It refers to an abnormal increase in plasma total cholesterol (TC) or triglyceride (TG).

LDL is the main factor causing AS, and together with VLDL, it is called an AS-causing lipoprotein, while HDL has a preventive effect on AS.

Oxidized LDL (ox-LDL) is the most important atherogenic factor and the main factor causing damage to endothelial cells and smooth muscle cells. Ox-LDL cannot be recognized by normal LDL receptors, but is easily recognized and rapidly taken up by the scavenger receptors of macrophages, promoting the formation of foam cells by macrophages.

HDL can remove cholesterol from the arterial wall through the reverse cholesterol transport mechanism to prevent the occurrence of AS. In addition, HDL also has antioxidant effects that can prevent the oxidation of LDL, and can competitively inhibit the binding of LDL to receptors on endothelial cells to reduce its uptake.

Abnormally increased values ​​of LDL, VLDL, and TG are the best indicators for judging AS and CHD.

Due to the pressure and impact of blood flow on the blood vessel wall due to high blood pressure, it causes damage to the vascular endothelium, increases the lipid permeability of the intima, and lipoproteins easily penetrate into the intima. Monocytes and platelets adhere to and migrate into the intima, and media SMC migrate into the intima. Thereby promoting the occurrence of AS.

Smoking increases the concentration of CO in the blood, causing hypoxic damage to vascular endothelial cells. It can also make LDL in the blood easily oxidized. Ox-LDL promotes blood mononuclear cells to migrate into the intima and transform into foam cells.

diabetes.

Hyperinsulinemia.

Hypothyroidism and nephrotic syndrome.

Patients with familial hypercholesterolemia have a genetic mutation in the LDL receptor, resulting in functional defects that lead to extremely elevated plasma LDL levels.

Because estrogen has the effect of improving the function of vascular endothelium and reducing plasma cholesterol levels, women before menopause. The incidence of AS is lower than that of men in the same age group.

It is a syndrome combined with hypertension and abnormalities in glucose and lipid metabolism, accompanied by an increase in LDL and a decrease in HDL.

Damaged endothelial cells secrete cytokines or growth factors, attracting monocytes to gather and adhere to the subendothelium, and migrate into the subendothelial space. Mediated by scavenger receptors on their surfaces, they are continuously absorbed into the body. Foam cells of monocyte origin are formed from oxidized lipids in the membrane.

Smooth muscle cells SMC phagocytose lipids through the LPL receptor on their surface, forming SMC-derived foam cells.

The migration of SMC into the intima and proliferation of the arterial media is an important step in the progression of atherosclerosis.

It is the earliest visible lesion of AS. To the naked eye, it appears as punctate or striped yellow lesions that are not raised or slightly raised in the intima.

Under a light microscope, there are a large number of foam cells (the most characteristic cell component) gathered under the intima of the lesion. The foam cells are large in size, round or oval in shape, and contain a large number of small vacuoles in the cytoplasm. Foam cells are derived from macrophages and SMCs

Developed from fingerprints, the surface of the endometrium can be seen with the naked eye as scattered irregular, raised patches in light yellowish-yellow or porcelain white color.

Under a light microscope, the surface of the lesion was a layer of fibrous cap, composed of a large number of collagen fibers, proteoglycans, and scattered SMC. Collagen fibers can undergo glass transition. Under the fibrous cap, varying numbers of foam cells, SMC, extracellular matrix and inflammatory cells were seen.

It develops from the necrosis of cells deep in the fibrous plaque and is a typical lesion of AS. With the naked eye, obvious gray-yellow plaques can be seen in the intima. The luminal surface of the plaque is white hard tissue, and the deep part is yellow soft atherosclerotic material.

Under a light microscope, there were a large amount of amorphous necrotic disintegration, cholesterol crystals, and calcium salt deposition (blue-purple dots under the microscope) under the fibrous cap. Granulation tissue and a small number of lymphocytes and foam cells appeared at the bottom edge of the plaque. The media becomes thinner due to plaque compression, SMC atrophy, and elastic fiber destruction.

