1. Coronary atherosclerosis is the most common stenotic coronary artery disease, especially the atherosclerosis of coronary artery branches outside muscle wall. The proximal segment of coronary artery is prone to atherosclerosis because it is closer to the ventricle than all organ arteries, so it bears the largest systolic pressure impact. Furthermore, because of the shape of the heart, the coronary vascular tree changes in most directions, so it also bears greater blood flow shear stress.
Common parts: According to the statistics of 6352 autopsy cases in China, the total detection rate, stenosis detection rate and average grading of anterior descending branch lesions are the highest, and the rest are right trunk, left trunk or left branch and posterior descending branch in turn. Gender difference: the detection rate of lesions in men aged 20 ~ 50 years is significantly higher than that in women; There is no obvious difference between men and women after 60 years old.
Characteristics of lesions: Atherosclerotic plaques are mostly distributed in the proximal segment, which is heavier at the branch mouth; The early plaques were scattered and distributed in segments. With the progress of the disease, adjacent plaques can fuse with each other. On the cross section, the plaques are mostly crescent-shaped and the lumen is narrow to varying degrees. Sometimes it can be complicated by thrombosis, which makes the lumen completely blocked. According to the degree of lumen stenosis caused by plaque, it is divided into four grades: grade ⅰ, lumen stenosis below 25%; Grade ⅱ, stenosis 26% ~ 50%; Grade ⅲ, stenosis 51%~ 75%; Grade ⅳ, lumen stenosis above 76%.
2. Coronary artery spasm For many years, academic circles have been arguing whether coronary artery spasm is the cause of ischemic heart disease. It has been found that the incidence of coronary thrombosis is only 30%, and only 50% of patients die within 12 hours after onset, so it is considered that at least a considerable number of cases are caused by coronary artery spasm. In recent years, due to the development of angiocardiography, it has been confirmed that coronary artery spasm can cause angina pectoris and myocardial infarction.
3. Inflammatory coronary artery stenosis Inflammation of the coronary artery can cause coronary artery stenosis or even complete occlusion, leading to ischemic heart disease, such as polyarteritis nodosa, giant cell arteritis, polyarteritis polyarteritis, Wegener granulomatosis, etc. , may involve the coronary artery. In addition, Syphilitic Takayasu's arteritis can also cause coronary artery stenosis, but it is rare.
First, angina pectoris
The most common clinical syndrome of angina pectoris is caused by the temporary imbalance of myocardial oxygen consumption and oxygen supply. Angina pectoris can be caused by the temporary increase of myocardial oxygen consumption over the oxygen supply capacity of narrow coronary artery (fatigue angina pectoris) (for example, it can occur under the influence of physical activity, emotional excitement, cold, overeating and so on). ), it may also be caused by insufficient oxygen supply to the myocardium caused by coronary artery spasm (spontaneous angina pectoris).
The occurrence of angina pectoris is due to the accumulation of metabolites caused by myocardial hypoxia. These substances stimulate local sympathetic nerve endings in the heart. After the afferent nerve is introduced into the brain through the sympathetic ganglia of the lower neck and upper chest and the corresponding spinal cord segments, discomfort occurs in the skin area where the spinal nerves of the corresponding spinal cord segments are distributed. Its nature is often not pain, but a feeling of oppression or contraction. So angina pectoris is a reflex symptom caused by myocardial ischemia.
1. Stable angina pectoris (stable angina pectoris) is also called mild angina pectoris. At this time, angina pectoris generally does not occur, but can be stable for several months, only when it occurs during heavy physical labor. This angina pectoris is caused by temporary acute or chronic relative myocardial ischemia.
2. Unstable angina pectoris Unstable angina pectoris (unstable angina pectoris) is quite unstable in clinic, which can occur during load or rest, or its intensity and/or frequency increase. Most of these patients have at least 1 coronary artery with high proximal stenosis. Stenosis of the main coronary artery and three coronary arteries is common in patients with increased intensity of angina pectoris. Microscopically, diffuse interstitial myocardial fibrosis caused by diffuse myocardial cell necrosis is more common, which can lead to chronic myogenic cardiac insufficiency with left ventricular dilatation.
3. Variant angina pectoris Variant angina pectoris, also known as primary angina pectoris, mostly occurs at rest, and there is no obvious inducement. Only a few people get sick when they are working. On the contrary, the ST segment of ECG increased during the attack. Angiography shows that coronary artery spasm can be seen in this type of angina pectoris until its lumen narrows. This vasospasm mostly occurs in patients with obvious coronary artery stenosis, but sometimes it can also be seen in patients with no obvious coronary artery lesions.
Second, myocardial infarction.
Myocardial infarction refers to large-scale myocardial necrosis caused by absolute coronary insufficiency, accompanied by persistent ischemia in the coronary blood supply area. The vast majority (95%) of myocardial infarction is confined to a certain range of the left ventricle, most of them involve all layers of the heart wall (transmural infarction), and a few cases only involve the myocardium endocardium (subendocardial infarction).
