The association between elevated plasma levels of lipoprotein (a) [Lp(a)] and atherosclerotic cardiovascular disease (ASCVD) has been discussed for many years.
Lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerosis-related events that is under strong genetic control (heritability = 0.68-0.98).
Novel therapeutic strategy for atherosclerosis: ribozyme oligonucleotides against apolipoprotein(a) selectively inhibit apolipoprotein(a) but not plasminogen gene expression.
The purpose of this review is to highlight our emerging understanding of lipoprotein(a) [Lp(a)]'s role in atherosclerotic cardiovascular disease (ASCVD), its structure-function relationship, and promising developments within the therapeutic pipeline.
Mechanistically, elevated Lp(a) levels may either induce a prothrombotic/anti-fibrinolytic effect as apolipoprotein(a) resembles both plasminogen and plasmin but has no fibrinolytic activity, or may accelerate atherosclerosis because, like LDL, the Lp(a) particle is cholesterol-rich, or both.
A considerable body of data from genetic and epidemiological studies strongly support a causal relationship between high lipoprotein(a) [Lp(a)] levels, and the development of atherosclerosis and cardiovascular disease.
Genetic dyslipidemias can be identified in over 75% of CAD patients and include the atherosclerosis susceptibility trait (low density lipoprotein [LDL] pattern B), hyperapobetalipoproteinemia, lipoprotein (a), apo E isoforms, and lipoprotein susceptibility to oxidative damage.
We identified circulating miR-212 as a novel marker of atherosclerosis. miR-212 enhanced the estimation of atherosclerosis presence in combination with hemoglobin A1c, high-density lipoprotein cholesterol, and lipoprotein(a).
The apo(a) [apolipoprotein(a)] gene is responsible for variations in plasma lipoprotein(a), high levels of which are a risk factor for atherosclerosis and myocardial infarction.
Increased concentrations of low-density-lipoprotein (LDL)-cholesterol (LDL-C) and lipoprotein a (Lp(a)) are scientifically accepted, independent risk factors for the development of atherosclerosis.
Evaluating the Potential Association Between Lipoprotein(a) and Atherosclerosis (from the Mediators of Atherosclerosis Among South Asians Living in America Cohort).
FV Leiden was not a useful predictor (p=0.23) of the presence of clinically defined atherosclerosis (> or = 50% stenosis) in a logistic regression model adjusting for age, lipoprotein (a), total cholesterol, triglycerides, high density lipoprotein cholesterol, and fibrinogen.
Elevated plasma levels of lipoprotein(a) [Lp(a)], referred to as lipoprotein(a)-hyperlipoproteinemia [Lp(a)-HLP], are an independent risk factor for atherosclerosis.
Defects in the low density lipoprotein receptor gene affect lipoprotein (a) levels: multiplicative interaction of two gene loci associated with premature atherosclerosis.
Transgenic mice expressing human apolipoprotein(a) develop aortic lesions resembling the early stages of human atherosclerosis after 3.5 months on a high fat diet.
Nontraditional cardiovascular risk factors such as lipoprotein(a) (Lp(a)), the genetic polymorphisms of apolipoprotein(a), apolipoprotein E (ApoE), and apolipoprotein B (ApoB) increase the prevalence of atherosclerosis in end-stage renal disease (ESRD) through quantitative and qualitative alterations.