Apolipoprotein B (apoB) is the causative agent in atherosclerosis. If your apoB is low, you will not develop atherosclerosis. However, if your apoB is high, you could die young.
We know this because of genetic studies of people with different levels of apoB and their health outcomes.
What is Atherosclerosis of the heart?
Atherosclerosis is a progressive laying down of "plaque" in the wall of the coronary arteries. Since the coronary arteries feed the heart, this can lead to three outcomes:
- The plaque impinges on the artery. Thus, the plaque will decrease blood flow to the heart. This can lead to angina or a poorly working cardiac muscle.
- The plaque can rupture (burst) into the artery. Next the body repairs this by clotting the blood. Thus, the blood flows to that portion of the heart is stopped. Without blood flow, the heart muscle starves, and if the flow isn't restored, that part of the heart will die. This is a heart attack or myocardial infarction.
- The plaque can have no result. Meaning, it isn't stopping blood flow to lead to angina, and it doesn't occlude the artery.
What is in the plaque?
In the above artery, you can see the yellow cholesterol in the wall. This is a "soft" plaque, like porridge.
The plaque is not inside the vessel. The artery is lined by a layer called the intima. So how does cholesterol get from the inside of the blood vessel to behind the layer?
The Process of Atherosclerotic Plaque Formation
Lipoprotein Entry into the Arterial Wall: The process begins when ApoB-containing lipoproteins pass through the endothelial layer of arteries. Normally, this layer acts as a barrier, but factors like high blood pressure or inflammation can make it more permeable, allowing these particles to accumulate beneath the endothelial cells.
Retention and Modification: Once inside the arterial wall, ApoB lipoproteins are trapped by proteoglycans (components of the extracellular matrix). These retained lipoproteins undergo modifications, such as oxidation, which makes them more likely to trigger inflammatory responses.
Inflammatory Response: The modified lipoproteins activate endothelial cells and attract immune cells like monocytes. These monocytes enter the arterial wall and transform into macrophages. Macrophages engulf the modified lipoproteins, turning into foam cells, which are a hallmark of early atherosclerotic plaque.
Plaque Development: Over time, foam cells accumulate, leading to the formation of fatty streaks in the arterial wall. Smooth muscle cells migrate into the intimal layer of the artery, contributing to the formation of a fibrous cap that covers the plaque. This cap consists of connective tissue, calcium, and cholesterol deposits.
Progression and Complications: As the plaque grows, it narrows the artery and restricts blood flow. If the fibrous cap ruptures, it can lead to the formation of a blood clot (thrombus), which may block the artery entirely, causing a heart attack or stroke.
Preventing Plaque Formation
Understanding how ApoB-containing lipoproteins contribute to atherosclerosis underscores the importance of managing blood cholesterol levels. Lifestyle changes such as diet, exercise, and medications like statins can reduce LDL levels, lowering the risk of plaque formation and subsequent cardiovascular events.
Atherosclerosis is a gradual process that starts with the seemingly harmless entry of ApoB lipoproteins into arterial walls. By addressing the risk factors that promote lipoprotein retention and inflammation, the progression of atherosclerosis can be slowed or prevented.
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