A modified form of LDL, structurally similar to plasminogen, which may impair fibrinolysis, increase plaque formation and thrombosis.

Association exists between higher circulating lipoprotein (a) concentrations and an increase risk of atherosclerotic cardiovascular disease, in addition there is support for it as a causal role for calcific valvular aortic stenosis.

High levels of Lipo, protein (A) a protein that carries cholesterol through the blood is tied to increased cardiovascular risk.

Composed of a low density lipoprotein-like moiety found covalently to apolipoprotein(a).

Circulating Lipoproteins (a) concentrations are almost exclusively, determined genetically, and do not affect by traditional approaches to cardiovascular risk reduction, including statins, and lifestyle modifications.

Lipoprotein (a) is produced from the binding of Apoloprortein (a) to April Loop proprotein B.

LPA gene encodes for Apolipoprotein a, a dominant and rate limiting component in the hepatic synthesis of the lipoprotein a particle.

It is a cholesterol carrying, apolipoprotein b containing lipoprotein that has an apoliporotein a moiety conveniently attached to its apolipoprotein b molecule.

The attached apolipoprotein a moiety interferes with the interaction between lipoprotein a and the apoliporotein b dependent low density lipoprotein receptor, resulting in a long circulating half-life and accumulation of oxidized phospholipids within Lipoprotein a.

Lipoprotein (a) potentially contributes to cardiovascular disease via pro atherogenic effects of its LDL like moiety, proinflammatory effects on its oxidized phospholipid content, and prothrombotic effects through its inactive, plasminogen-like protease domain on apolipoprotein (a).

Elevated levels are a recognized causal risk factor in atherosclerotic cardiovascular disease.

Lipoprotein a can become trapped within the artery wall to participate in the initiation and progression of atherosclerotic plaque.

Because of its long circulating half-life and high concentration of oxidized phospholipids, lipoprotein a particles may be more atherogenic and other Apo B  be containing Lipoproteins despite carrying less cholesterol.

It is a heritable risk factor, and is recommended that at least a single measurement of LP(a) be done  in one’s lifetime, as it is relatively stable over a lifetime and repeated measurements are generally not necessary.

Unlike low density lipoprotein and other apolipoproteins B containing Lipoproteins, plasma concentrations of lipoprotein are stable throughout life and are not affected by diet or lifestyle choices.

Lipoprotein levels can only be lowered with biological pharmacological interventions or by apheresis.

Synthesized by the liver and consists of an apolipoprotein(a B100 molecule covalently linked to a very large glycoprotein known as apolipoprotein(a).

Genetic, epidemiologic, and mechanistic evidence supports the fact that elevated plasma Lipo protein(a) is an independent genetic risk factors for cardiovascular disease and calcific aortic-valve stenosis.

Patients with lipoprotein a concentrations in the highest decile of approximately 350 nmol per liter have a lifetime risk of cardiovascular disease equivalent to those with familial hypercholesterolemia.

Elevated levels of lipoprotein a are associated with aortic valve calcification, development and more rapid progression of aortic stenosis, and a higher rate of aortic valve replacement.

Genetically related low levels of lipoprotein (a) is associated with decreased risk of cardiovascular disease but not of other non-cardiovascular disease adverse phenotypes.

No data indicates that lowering lipoprotein(a) levels leads to clinical benefit.

No pharmacological agent has been approved for treatment of elevated lipoprotein a.

Randomized clinical trials of several classes of lipid lowering therapies that reduce lipoprotein a by 20 to 25% have consistently failed to demonstrate that the lower lipoprotein a reduces the risk of cardiovascular events beyond what would be expected from the corresponding reduction of low density lipoprotein and other apo-B containing Lipoproteins alone.

Patients with the highest levels have a 70% increase in coronary artery risk over patients with the lowest levels.

The plasma concentration of Lipoprotein (a) is  primarily genetically determined with approximately 70 to 90% expression by the apolipoprotein (a) gene LPA.

Measurement of lipoprotein(a) (Lp(a)) at least once in each adult’s lifetime should be done to identify those with very high inherited Lp(a) levels above 180 mg/dL (>430 nmol/L) who may have a lifetime risk of atherosclerotic CV disease (ASCVD) that is equivalent to the risk associated with heterozygous familial hypercholesterolemia (FH).

A LDL particle bound to a plasminogen like lipoprotein, apolipoprotein(a).

Levels can vary up to 1000 fold.

Enters the arterial intima and can promote thrombosis, inflammation and foam cell formation.

Levels are partly determined by polymorphisms in the LPA gene coding for the apolipoprotein(a) moiety of lipoprotein(a).

Kringle IV type 2 is the most influential LPA polymorphism.

The number of kringle IV type 2 (KIV-2) repeats correlates inversely with levels of lipoprotein(a).

In prospective population study with 16 years of follow-up 8637 patients with 599 myocardial infarction events demonstrated an association between lipoprotein(a) level and MI , and association with KIV-2 to genotype and lipoprotein(a, and an association between KIV-2 genotype and MI.

Concentrations are modulated prinarily by polymorphisms in the LPA gene affecting its production.

Concentrations are higher in pateitns with familil hypercholesterolemia than in people with healthy lipids.

Is similar to LDL which has a reduced plasma clearance in familial hypercholesterolemia

Studies suggest lipoprotein(a) (Lp[a]) is both proatherosclerotic and prothrombotic.

Elevated plasma levels of Lp(a) have been linked to increased risk for coronary heart disease and stroke.

Lp(a) is also associated with atherosclerotic cardiovascular disease which, in turn, is linked with atrial fibrillation (AF).

Lp(a) levels are about three times higher in blacks vs whites and 15% to 20% higher in women vs men,however the incidence of AF in blacks and women is lower.

No currently approved pharmacological therapy specifically targets lipoproteins(a).

A hepatocyte directed anti-sense oligonucleotide AKCEA-APO(a)-L reduces lipoprotein (a) levels in a dose dependent manner.

Olpasiran, a small interfering RNA molecule that disrupts expression of LPA, degrading apolipoprotein (a) mRNA preventing assembly of the lipoprotein (a) particle in the hepatocyte: significantly reduced lipoprotein(a) concentrations in patients with established atherosclerotic cardiovascular disease (O’Donoghue ML).



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