Arteriosclerosis

Introduction to arteriosclerosis Arteriosclerosis is a non-inflammatory disease of the arteries. It is a general term for degenerative and proliferative lesions of arterial wall thickening, hardening, loss of elasticity and narrow lumen. Common atherosclerosis, arterial calcification There are three types of arteriosclerosis. Arteriosclerosis is a vascular disease that occurs with the age of a person. Its regularity usually occurs in adolescence, and it is aggravated in the middle-aged and elderly. The incidence is more men than women. In recent years, the disease has gradually increased in China, and it has become the main cause of death in the elderly. One of the reasons, the most important causes of arteriosclerosis are hypertension, hyperlipidemia, smoking three major risk factors, other obesity, diabetes, lack of exercise, nervousness, advanced age, family history, temper and so on. basic knowledge The proportion of illness: 0.035% Susceptible population: hypertensive patients, diabetic smokers, lack of exercisers, obese patients. Mode of infection: non-infectious Complications: angina pectoris, arrhythmia

Cause of arteriosclerosis

Causes

Arteriosclerosis is a vascular disease that occurs with the age of a person. Its regularity usually occurs in adolescence, and it is aggravated in the middle-aged and elderly. The incidence is more men than women. In recent years, the disease has gradually increased in China, and it has become the main cause of death in the elderly. One of the reasons, the most important causes of arteriosclerosis are hypertension, hyperlipidemia, smoking three major risk factors, other obesity, diabetes, lack of exercise, nervousness, advanced age, family history, temper and so on.

High blood pressure (25%):

Long-term impact of high-pressure blood flow on the arterial wall causes mechanical damage to the arterial intima, resulting in blood lipids easily depositing on the arterial wall, forming fatty plaques and causing arteriosclerosis stenosis, blood pressure is not controlled, the incidence of myocardial infarction is increased by about 2 to 3 times, and stroke Then about 4 times.

Lack of exercise (20%):

Exercise can increase high-density lipoprotein, reduce low-density lipoprotein, help the body excrete excess cholesterol from the biliary tract and intestines, and prevent excess cholesterol from depositing on the inner wall of blood vessels. In addition, exercise can promote blood circulation, increase blood vessel elasticity, and lower blood pressure. Excessive calories burn, reduce body fat weight, increase muscle mass, and lose weight, so people who lack exercise can easily get atherosclerotic arteriosclerosis.

Hyperlipidemia (20%):

The amount of fat in the blood is too high to deposit on the inner wall of the blood vessel to form plaque, resulting in narrowing of arteriosclerosis.

Diabetes (15%):

Diabetes people have problems with fat metabolism. Proteins that transport fat in the blood (called lipoproteins) are degenerated, and fat is easily deposited on the inner wall of blood vessels to form fat plaques during transport.

Smoking (10%):

Nicotine in cigarettes, carbon monoxide, etc. will damage the inner wall of the artery. The inner wall of the injured artery will trap cholesterol, causing platelet accumulation to form fatty plaque. At the same time, smoking can cause coronary artery contraction and reduce blood flow.

Obesity (5%):

People who are obese or overweight have a higher cardiac load and a higher chance of abnormal blood fat, which increases the risk of atherosclerosis, obesity, easy to promote high blood pressure, diabetes, hyperlipidemia, and insulin resistance syndrome.

Excessive pressure: People will increase the secretion of adrenaline due to stress, thus causing blood pressure to rise, heart rate to accelerate, and damage to the inner wall of arterial blood vessels.

Family history: refers to the genetic factors, so that some people have early inherited atherosclerotic disease, the cause is still unknown, and some are severe hypercholesterolemia, which accumulates in the blood, which promotes arteriosclerosis, and some are early. Hypertension, or prone to thrombosis.

Pathogenesis

The pathogenesis of this disease has not been fully elucidated. Although research has progressed in recent years, it is still elaborated from different perspectives by various theories or hypotheses.

I. Lipid Infiltration Theory: It is believed that Jiuyi of this disease is closely related to lipid metabolism disorders. Its essence is the reaction of the arterial wall to lipids invading from plasma. The main pathological change of this disease is the appearance of floor plaque on the arterial wall. Cholesterol and cholesterol esters are the main components of atherosclerotic plaque. Although the arterial wall can also synthesize cholesterol and other lipids, in recent years, physiological and pathological studies of arterial wall and endothelial cells and atherosclerotic lesions. The results of histochemical and immunochemical examinations confirmed that the lipids in atherosclerotic plaques mainly come from plasma. Plasma cholesterol, triglycerides and phospholipids are dissolved and actuated by apolipoproteins to form lipoproteins. LDL contains Cholesterol and cholesterol esters are the most, VLDL contains the most triglycerides, HDL contains the most protein, and the lipids in plasma are decomposed into fragments by LDL and VLDL or by the action of arterial intimal lipoprotein lipase. Route to invade the arterial wall:

1. Endothelial cells are directly swallowed.

2, through the gap of endothelial cells.