The new blood vessels within the plaque rupture to form a hematoma. It can block or even completely occlude the lumen, causing acute blood supply interruption.

When the fibrous cap ruptures, atherosclerotic material enters the bloodstream, and the necrotic material and lipids that enter the bloodstream form cholesterol emboli, causing embolism.

After plaque ruptures and forms an ulcer, exposure of collagen can promote thrombosis.

Calcium salt deposition can be seen in the fibrous cap and atheroma lesions, causing the tube wall to become hard and brittle.

The smooth muscle in the media at the base of severe atherosclerotic plaques may atrophy and decrease in elasticity. Under the action of intravascular pressure, the arterial wall expands locally to form an aneurysm. The rupture of the aneurysm can lead to massive bleeding (the most dangerous secondary disease of AS).

Elastometrial arteries (medium arteries) have luminal narrowing due to atheromatous plaque. Causes blood supply to decrease, causing ischemic lesions in corresponding organs.

It commonly occurs in the posterior wall of the aorta and the openings of its branches, with the abdominal aorta being the most severely affected. Due to the large lumen of the aorta, even if there is severe atherosclerosis, it will not cause obvious symptoms. However, in severe cases, aneurysms can easily form and aneurysm rupture can lead to fatal bleeding.

Coronary atherosclerosis.

Coronary heart disease. (CHD)

Chronic ischemic heart disease.

It is most commonly found at the origin of the internal carotid artery, basilar artery, middle cerebral artery, and circle of Willis. Fibrotic plaques and atherosclerotic plaques often lead to lumen stenosis or even occlusion. Due to stenosis of cerebral artery lumen, long-term insufficient blood supply to brain tissue can lead to brain atrophy. Those with severe atrophy may suffer from mental retardation or even dementia.

Renal tissue infarction occurs due to plaque combined with thrombosis. After the infarction becomes organized, large sunken scars are left behind. Multiple scars can cause the kidney to shrink, which is called AS pyknosis.

The most severe disease is in the arteries of the lower extremities, often occurring in the iliac arteries, femoral arteries, and anterior and posterior tibial arteries. When the lumen of the larger artery is narrowed, it causes insufficient blood supply to the lower limbs, causing pain in the lower limbs and making it impossible to walk, but it gets better after rest, which is the so-called intermittent walking.

When the lumen is narrowed or even blocked, patients will have symptoms of severe abdominal pain, abdominal distension, and fever, which can lead to serious consequences such as intestinal infarction, paralytic intestinal obstruction, and shock.

It is estimated that at least 20% to 40% of the variation in blood pressure in the population is genetically determined.

Salt intake is positively correlated with blood pressure, but not everyone is sodium sensitive.

The increase in blood pressure caused by drinking alcohol may be related to the increased levels of catecholamines and corticotropin in the blood.

People who are in a state of long-term or repeated stress or who are engaged in corresponding undertakings are prone to dysfunction of the cerebral cortex, which can increase blood pressure.

Physical activity has a blood pressure lowering effect and can reduce the dose of antihypertensive drugs to maintain the antihypertensive effect.

It is generally believed that increased excitability of sympathetic nerve fibers in arterioles is the main neurological factor in hypertensive lesions.

Hypertension is the product of multiple genes.

The renin-angiotensin-aldosterone system (RASS) mechanism is:

Sympathetic nervous system.

Vascular endocrine dysfunction.

Insulin resistance.

Hypertensive vascular remodeling is divided into four types.

The small arteries throughout the body spasm and contract intermittently, and the blood pressure rises. Since there is no organic disease in the arteries, the blood pressure can return to normal after the spasm is relieved.

Arteriosclerosis.

Arteriolar sclerosis.

Hardening of the arteries.

The clinical manifestations of this period are obvious elevated blood pressure, loss of volatility, and the need to take antihypertensive drugs.

Heart disease.

kidney disease

Brain lesions.

Retinopathy.

