Symptoms of atherosclerosis

1、 Clinical manifestations

（1） Generally, mental and physical strength decline. Palpation of body surface arteries such as temporal artery, radial artery, brachial artery, etc. can reveal widening, lengthening, tortuous and hardening.

（2） Most of aortic atherosclerosis has no specific symptoms. On percussion, the dullness area of the aorta behind the sternal handle was widened; The second heart sound in aortic valve area is hyperintense with metallic tone and systolic murmur. Systolic blood pressure rises, pulse pressure widens, and radial artery palpation can be similar to pulse stimulation. X-ray examination showed that the aortic node protruded to the upper left, the aorta was dilated and twisted, and sometimes calcareous deposits in patches or arcs could be seen.

Aortic atherosclerosis can also form aortic aneurysms, most of which occur in the abdominal aorta below the opening of the renal artery, followed by the aortic arch and descending aorta. Abdominal aortic aneurysm is often found due to pulsatile mass swelling in the abdomen during physical examination, murmurs can be heard on the corresponding parts of the abdominal wall, and the pulse of the femoral artery can be weakened. Thoracic aortic aneurysm can cause chest pain, dyspnea, dysphagia, hemoptysis, vocal cord paralysis due to compression of recurrent laryngeal nerve, tracheal displacement or obstruction, and compression of superior vena cava and pulmonary artery. X-ray examination showed that the corresponding part of the aorta was enlarged; Aortography can show spindle or cystic aneurysms. Two dimensional ultrasound imaging, computerized X-ray tomography, and magnetic resonance tomography can show aneurysmal aortic dilatation. Once an aortic aneurysm ruptures, it can be quickly fatal. Atherosclerosis can also form dissecting aneurysm, but it is rare.

（3） Coronary atherosclerosis can cause angina pectoris, myocardial infarction and myocardial fibrosis, which will be detailed in the next section.

（4） Cerebral atherosclerosis and cerebral ischemia can cause dizziness, headache and syncope. Cerebrovascular accidents caused by cerebral artery thrombosis or rupture and bleeding, including headache, dizziness, vomiting, sudden loss of consciousness, limbs, paralysis, hemianopsia or aphasia (see "acute cerebrovascular disease" for details). Brain atrophy can cause dementia, psychopathy, dyskinesia, loss of intelligence and memory, and even complete personality changes (see "Mental disorders associated with cerebral arteriosclerosis").

（5） Renal atherosclerosis is rare clinically and can cause intractable hypertension. If hypertension suddenly occurs when you are over 55 years old, you should consider the possibility of this disease. If there is a renal artery thrombosis, it can cause pain in the renal area, urinary obstruction and fever.

（6） Mesenteric atherosclerosis may cause indigestion, decreased intestinal tension, constipation, abdominal pain and other symptoms. When thrombosis occurs, there are severe abdominal pain, abdominal distension and fever. When the intestinal wall is necrotic, it can cause symptoms such as bloody stool, paralytic intestinal obstruction and shock.

（7） Atherosclerosis of limbs is more common in the lower limbs, especially in the arteries of the legs. The lower limbs are cold, numb and intermittent claudication due to blood supply obstacles, that is, gastrocnemius numbness, pain and even spasm occur when walking, disappear after rest, and reappear when walking again; In severe cases, there may be persistent pain, and the pulse of the lower limb artery, especially the dorsalis pedis artery, is weakened or disappears. Gangrene may occur if the arterial lumen is completely occluded (see "occlusive arteriosclerosis").

2、 Pathology

It is not difficult to diagnose the disease when it develops to a certain extent, especially when there are obvious organ lesions, but it is not easy to diagnose early. If the elderly patient is found to have high blood lipid and angiographic findings of vascular stenosis, it is conducive to the diagnosis of this disease.

[Pathological changes] The pathological changes of atherosclerosis mainly involve the large elastic arteries (such as aorta) and medium-sized muscle elastic arteries of the systemic circulation system (the coronary and cerebral arteries are the most affected, followed by the limb arteries, renal arteries and mesenteric arteries, and the splenic artery can also be affected), while the pulmonary circulation arteries are rarely affected. The distribution of lesions is mostly that several tissues and organs are involved at the same time, but sometimes they can be concentrated in the arteries of one organ, while other arteries are normal. The earliest lesion was found in the posterior wall of aorta and the opening of intercostal artery; The blood pressure in these parts is high, and the impact of blood flow on the pipe wall is large, so the lesions are also obvious.