3. LDL receptors via endothelial cells.

4. Endothelial cells with increased permeability after impaired.

5, through the endothelium directly exposed to the bloodstream due to endothelial cell loss, lipoprotein into the middle membrane, accumulated in smooth muscle cells, collagen and elastic fibers, causing smooth muscle cell proliferation, smooth muscle cells and blood from the blood Monocytes phagocytose large amounts of lipids into foam cells; lipoproteins degrade and release cholesterol, cholesterol esters, triglycerides and other lipids. LDL also binds to the proteoglycans of the arterial wall to produce insoluble precipitates, which can stimulate fibrous tissue proliferation. All of these together form atheromatous plaques.

HDL in lipoprotein can send cholesterol to the liver to decompose, inhibit the uptake of LDL by cells and inhibit the proliferation of smooth muscle cells. Therefore, it is considered to have anti-atherosclerosis effect, and lipid peroxide produced by oxidation of lipids. It is cytotoxic, damages the cell membrane and promotes the formation of atherosclerosis.

Second, thrombosis and platelet aggregation theory: The former believes that the disease begins with local coagulation mechanism, arterial intimal surface thrombosis, after the thrombus is covered by proliferating endothelial cells and merged into the arterial wall, platelets and leukocyte disintegration in the thrombus The release of lipids and other active substances gradually form atheromatous plaques. The latter believes that the disease begins with arterial intimal injury, platelet activating factor (PAF) increases, platelets adhere to it and then aggregate, followed by fibrin Deposition, formation of microthrombus, and release of some active substances after platelet aggregation, wherein thromboxane A2 (TXA2) can counteract the synthesis of prostacycline (PGI2) of blood vessel wall to depolymerize and vasodilate platelets. Role, and promote platelet aggregation and vasoconstriction; platelet derived growth factor can stimulate smooth muscle cell proliferation, contraction and migration to the intima; serotonin and fibroblast growth factor Stimulates fibroblasts, smooth muscle cells and endothelial cells, adrenaline and diphosphate Adenosine promotes further platelet aggregation: factor VIII further binds platelets; platelet factor 4 causes vasoconstriction; plasminogen activator inhibitor (PAI) inhibits thrombus lysis, these substances Further damage to endothelial cells, resulting in LDL, fibrinogen entering the intima and intima; allowing monocytes to accumulate in the intima and develop into foam cells; smoothing smooth muscle cells, moving into the intima, phagocytizing lipids; Endothelial cell proliferation is beneficial to the formation of atherosclerosis.

III. Injury response theory: It is believed that the formation of atherosclerotic plaque is the response of arteries to intimal injury. Intimal injury can be manifested as endometrial dysfunction such as increased intimal permeation, surface is prone to thrombosis, and can also be expressed as internal Membrane integrity is compromised, long-term hyperlipidemia, turbulence, shear stress, and diabetes due to hemodynamic changes due to elevated blood pressure, specific angles and orientations of arterial branches, local stenosis, etc. , long-term repetitive effects of bacteria, viruses, toxins, immune factors and vasoactive substances such as catecholamines, serotonin, histamine, kinins, endothelin, angiotensin, etc.; are sufficient to damage the intima or cause functional changes, Conducive to the deposition of lipids and the adhesion and aggregation of platelets to form atherosclerosis.

4. Monoclonal theory, ie, the theory of unitary reproduction: It is believed that every lesion of atherosclerosis is derived from the proliferation of a single smooth muscle cell, which is the ancestor of many cells later, and some factors such as platelet-derived growth factor Endothelial cell-derived growth factor, monocyte-derived growth factor, LDL, and possibly viruses, proliferate and phagocytose lipids, thus resembling benign tumors and forming atherosclerosis, although through glucose-6-phosphate Determination of dehydrogenase (G6PD) isoenzymes, found that most of the diseased arterial wall fiber plaques contain only one G6PD isoenzyme, showing the monoclonal characteristics of fiber plaques, but also the single enzyme phenotype Does not necessarily mean that the origin of the lesion is clonal, or it may be derived from multiple cells containing the same isozyme, however, due to repeated cell death and growth, the assay results in a single enzyme phenotype, in fact The culture of smooth muscle cells in atheromatous plaques has not shown that these cells will proliferate indefinitely like tumors.

