Atherosclerosis is initiated by inflammatory processes in the endothelial cells of the vessel wall associated with retained low-density lipoprotein (LDL) particles. This retention may be a cause, an effect, or both, of the underlying inflammatory process. Lipoproteins in the blood vary in size. Some data suggests that small dense LDL particles are more prone to pass between the endothelial cells, going behind the cellular monolayer of endothelium. LDL particles and their content are susceptible to oxidation by free radicals and the risk is higher while the particles are in the wall than while in the bloodstream. However, LDL particles have a half-life of only a couple of days, and their content with time.
Once inside the vessel wall, LDL particles can become more prone to oxidation. Endothelial cells respond by attracting monocyte white blood cells, causing them to leave the blood stream, penetrate into the arterial walls and transform into macrophages. The macrophages’ ingestion of oxidized LDL particles triggers a cascade of immune responses which over time can produce an atheroma if HDL removal of fats from the macrophages does not keep up. The immune system’s specialized white blood cells absorb the oxidized LDL, forming specialized foam cells. If these foam cells are not able to process the oxidized LDL and recruit HDL particles to remove the fats, they grow and eventually rupture, leaving behind cellular membrane remnants, oxidized materials, and fats (including cholesterol) in the artery wall. This attracts more white blood cells, resulting in a snowballing progression that continues the cycle, inflaming the artery. The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial lining thickens, increasing the separation between the plaque and lumen. This somewhat offsets the narrowing caused by the growth of the plaque, but it causes the wall to stiffen and become less compliant to stretching with each heart beat.
The Risk Factors of the Atherosclerosis
1. Hypertension: Long-term hypertension cause the arterial wall damages physically and chemically. It makes easy deposition of lipids, the formation of fatty plaque and cause atherosclerotic stenosis. If blood pressure can’t be in normal, the incidence of myocardial infarction can increases about 2 to 3 times, stroke is about 4 times.
2. Hyperlipidemia: The higher amount of the fats in the plasma is more easily deposit in the blood vessel wall to form plaques, resulting in arteriosclerosis stenosis.
3. Diabetes: The diabetes patient will have a problem of lipoprotein metabolism (Fat Protein), the transport of lipoprotein will be denatured in the blood. It causes fat deposition and formation of fatty plaque in the vessel wall.
4. Smoking: The toxic substances like nicotine and carbon monoxide in cigarettes will cause the arterial wall damaged. The injured wall will adhere to cholesterol easily, leading to platelet accumulation and the formation of fatty plaques. Meanwhile, smoking can cause coronary artery spasm and reduce blood supply in the body.
5. Lack of exercise: Exercise can increase the amount of high-density lipoprotein and reduce the amount of low-density lipoprotein, it helps the body to excess cholesterol from the biliary tract and intestinal excreted. It avoids the excess cholesterol deposition in the vascular wall. In addition, exercise can enhance blood circulation, increase blood vessel elasticity, reduce hypertension and consume excess calories, so that the proportion of body fat decreased and muscle weight increased. The good result is weight loss. Therefore, lack of exercise gets atherosclerosis easily.
6. Obesity: The obesity or overweight one, which increases the cardiac load, the probability of abnormal lipoprotein is high. Thus it increases the risk of atherosclerosis. Obesity is likely to trigger hypertension, diabetes, hyperlipidemia and insulin resistance syndrome.
7. Overpressure: We will increase the adrenaline secretion if we get overpressure. This would cause hypertension, increase the heart rate and damage the arterial wall.
8. Family history: Genetic factors, some people will occur atherosclerosis early. The reason is still unknown. Some is severe hypercholesterolemia; LDL and WBCs are accumulated in the vessel, so it contributes to the occurrence of atherosclerosis. Some is hypertension or thrombosis.
9. Nutrition: First of all, atherosclerosis risk factors – cholesterol. Large amount of intake of greasy foods is the main cause of atherosclerosis. Cholesterol is one of the main substances to synthesis the cell membrane, important brain and nerve tissue, and formation of hormone and vitamin D. However, if excessive intake of cholesterol, the cholesterol levels will be over the normal range. As a result, atherosclerosis will be induced. Excessive cholesterol, one of the important risk factors, in the blood is the occurrence of coronary artery disease and cardiovascular disease in the clinical study.
Secondly, fat diet and arteriosclerosis are closely related. Balanced diet is important. If you are likely to have fatty foods and not pay attention to the intake of other minerals, you will make too much LDL deposited in the blood vessel wall, it may induce arteriosclerosis and other cardiovascular diseases.