How Does Vascular Occlusion Occur?

• Because of the importance and curiosity of the subject, I will give you some information gradually and in detail. If you are interested, continue. It is long but you can understand the subject in all its aspects.

• Despite all the developments, the disease that kills the most in the world is still cardiovascular diseases. When Cardiovascular Diseases are mentioned, Cardiovascular Occlusion, Cardiovascular Occlusion and Leg Vascular Occlusion come to mind. The veins here are the arteries. They are the vessels that carry clean blood.

• Hardness of the arteries can occur in all arteries. It can also occur in the arteries in the kidney and brain.

• Atherosclerosis is known as "calcification" or "hardening of the arteries" among the people. THE RESULT IS VACULAR OBSTRUCTION. It manifests itself in the form of heart attack and stroke. It is correct to define arteriosclerosis as calcification.

• The plaque formed by atherosclerosis (the area with thickening of the vessel wall) contains plenty of calcium. The calcium load in the coronary arteries, which are the heart vessels, is important for atherosclerosis and plaque development. You can read how the score of this load is calculated in the Calcium Scoring section.

• Vascular occlusion is a process. IT HAPPENS STEP BY A SERIES OF CONNECTED EVENTS..

• First, let's take a look at the basics. Veins consist of three layers. There are inner, middle and outer layers.

• There are three layers in arteries and veins. However, the structures of arteries and veins are different. Smooth muscle cells are found in the middle layer of the artery. In the arteries, smooth muscle cells that allow the vessel to contract and relax are more dense in the middle layer.

• There are single-layered flat cells called endothelium that line the inner layer of arteries. I will call them “vascular h, crleri” for easy understanding. Think of these cells as square paving stones that line the street. Do not refer to them as cells. They secrete many chemicals, especially nitric oxide, that protect us but somehow also contribute to atherosclerosis. One of these features is vascular occlusion. considered as a role player. In the first step, we will see these cells.

VASUS CELL (ENDOTEL) ) DAMAGE

Smoking, high blood sugar and cholesterol, high blood pressure cause damage to these cells. The structure of the cells changes. Mechanical stress (blood flow) plays an important role in the change of the structure. Stress is higher in the branching regions of the vessels. The stress created by the blood flow has an effect on the layers. Atherosclerosis is more common here.

STRESS IN THE VESSEL.

Is there any stress in the vein?. It is possible. This is mechanical stress. Stress depends on two factors. To the blood flow and its effect on the vessel wall. We said above that the vessel wall consists of three layers. The stress of blood flow is directed to one point. As you can see in the figure, the stress characteristics created by the unidirectional and regular blood flow change.

It is more common in the posterior wall of the veins and in the areas where the veins branch. Atherosclerosis and occlusion begin in these areas.

It can also be evaluated as a result of the shear stress of the vascular layers as a result of the stress created by the blood flow. In summary, some changes begin in the vessel cells (endothelium) due to stress in the vessel.

FAT IN THE BLOOD THEY PASS.

As a result of the damage, the endothelial cells are separated. Thus, the passage of LDL bad cholesterol, other substances and cells through the gap becomes easier. The higher the LDL bad cholesterol, the greater the transition. This transition explains why LDL cholesterol is a risk factor. Small "fatty dots" are formed with the accumulation of fat on the vessel wall. When these points come together, fat streaks are formed. Now we can say that lime (plaque) has started to form in the vein.

HOOKS IN THE VESSEL CELLS FORMATION AND TRANSFER OF WARRIOR CELLS INTO THE VESSEL.

Vessel (endothelium) cells Some hooks (chemicals: VCAM: Vascular Cell Adhesion Molecule) are formed on the i surface. These hooks are precipitation. Warrior white blood cells (mono=monocytes) are attached to these sticky hooks. The warrior cells we call monocyte pass through the vascular layer. They transform into macrophages, which are tissue warrior cells.

Some hooks (chemicals: VCAM) are formed on the surface of vascular (endothelial) cells. These hooks catch the warrior white blood cells (monocytes). These warrior cells follow the fat passing through the spaced vascular cells.

OXIDATION OF BAD CHOLESTEROL TRANSMITTING INTO THE VESSEL.

• The oils that pass into the vein (LDL bad cholesterol) are oxidized in this region.

• Oxidation is important for the next step. Oxidized LDL becomes more palatable.

LDL CHOLESTEROL IS SWALLOWED BY WARRIER CELLS.

Oxidized and palatable Incoming LDL warrior cells (monocyte name became macrophage) become food. These warrior cells cannot get enough of LDL. As they swallow, they swallow and begin to swell. These swollen warrior cells are called foam cells.

INHALED REACTION

Fighter cells secrete some chemical substances (such as cytokines: TNF and IL-4) after they pass into the vessel. After transforming into foam cells, they secrete more. These substances are chemical messengers. Summon more warrior cells. An inflammatory reaction begins in the vein. Remember, every disease is an inflammatory reaction.

MIGRATION OF STRAIGHT MUSCLE CELLS

It is located in the middle layer and provides contraction and relaxation of the vessel by contraction and relaxation. Smooth muscle cells leave their places and migrate to the upper layer, that is, to the inner layer.

During this migration, they both grow and their functions change. When their functions change, they start ingesting delicious bad cholesterol (LDL) even though they have no strikes. skewers as you eat them

OIL SEED

These foam cells, which are increasing in number and accumulating, form a "LIPID CORE" in the inner layer of the vessel. More and more oxidized LDL accumulates on this core. We begin to call this new structure PLAK.

FIBROUS CAP

Immediate layer of the inner layer of the vessel On the one hand, these foam cells accumulating under the surface synthesize hard extracellular substances and cause calcium accumulation. This can be considered as a kind of healing tissue. A fibrin cap forms above the lipid core. A cap (cap) is placed on the core.

When the fibrous cap is thinner at the beginning, the plaque formed is called HASSAs PLAK. Fibriase healing tissue fibrin cap increases over time. The plate hook becomes stiffer. When it hardens, it takes the name STABLE PLAK. The risk of ser plaque is considered lower.

CONTRACTING IN THE VESSEL

As the plaque grows, it forms a bulge and rises into the vein (lumen). This causes the vessel to narrow over time and send less blood to the areas it feeds.

FORMATION OF NEW VESSELS IN THE PLATE

As this lime (PLAC) formed in the vein grows, new veins (neovascularization) begin to form on the edges to feed it.

BLEACHING AND BLEEDING IN PLATE

Bleeding in newly formed vessels and/or breaking in the plaque attracts the coagulation cells within the vessel. At this point, clot formation begins in the vein.

As the clot progresses and grows, it completely covers and fills the inside of the vein. A plug is formed. With this sudden blockage, the blood flow to the area it feeds is reset. A heart attack or stroke develops.

In the process that I have summarized in roughly 13 stages, some strategic points are evaluated for treatment.

Vessel cells (endothelium) damage,

Importance and reduction of LDL bad cholesterol,

Oxidation and prevention of LDL bad cholesterol

Foam cell formation and inflammatory reaction prevention

Preventing the growth of calculus in the vein (PLAK),

Stable and not breaking the limestone plaque,

Prevention of clot formation.

If you look at 13 stages and strategic points, you can understand that vascular occlusion is a multi-factor event. In addition, the differences of the patients reveal the necessity of personal evaluation and individual treatment planning. Changing lifestyle with smoking, sugar, hypertension, high cholesterol, smoking, obesity and exercise (inactivity) is important in terms of controlling these factors.

Concentrate on small experimental small group human studies, predominantly on Vitamin E, Resveratrol, quercetin, and magnesium supplements for the prevention of plaque development.

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