(1) subendocardial myocardial infarction
Subendocardial myocardial infarction's characteristic is that necrosis mainly involves 65,438+0/3 myocardium in the inner wall of the ventricle, as well as sarcomatoid muscle and papillary muscle. It often shows multiple small focal necrosis with the size of 0.5 ~ 1.5 cm. The distribution of lesions is often not limited to the blood supply range of 1 coronary artery, but irregularly distributed around the left ventricle. In the most serious case, the necrotic focus expands and merges into necrosis involving the whole subendocardial myocardium, which is called circular infarction. Patients usually have severe stenotic atherosclerosis of three main coronary arteries, but most of them are neither thrombotic nor atherosclerotic, indicating that severe and diffuse coronary artery disease is the premise of this type of myocardial infarction. When the patient has insufficient blood supply to the coronary artery due to some reasons (such as shock, tachycardia and inappropriate physical activity), it can cause hypoxia in the farthest area of each coronary artery (subendocardial myocardium), while the three major coronary arteries have been severely narrowed, and collateral circulation can hardly improve the blood supply to the myocardium, resulting in myocardial necrosis, and it is multifocal necrosis.
(ii) Regional myocardial infarction
Local myocardial infarction, also known as transmural myocardial infarction, is a typical type of myocardial infarction. The infarct area varies in size, mostly several centimeters or more. Most of them are located in the left ventricle and involve three layers of tissue in the heart wall.
Etiology and pathogenesis
1. Coronary Thrombosis Many scholars believe that coronary thrombosis is the cause of myocardial infarction because it is found in many autopsy cases that there is narrow atherosclerosis complicated with occlusive thrombosis in the coronary branches supplying the infarcted area. However, the incidence of coronary thrombosis in myocardial infarction cases varies greatly from report to report, so the relationship between coronary thrombosis and myocardial infarction is still controversial.
2. Coronary artery spasm Due to the progress of cardiovascular imaging technology, the problem of coronary artery spasm has made a breakthrough. It has been proved that variant angina pectoris is caused by coronary artery spasm. Some people used coronary angiography to study a large number of cases of transmural myocardial infarction, and found that with the extension of time after the attack, the coronary artery occlusion rate decreased, suggesting that coronary artery spasm was relieved. Recent studies have proved that severely narrowed coronary arteries can still contract.
3. Insufficient myocardial blood supply On the basis of coronary atherosclerosis stenosis, insufficient myocardial blood supply due to overload can also cause myocardial infarction.
Location and scope of preference
The location of this type of myocardial infarction is consistent with the occluded coronary artery blood supply area. Because left coronary artery disease is more common than right coronary artery disease, myocardial infarction mostly occurs in the left ventricle. Among them, the anterior wall, apex and anterior 2/3 of ventricular septum account for about 50% of all myocardial infarction, and they are the blood supply areas of the anterior descending branch of left coronary artery. About 25% of myocardial infarction occurs in the posterior wall of left ventricle, interventricular septum and posterior right ventricle 1/3, which is the blood supply area of right coronary artery. In addition, it is also found in the lateral wall of the left ventricle, which is equivalent to the blood supply area of the left coronary artery.
The distribution of coronary arteries varies greatly. According to statistics, there are three types: ① Right dominant type: the right coronary artery branch supplies blood to the diaphragm of the right ventricle and a part of the left ventricle in addition to the posterior descending branch. ② Balanced type: The diaphragmatic surface of two ventricles is supplied with blood by their respective coronary arteries, and there may be two posterior descending branches without crossing the junction of two atria and ventricles. ③ Left dominant type: the left coronary artery is distributed on the diaphragm of the left ventricle, sending out the descending branch, and some branches to the diaphragm of the right ventricle. This variation not only affects the distribution of myocardial infarction, but also when one dominant coronary artery is blocked, the anastomotic branch of the other weak coronary artery often cannot meet the oxygen demand of the myocardium in the blood supply area of the blocked branch, resulting in necrosis in this area.
pathological change
Macroscopically, the shape of myocardial infarction focus is irregular. Generally, infarction can only be recognized by naked eyes after 6 hours. After 8-9 hours, the infarct is yellowish or khaki, dry and hard, and loses its normal luster (Figure 8-30). On the fourth day, there were obvious hyperemia and bleeding areas around the infarct. After 2 ~ 3 weeks, it turns red due to granulation tissue hyperplasia. After 5 weeks, the infarct was gradually replaced by scar tissue, which was gray (old infarct).
Figure 8-30 Myocardial Infarction
From bottom to top, the cross section of the heart shows the anterior wall of the heart, the anterior wall of the left ventricle and the infarction of the anterior ventricular septum (the gray area in the figure).
Microscopically, the most common manifestation of myocardial infarction is coagulation necrosis, eosinophils in the cytoplasm of myocardial cells increase, and then the nucleus disappears. The myofibril structure can be maintained for a long time and finally fused into a uniform red dye (Figure 8-3 1). Congestion zone and neutrophil infiltration can be seen at the edge of infarction, and myocardial cells are swollen, and granules and irregular horizontal bands appear in cytoplasm (Figure 8-32). On the other hand, some cardiomyocytes showed vacuolar degeneration, and then myofibrils and nuclei dissolved and disappeared, leaving the myomembrane of cardiomyocytes, like an empty dilated myomembrane tube (Figure 8-3 1).