The normal arterial wall consists of three layers: the inner wall, the middle membrane and the outer membrane. The intima is composed of a single layer of endothelial cells, connective tissue and perforated internal elastic plates. Between the endothelial cells and elastic plates (also called subendothelium), in addition to the connective tissue, there are smooth muscle cells and matrices (including acidic proteoglycans, soluble proteins, lipids, glucose and electrolytes). Smooth muscle cells in childhood are extremely rare, and smooth muscle cells and matrix components in intima gradually accumulate with age. In the muscular elastic artery, the middle membrane is almost all composed of oblique smooth muscle cells, and there are an indefinite number of collagen, elastic fibers, glycoproteins and other surrounding smooth muscle cells. Its shape generally does not change with age. The outer membrane contains fibroblasts, collagen, glycoprotein and smooth muscle cells. A discontinuous external elastic plate is also separated between the outer membrane and the middle membrane. When atherosclerosis occurs, there are three types of changes in the arterial wall: lipid stripes, fibrous plaques and complex lesions.

（1） Lipid stripe disease is an early disease, which is common in young people. It is limited to the intima of arteries and presents yellow fat spots several millimeters in size or yellow fat stripes up to several centimeters in length. It is characterized by focal accumulation of macrophages and a few smooth muscle cells in the intima, and lipid deposition inside and outside the cells. The lipid components are mainly cholesterol and cholesterol esters, as well as phospholipids and triglycerides; As the lipid stripe is a flat or slightly higher lesion than the intima, it will not block the involved artery and cause clinical symptoms. Its importance is that it may develop into plaque.

（2） Fibrous plaque lesion is the most characteristic lesion of progressive atherosclerosis, which is generally pale yellow, slightly raised and protrudes into the artery lumen or around the opening of vascular branches, causing lumen stenosis. Such lesions are mainly composed of connective tissue with intimal hyperplasia, smooth muscle cells and macrophages containing lipid. Lipids are mainly cholesterol and cholesterol esters, and the periphery of cells is surrounded by lipids, collagen, elastic fibers and glycoproteins. Fibrous tissue at the focus proliferates to form a fibrous membrane, which covers a large amount of lipid in the deep. The lipid deposit is mixed with cell fragments and cholesterol crystals. When the size of the plaque increases, it expands to the middle membrane of the tube wall, which can destroy the muscle fibers and elastic fibers of the tube wall and replace them with connective tissue and proliferative new capillaries. After more lipid deposition, the bottom of the central base is often disintegrated due to malnutrition, degeneration and necrosis. These disintegrated substances are mixed with lipids to form atherosclerotic substances, which are atherosclerotic plaques or atheroma.

（3） The complex lesion was caused by bleeding, necrosis, ulcer and calcification of fibrous plaques. Atheromatous plaque may form so-called atherosclerotic ulcer due to the collapse of the inner membrane surface; After the ulceration, the porridge enters the blood stream and becomes an embolus. The ulceration can cause bleeding. The surface of the ulcer is rough and easy to produce thrombus. The formation of mural thrombus aggravates the stenosis of the lumen and even blocks it. At the same time of gradual occlusion of blood vessels, collateral circulation from nearby blood vessels gradually appears. After the thrombus is organized, it can be reopened, so that local blood flow can be partially restored. The compound lesion is also characterized by calcification of the middle membrane.

The affected artery has weakened elasticity, increased brittleness, and is prone to rupture. Its lumen gradually narrows or even completely occludes, and can also expand to form an aneurysm.

Depending on the establishment of the involved artery and collateral circulation, this disease can cause functional disorder of the whole circulatory system or individual organs:

1. The elasticity of the aorta wall is reduced due to atherosclerosis. When the heart contracts, it temporarily expands and retains part of the blood drained by the heart, which weakens. The systolic pressure will rise and the pulse pressure will widen. When atherosclerotic aneurysms form in the aorta, the tube wall is replaced by fibrous tissue, which not only loses tension but also expands outwards. These are enough to affect the regulation of blood flow throughout the body, and also increase the burden on the heart.

2. Stenosis or occlusion of internal organs or limbs' artery lumen, in the case that the lateral right circulation can not compensate, causes the blood supply of organs and tissues to be obstructed, resulting in ischemia, fibrosis or necrosis. If coronary atherosclerosis can cause angina, myocardial infarction or myocardial fibrosis; Cerebral atrophy caused by cerebral atherosclerosis; Renal atherosclerosis causes hypertension or renal atrophy; Atherosclerosis of lower limbs causes intermittent claudication or gangrene of lower limbs.

3. The elastic layer and muscular layer of the arterial wall are damaged, making the wall fragile and prone to rupture and bleeding in the case of blood pressure fluctuations. The death caused by cerebrovascular accident and aneurysm rupture is more common.

The pathological changes of this disease progress slowly, and the obvious lesions are mostly seen after the prime of life, but the obvious symptoms mostly appear in the old age. According to the pathological anatomy data, the pathological changes of aortic atherosclerosis of the same degree in Chinese people were 10 to 15 years later than that in European and American people on average, and the pathological changes of coronary atherosclerosis of the same degree occurred about 15 to 20 years later.

There are many data proving that the atherosclerotic lesions of experimental arteries can subside in a period of time after drug treatment and cessation of atherogenic feed, no matter in the early or late stage.