5. Other mechanisms related to the pathogenesis include neuronal, endocrine changes, changes in the acid proteinaceous substance and amount in the arterial wall matrix (increased dermatan sulfate, and decreased chondroitin sulfate A and C), and the activity of the arterial wall enzyme Lowering, etc., these conditions can be beneficial to the formation of atherosclerotic lesions by affecting vascular movement, lipid metabolism, anabolism of blood vessel walls, and the like.

Arteriosclerosis prevention

Eliminate the fear and pessimism of the patient and establish a confidence to heal.

Arteriosclerosis complications Complications, angina, arrhythmia

The complications that may occur in arteriosclerosis are as follows:

1, coronary atherosclerosis, if the diameter of the tube is more than 75%, angina, myocardial infarction, arrhythmia, and even sudden death may occur.

2, cerebral arteriosclerosis, can cause cerebral ischemia (including temporary ischemic attacks), brain atrophy, or cause cerebral vascular rupture, early stage of cerebral arteriosclerosis: neurasthenia (often dizziness, dizziness, headache, Tinnitus, lethargy, memory loss, fatigue), emotional abnormalities (emotional irritability, lack of self-control, as the condition worsens, will gradually become indifferent, lack of interest in things around), low judgment ability (expressed as unable to hold Focusing attention, reducing imagination, and dealing with problems depends on others.) When cerebral arteriosclerosis reaches the middle and late stages, gait stiffness or walking instability, dementia, epileptic seizures, and strokes may occur.

3, renal atherosclerosis, often cause nocturia, refractory hypertension, severe cases may have renal insufficiency.

4, mesenteric atherosclerosis, can be expressed as a pain after the meal, abdominal pain and blood in the stool.

5, lower extremity atherosclerosis, early symptoms mainly manifested as intermittent claudication, pain at rest is the performance of severe ischemia of the lower extremities, often accompanied by numbness of the extremities, disappearance of the dorsal artery pulsation, etc. End ulcers and gangrene.

Symptoms of arteriosclerosis Common symptoms Atherosclerosis Dizziness Pulse pressure Widening Brain stem Infarction Syringacic murmur Heart blood obstruction Low temperature coma Blood pressure High cerebral ischemia

First, the general performance of mental and physical decline, palpation of the surface arteries such as the radial artery, radial artery, radial artery, etc. can be found widening, lengthening, distortion and hardening.

Second, most of the aortic atherosclerosis has no specific symptoms. In the percussion, the dural area of the posterior sternum can be found widened, the second heart sound of the aortic valve area is followed by metal tone, and there is systolic murmur, systolic blood pressure. Increased, pulse pressure widened, palpation of the radial artery can be similar to the pulse, X-ray examination shows that the aortic node protrudes to the left upper, aortic dilatation and distortion, sometimes visible in the plaque or arc plaque .

Aortic atherosclerosis can also form an aortic aneurysm, which is most common in the abdominal aorta below the renal artery opening, followed by the aortic arch and descending aorta. The abdominal aortic aneurysm is often seen as a pulsating abdomen during physical examination. Block swelling found that the corresponding part of the abdominal wall can hear murmur, femoral artery pulsation can be weakened, thoracic aortic aneurysm can cause chest pain, shortness of breath, difficulty swallowing, hemoptysis, vocal cord paralysis due to recurrent laryngeal nerve compression, tracheal displacement or obstruction , superior vena cava and pulmonary artery compression, X-ray examination showed that the corresponding part of the aorta increased, aortic angiography can show a fusiform or cystic aneurysm, two-dimensional ultrasound imaging, computerized tomography For example, magnetic resonance tomography can show tumor-like aortic dilatation. Once the aortic aneurysm ruptures, it can be fatal quickly. Atherosclerosis can also form a dissection aneurysm, but it is rare.

Third, coronary atherosclerosis can cause angina, myocardial infarction and myocardial fibrosis.

Fourth, cerebral atherosclerosis cerebral ischemia can cause dizziness, headache and fainting, cerebral arterial thrombosis or rupture caused by cerebrovascular accident, headache, dizziness, vomiting, sudden loss of consciousness, limbs, paralysis, hemianopia or Aphasia and other manifestations (see "Acute Cerebrovascular Diseases" for details), dementia caused by brain atrophy, psychopathic, dysfunctional, mental and memory loss and even complete changes in personality (see "Psychotic disorders associated with cerebral arteriosclerosis") .

