation in factors such as low-density lipoprotein cholesterol, apolipoprotein E, high-density lipoprotein cholesterol, apolipoprotein A-I/CIII/A-IV, lipoprotein lipase, cholesteryl ester transfer protein, lipoprotein (a), and homocysteine may affect CHD risk via genetic or environmental mechanisms or their interactions.
These results suggest that APO(a) phenotyping might be used in subjects with hyperlipoproteinemia a as a powerful marker to assess the risk of premature CHD because heterozygous status, mainly when both isoforms are equally expressed, is associated with higher cardiovascular risk.