Also known as rapidly progressive hypertension, it is more common in teenagers. Blood pressure increases significantly, often exceeding 230/130mmHg. Hypertensive encephalopathy or renal failure may occur early (the kidney is the organ with the most obvious lesions in malignant hypertension), and retinal hemorrhage and optic disc edema often occur. Can develop from good hypertension

Characteristic lesions are proliferative arteriolar sclerosis and necrotizing arteritis (fibrinoid necrosis of arterioles), primarily involving the kidneys.

The lesions mainly invade the heart valves, with the mitral valve most commonly affected, followed by the mitral valve and aortic valve being affected simultaneously.

In the early stage of the disease, the involved valves are swollen, and myxoid degeneration and fibrinoid necrosis, serous exudation, and inflammatory cell infiltration occur within the valves. Verrucous excrescences with a diameter of 1-2mm form on the surface of the diseased valve. These wart-like growths. It is off-white and translucent. Not easy to fall off. When the verrucous excrescences are present for a long time, they may appear in sheets and involve the chordae tendineae and adjacent intima.

Under light microscopy, the vegetations are composed of platelets and fibrin, accompanied by small focal fibrinoid necrosis, and a small number of rheumatoid cells may appear around it.

In the later stage of the disease, due to recurrence of the disease, fibrous tissue proliferates, resulting in valve thickening, hardening, curling, and shortening. The valves adhere to each other and the chordae tendineae become thickened and shortened, eventually forming chronic valvular heart disease.

The lesions mainly involve the myocardial interstitial connective tissue, often manifesting as focal interstitial myocarditis, interstitial edema, rheumatic bodies (characteristic lesions of rheumatic myocarditis) and a small amount of lymphocyte infiltration near interstitial blood vessels.

Lesions commonly occur in the left ventricle, interventricular septum, left atrium, and left atrial appendage. When the conduction system is involved, conduction block may occur.

The lesions mainly involve the visceral layer of the epicardium. When a large amount of serous fluid mainly leaks out, epicardial effusion is formed. When the exudation is mainly cellulose, the cellulose covering the epicardial surface is pulled by the heart beat to form a villi-like shape called a villous heart.

If a large amount of exuded cellulose cannot be absorbed, it will become organized, causing the visceral layer and wall layer of the epicardial cavity to adhere to each other to form constrictive epicarditis.

It is an exudative lesion and is more common on the skin of the trunk and limbs. It is a light red annular blush with normal skin color in the center. The lesions often resolve within one to two days.

It is a proliferative disease. It is more common in the connective tissue under the skin on the extensor sides near the elbow, wrist, knee, and ankle joints. A hard, non-tender nodule forms. Under a light microscope, the center of the nodule was a large area of ​​fibrinoid necrosis, surrounded by radially arranged rheumatoid cells and fibroblasts, accompanied by infiltration of inflammatory cells, mainly lymphocytes.

In the early stage, the heart is affected by infection through catheter or intravenous infusion during surgery. The main pathogenic bacteria are Staphylococcus epidermidis and Staphylococcus aureus.

The late stage is mostly caused by transient bacteremia, and Staphylococcus aureus accounts for more than 50%.

The mitral and aortic valves are most commonly affected. The characteristic feature of the disease is the formation of vegetations on the affected semimembrane. The excrescences are polyp-like or cauliflower-like in texture and are brittle and easy to break and fall off.

Affected valves are prone to deformation, ulceration and perforation. Under a light microscope, the vegetations are composed of platelets, fibrin, bacterial colonies, necrotic tissue, and neutrophils. Hyperplasia of granulation tissue and infiltration of lymphocytes and monocytes can be seen at the base of the ulcer.

Arterial embolism and vasculitis are caused by emboli formed by bacterial toxins and vegetations breaking off. Embolism is more common in the brain, followed by the kidney and spleen.

Because the embolus is not sterile or contains very few bacteria and the bacteria are weak, it is often aseptic infarction.

Focal or diffuse glomerulonephritis can occur due to allergic reactions or microemboli.

Bacteria in the shed vegetation invade the bloodstream and multiply in the bloodstream, causing the patient to have long-term fever, splenomegaly, leukocytosis, frequent small bleeding spots in the skin, mucous membranes and fundus of the eyes, and anemia.