Atherosclerosis, the number one killer of human health

Author: Xu Jiayin, Guo Weina, School of Health Sciences, Three Gorges University, Lu Hua, School of Basic Medicine, Three Gorges University

Illustration: Guo Weina, Xu Jiayin, Health and Medical College of China Three Gorges University

Reviewer: Huang Yiling, Associate Professor, School of Basic Medical Sciences, Three Gorges University

Atherosclerosis is the main cause of coronary heart disease, cerebral infarction and peripheral vascular disease, and is the number one killer of human health. Its main feature is the appearance of atherosclerotic plaques or fibrous plaques in the vascular endothelium, usually involving large and medium arteries, causing the vascular wall to harden, reduce elasticity, and narrow the lumen, thus causing a series of lesions.

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How does atherosclerosis develop? What are the basic pathological changes? How can it be prevented? The following will reveal the answers one by one.

1. Formation of Atherosclerosis

Let's use an analogy to give a general understanding of the formation of atherosclerosis. Clear water flows in a river. When there is too much sediment in the water, the flow rate will slow down, and the sediment will easily settle in the potholes at the bottom of the river, gradually forming silt at the bottom of the river. In the process of atherosclerosis, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) in the blood are like sediment, and the damage to vascular endothelial cells caused by stimuli such as high blood pressure and smoking is like the potholes at the bottom of the river. Low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) are easily deposited under the damaged vascular endothelial cells, gradually forming atherosclerosis.

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The formation of foam cells, an important event in the lipid deposition process, has two main sources. First, after the vascular endothelium is damaged, low-density lipoprotein (LDL) in the blood enters the subendothelium and is oxidized into oxidized low-density lipoprotein (ox-LDL). At the same time, monocytes aggregate, adhere and migrate into the subendothelium to activate as macrophages. Oxidized low-density lipoprotein (ox-LDL) is recognized and taken up by the scavenger receptors of macrophages to form macrophage-derived foam cells. Second, damaged endothelial cells secrete growth factors, activate smooth muscle cells in the arterial media, migrate into the intima and proliferate. On the one hand, smooth muscle cells can synthesize extracellular matrices such as collagen and proteoglycans, and on the other hand, they can take up low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) by binding to lipoprotein receptors to become myogenic foam cells.

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2. Basic pathological changes of atherosclerosis

The basic pathological changes of atherosclerosis can be divided into the following four stages.

1. Fat streak formation stage

As the above-mentioned lesions continue to develop and accumulate to a certain extent, visible dot-like or stripe-like yellow lesions that are not raised or slightly raised on the intima will appear on the vascular endothelium, namely fatty streaks.

2. Fibrous plaque formation stage

Part of the extracellular matrix in the fatty streak continues to develop, forming a fibrous cap composed of collagen fibers, proteoglycans, etc. on the surface of the lesion, while the remaining components continue to develop and deposit in the lesion. At this stage, scattered irregular raised light yellow, grayish yellow or porcelain white plaques, namely fibrous plaques, can be seen on the surface of the endometrium.

3. Stage of atherosclerotic plaque formation

After the fibrous plaque necrosis, a large number of amorphous necrotic disintegration products, cholesterol crystals, calcium salt deposits, etc. may appear under the fibrous cap. At this stage, obvious gray-yellow plaques can be seen, namely atheromas, also known as "atheromas".

4. Secondary lesion stage

Secondary lesions mainly include the following three aspects.

1. Blood vessel blockage Plaques continue to grow or bleeding within the plaques causes the plaques to bulge, resulting in narrowing of the blood vessel lumen or even complete occlusion. Plaques are constantly impacted by blood flow. If they rupture, their contents will enter the blood flow and become emboli, causing embolism. Embolism can cause acute interruption of blood supply, leading to ischemic lesions in the corresponding organs, often occurring in the brain, heart, kidneys, lower limbs and other parts.

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2. Atherosclerosis The middle membrane of the artery becomes hardened and thinned due to the compression of plaques, and the calcium salt deposition after necrosis makes the middle membrane more brittle.

3. Aneurysm After arteriosclerosis, the arterial wall expands under the action of intravascular pressure, forming an aneurysm. Rupture of an aneurysm can cause heavy bleeding.

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It can be seen that most diseases caused by atherosclerosis are acute and dangerous. It is also the most common disease of the cardiovascular system and is therefore called "the number one killer of human health."

3. Prevention of Atherosclerosis

In the face of this "killer", we must take precautions before it happens and do the following in our lives.

On the one hand, we should maintain a healthy lifestyle and do appropriate exercise to promote blood circulation and lower blood lipids. We should also quit smoking, limit alcohol, eat a light diet, and eat more foods rich in vitamin C and plant protein. On the other hand, if you suffer from high blood pressure, hyperlipidemia, diabetes, obesity and other diseases that are prone to cause atherosclerosis, you should actively seek treatment under the guidance of a doctor to avoid further development of the disease into atherosclerosis.

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