Lipoprotein (a)

Lipoprotein (a) or Lp(a) is a type of lipoprotein closely related to LDL cholesterol, but it includes a protein called apolipoprotein (a), which is attached to the LDL-like particle. The structure of Lp(a) is similar to that of plasminogen, which plays a key role in the body's process of breaking down blood clots. This similarity in structure is thought to interfere with the body's ability to dissolve clots, potentially leading to an increased risk of cardiovascular disease (CVD).

Structure and Function[edit | edit source]

Lp(a) consists of an LDL-like particle and one molecule of apolipoprotein (a), which is covalently linked to the apolipoprotein B-100 on the LDL particle. The apolipoprotein (a) component varies greatly in size among different individuals due to a genetic variation in the number of kringle IV type 2 repeats. This genetic variation is the primary determinant of Lp(a) levels in blood, which are highly heritable and vary widely between individuals and different ethnic groups.

The exact physiological function of Lp(a) is not fully understood, but it is believed to play a role in wound healing, cellular repair, and angiogenesis, possibly due to its structural similarity to plasminogen. However, its resemblance to plasminogen also suggests a potential role in thrombosis and atherogenesis, contributing to its association with cardiovascular diseases.

Health Implications[edit | edit source]

Elevated levels of Lp(a) in the blood are associated with an increased risk of cardiovascular diseases such as coronary artery disease (CAD), stroke, and peripheral arterial disease. High Lp(a) levels are considered an independent risk factor for CVD, meaning that individuals with high Lp(a) levels have a higher risk of developing CVD regardless of other risk factors such as high LDL cholesterol levels, hypertension, or diabetes.

The mechanisms by which Lp(a) contributes to cardiovascular risk are not entirely clear but are thought to involve promotion of atherosclerosis through the deposition of cholesterol in the arterial wall, inhibition of fibrinolysis leading to increased clot formation, and inflammatory effects within atherosclerotic plaques.

Measurement and Treatment[edit | edit source]

Lp(a) levels are measured through a blood test. However, there is currently no consensus on the optimal levels of Lp(a), partly due to the variability in measurement methods and the lack of standardized units. Treatment options for high Lp(a) levels are limited. Niacin (vitamin B3) has been shown to lower Lp(a) levels, but its use is limited by side effects and a lack of evidence that it reduces cardiovascular risk. Recently, new cholesterol-lowering drugs such as PCSK9 inhibitors have been shown to reduce Lp(a) levels, but their long-term effects on cardiovascular outcomes are still being studied.

Lifestyle changes such as diet and exercise have not been shown to significantly affect Lp(a) levels, highlighting the importance of genetic factors in determining these levels. As research continues, more effective treatments for high Lp(a) levels and their impact on cardiovascular disease may be discovered.