5. Renal atherosclerosis is rare in clinical practice and can cause refractory hypertension. Those who are over 55 years old and suddenly have high blood pressure should consider the possibility of this disease. If there is renal artery thrombosis, it can cause kidney. Area pain, urinary closure and fever.

6, mesenteric atherosclerosis may cause indigestion, intestinal tension reduction, constipation and abdominal pain and other symptoms, thrombosis, severe abdominal pain, abdominal distension and fever, intestinal wall necrosis, can cause blood in the stool, paralytic ileus and shock And other symptoms.

Seventh, atherosclerosis of the extremities is more common in the lower extremities, especially the leg arteries. Due to blood supply disorders, the lower extremities are cold, numbness and intermittent claudication, that is, the gastrocnemius muscles are numb when walking, pain and even sputum, disappear after rest, and then Severe cases may have persistent pain, lower extremity arteries, especially the dorsal artery of the foot, weakened or disappeared, and the arterial lumen may produce gangrene if it is completely occluded (see "occlusive arteriosclerosis").

Arteriosclerosis examination

1. Laboratory inspection:

The disease still lacks sensitive and specific early laboratory diagnosis methods. Patients have abnormal lipid metabolism, which is mainly caused by increased total cholesterol, increased LDL cholesterol, decreased HDL cholesterol, increased blood triglyceride, and increased blood -lipoprotein. Increased apolipoprotein B, decreased apolipoprotein A, increased lipoprotein (), abnormal lipoprotein electrophoresis pattern, more than 90% of patients showed type II or IV hyperlipoproteinemia.

2, blood rheology examination often shows increased blood viscosity, platelet activity can be increased.

3, X-ray examination In addition to the aforementioned aortic atherosclerosis, selective or electronic computer digital subtraction angiography can show the lumen of the coronary artery, cerebral artery, renal artery, mesenteric artery and extremity atherosclerosis Stenosis or aneurysm lesions, as well as the location, extent and extent of the lesion, help to determine the indications for surgical treatment and the manner in which surgery is chosen.

4, Doppler ultrasound examination, help to determine the blood flow of the arteries and renal arteries of the extremities.

5. Intravascular ultrasound and angioscopy are methods for directly observing atherosclerotic lesions from the arterial lumen.

6, radionuclide examination helps to understand the blood supply of brain, heart, kidney tissue.

7, echocardiography, electrocardiogram and its load test showed characteristic changes to help diagnose coronary atherosclerosis.

8, other: limb electrical impedance map, brain electrical impedance map and EEG, brain X-ray, computerized X-ray or magnetic resonance tomography to help determine the function of limbs and cerebral arteries and brain tissue lesions.

Diagnosis of arteriosclerosis

The disease has developed to a considerable extent, especially when there are obvious lesions of the organs. It is not difficult to diagnose early, but early diagnosis is not easy. Elderly patients such as examination found that blood lipids increase, angiography found vascular stenosis, which is conducive to the diagnosis of this disease.

Differential diagnosis

Aortic atherosclerosis caused by aortic changes and aortic aneurysm, must be differentiated from syphilitic aortitis and aortic aneurysm and mediastinal tumor, coronary atherosclerosis caused by angina and myocardial infarction, and other coronary lesions The cause of the differentiation, myocardial fibrosis must be differentiated from other heart diseases, especially cardiomyopathy, cerebrovascular accident caused by cerebral atherosclerosis, need to be differentiated from other causes of cerebrovascular accident, renal atherosclerosis The hypertension caused must be differentiated from other causes of hypertension. Renal artery thrombosis must be differentiated from kidney stones. Symptoms caused by atherosclerosis of the extremities must be differentiated from those caused by arterial lesions of other causes.

Clinically, it is necessary to identify the different development processes of this disease, which can be divided into four phases:

1. Asymptomatic or occult period: The length of the process varies from early pathological changes until atherosclerosis has formed, but there is no clinical manifestation of organ or tissue involvement.

2. Ischemic period: Symptoms are caused by vascular stenosis and organ ischemia.

3. Necrotic phase: Symptoms of organ tissue necrosis due to intravascular thrombosis or luminal occlusion.

4, hardening period: long-term ischemia, organ hardening (fibrosis) and atrophy caused by symptoms.

Many patients enter the sclerosing phase without undergoing a necrotic phase, and patients in the cirrhotic phase can re-occur the manifestations of the ischemic phase.

According to the location of the affected artery, the disease has the following categories:

1, the aorta and its main branches atherosclerosis.

2, coronary atherosclerosis.

3. Cerebral atherosclerosis.

4, renal artery atherosclerosis.

5. Mesenteric atherosclerosis.

6, atherosclerosis of the extremities and so on.

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