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Lipoprotein (a), often known as Lp(a), is a less well-known lipoprotein that has recently come to light as a significant risk factor for cardiovascular (ASCVD) disease. The intricate nature of Lp(a) will be thoroughly examined in this article. We will also address how Lp(a) affects ASCVD and distinguish it from apoB.
LDL-C, apoB, and Lp(a) – Understanding the Differences
In the realm of cardiovascular health, understanding the intricate interplay between LDL-C, apoB, and Lp(a) is crucial. These lipid markers play significant roles in shaping an individual’s risk of atherosclerotic cardiovascular disease (ASCVD). In this section, we will delve into their relationship and distinctive characteristics, shedding light on their impact on heart health.
- LDL-C (Low-Density Lipoprotein Cholesterol): Low-density lipoprotein (LDL) particles are packages that carry cholesterol around the body. The cholesterol is wrapped with a protein called Apolipoprotein B (ApoB) to make the particle water-soluble. LDL particles can end up in the artery wall and become oxidized and form atherosclerotic plaques, which are the cause of heart attacks and strokes.
- apoB (Apolipoprotein B): Several lipoproteins, mainly LDL and VLDL, contain the protein apoB. One apoB molecule is present in each LDL particle.
- Lp(a) (Lipoprotein (a)): Lp(a) is a lipoprotein particle that is similar to an LDL particle. It has an extra protein termed apo(a) attached to the ApoB molecule. It encourages the development of atherosclerotic plaques, and thrombosis, and is largely genetically predetermined.
- Relationship with cardiovascular disease: The risk of cardiovascular disease is increased by elevated apoB and LDL-C values. Lp(a) elevates the risk of heart attack and stroke independently of LDL.
The Biology of Lp(a)
Apolipoprotein(a) gene, is expressed in the liver and is the origin of Lp(a) particles. The manner in which it generates Lp(a) is unclear. Apo(a) may bind to LDL within the circulatory system or during its departure from liver cells.
Recent investigations lend support to the concept of Lp(a) generation within hepatic cells, where apolipoprotein(a) associates with apoB situated on an LDL particle. This interaction within liver cells culminates in the formation of the distinctive Lp(a) structure.
The process by which Lp(a) undergoes degradation remains unclear, thus rendering its levels primarily reliant on the rate of its production.
The liver’s role in catabolism is pivotal, yet the precise receptor accountable for the removal of Lp(a) from the bloodstream remains elusive.
The plasminogen receptor or the LDL receptor are the most plausible candidates for this role. The concentration of Lp(a) is predominantly shaped by the production of apolipoprotein(a).
Diseases With High Levels of Lipoprotein (a)
Raised levels of Lp(a) have been associated with an increased risk of several cardiovascular diseases.
- Atherosclerotic Cardiovascular Disease (ASCVD): Elevated Lp(a) levels serve as an independent risk determinant for ASCVD, encompassing diseases such as coronary artery disease, myocardial infarctions, and cerebrovascular incidents.
- Ischemic Stroke: Heightened concentrations of Lp(a) have been linked to an escalated risk of ischemic stroke, stemming from the occlusion of cerebral blood vessels by thrombi, hampering the delivery of oxygen and nutrients to cerebral tissues.
- Peripheral Artery Disease (PAD): Characterized by the buildup of atherosclerotic plaques in arteries supplying the limbs, peripheral artery disease entails impaired blood circulation, discomfort, and an elevated potential for complications such as ulcers and gangrene. Elevated Lp(a) levels have been correlated with an augmented proneness to PAD.
- Aortic Stenosis: The narrowing of the aortic valve orifice, has been associated with raised Lp(a).
- Thrombosis: Elevated concentrations of Lp(a) can increase the risk of clotting, including deep vein thrombosis (DVT) and pulmonary embolism (PE).
It is imperative to acknowledge that while elevated Lp(a) levels increase susceptibility to specific diseases, their influence does not operate in isolation. Traditional risk factors such as elevated LDL cholesterol, hypertension, tobacco consumption, and familial predisposition, retain substantive relevance.
How to get a Lipoprotein (a) Test
Guidelines recommend that everyone should have their Lp(a) checked once in their life. However, your healthcare practitioner may never have heard of the test. Ask specifically for them to add it to your lipid blood work. The test is widely available and cheap.
How do you treat Lp(a)?
There is currently no evidence that lowering Lp(a) prevents heart attacks and strokes. There are treatments currently in development that target Lp(a) and their results will be published in the next few years.
Check out my article on its treatment here.
LP(a) is a lipid particle that is created by the binding of the protein Apo(a) to an LDL particle. It is largely genetically determined. It increases the risk of cardiovascular disease. Everyone should have it checked once in their lives.