Lp(a) stands for Lipoprotein little a. It is a small, cholesterol-rich protein produced in the liver that can enter the bloodstream, allowing for measurement of Lp(a) levels. These levels are genetically determined, meaning individuals are born with them. High levels of Lp(a) are common, affecting about 1 in 5 people or 20% of the population.

Elevated levels of Lp(a) have been associated with increased cardiovascular risk in the general population and particularly in individuals with familial hypercholesterolemia. Those with high Lp(a) levels are at a greater risk of stroke and heart attacks, with a 2 to 4 times increased risk of cardiovascular disease compared to those with lower Lp(a) levels.

Lp(a) is known to be pro-inflammatory, proatherogenic, and prothrombogenic, making artery walls more prone to inflammation, clot formation, and potential blockages. Structurally, Lp(a) has a unique composition with a shell made of LDL cholesterol attached to a protein called Apo(a). Apo(a) shares structural similarities with plasminogen, which may competitively inhibit the conversion of plasminogen to plasmin. This can lead to increased fibrin levels, promoting thrombogenesis.

Most individuals typically have Lp(a) levels ranging from 5 to 30 mg/dL. Cardiovascular risk begins to rise at 30 mg/dL and escalates more sharply at 50 mg/dL. Levels exceeding 50 mg/dL are currently considered pathological, although this remains a topic of debate. Routine measurement of Lp(a) is not common, and guidelines are evolving on when and in whom to measure it, often based on available treatment options.

Various treatment options are being explored to reduce Lp(a) levels, such as niacin, lipid apheresis, or PCSK9 inhibitors. Notably, statin therapy has shown limited impact on Lp(a) levels and associated cardiovascular risk.