Fig. 8-3 1 myocardial infarction
On the left side of the picture, the myocardial fibers are swollen, the striations disappear, eosin is concentrated, and nuclear dissolution disappears (coagulative necrosis); The fibers of right myocardial cells and some myocardial nuclei dissolved and disappeared (liquefied myolysis) ×68.
Figure 8-32 Myocardial Infarction
The myocardial cells at the edge of the infarct were swollen, and granules and transverse bands with different widths appeared in the cytoplasm. Semi-thin sections were stained with toluidine blue ×225.
Biochemical changes in myocardial infarction
The decrease or disappearance of glycogen in infarcted myocardial cells occurs earlier, usually 5 minutes after coronary artery occlusion. This is because the sources of oxygen and glucose needed by this part of the myocardium are interrupted after a certain coronary artery is blocked, and the glycogen stored in the cells is glycolyzed. Recently, it has been reported that early myocardial ischemia can cause the loss of myoglobin. When the myocardium is damaged, myoglobin is quickly released from muscle cells, enters the blood and is excreted from urine, so the myoglobin value can be quickly detected from blood and urine during acute myocardial infarction. When myocardial necrosis occurs, some enzymes, such as glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), creatine phosphokinase (CPK) and lactate dehydrogenase (LDH), can be released into the blood, which increases the concentration of these enzymes in the blood. Among them, CPK is helpful for the clinical diagnosis of myocardial infarction.
Complications and consequences
1. Cardiac rupture is rare, accounting for about 3% ~ 13% of myocardial infarction deaths. It often occurs within 1 ~ 2 weeks after myocardial infarction, which is mainly caused by proteolytic enzymes released by neutrophils and monocytes around the infarction and lysosomal enzymes of necrotic myocardium dissolving necrotic myocardium. The most common sites are: ① under the anterior wall of left ventricle 1/3. After the heart breaks, blood flows into the pericardium, causing pericardial tamponade and sudden death. ② Ventricular septum rupture, left ventricular blood flows into the right ventricle, causing right ventricular dysfunction. ③ Rupture of papillary muscle of left ventricle leads to acute mitral insufficiency and acute left heart failure.
2. Ventricular aneurysm About 10% ~ 38% of myocardial infarction cases are complicated with ventricular aneurysm, which can occur in the acute phase of myocardial infarction, but more often in the healing phase. Due to the necrotic tissue or scar tissue in the infarct area, local tissue bulges outward under the action of indoor blood pressure. Most of them occur near the left ventricular apex, which can cause cardiac insufficiency or secondary mural thrombosis.
3. mural thrombus is more common in left ventricle. Due to the rough endocardium in the infarcted area, eddy current and ventricular fibrillation in ventricular aneurysm provide conditions for thrombosis. Thrombosis can be organized or fall off to cause arterial embolism in the large circulation.
4. Epicarditis When myocardial infarction spreads to the epicardium, aseptic cellulose epicarditis can occur.
5. Myocardial contractility of myocardial infarction with cardiac insufficiency is obviously weakened or even lost, which can cause left heart, right heart or whole heart congestive heart failure, which is one of the most common causes of death.
6. Cardiogenic shock Some people think that when the left ventricular infarction reaches 40%, the ventricular contractility is extremely weakened and the cardiac output is significantly reduced, which can lead to cardiogenic shock and lead to the death of the patient.
7. After myocardial infarction caused by organized scar, if the patient is still alive, the infarction focus will be mechanically repaired into scar. It takes about 2 weeks for small infarction and 4 ~ 6 weeks for large infarction to be organized.
Third, sudden death of coronary heart disease.
Sudden death of coronary heart disease is more common. It is more common in people aged 30-49, and the male is 3.9 times that of the female. There are two kinds of diseases: ① Under some inducement, such as drinking, fatigue, smoking, exercise, quarreling and fighting. The patient may suddenly faint to the ground, twitch the muscles of the limbs, urinate incontinently, or suddenly have difficulty breathing, foaming at the mouth, sweating profusely, and soon fall into a coma. He died immediately after symptoms appeared, or died within 1 to several hours. ② onset during sleep at night: most of them died at home or dormitory, often unnoticed, so there were no witnesses.
Causes of sudden death: most cases have/kloc-0 or more coronary artery stenosis atherosclerosis, and some cases are complicated with thrombosis. Autopsy report showed that 128 cases of sudden death of coronary heart disease, 89 cases had severe coronary atherosclerosis, 18 cases were complicated with thrombosis, and 17 cases had intra-plaque hemorrhage. However, in some cases, the coronary artery has only mild or even no atherosclerotic lesions, and the occurrence of sudden death in these cases may be caused by coronary artery spasm. In addition, coronary artery malformation (such as left coronary artery originating from right coronary sinus or coronary artery trunk originating from pulmonary artery trunk). ), Syphilitic Takayasu's arteritis caused by coronary artery stenosis or occlusion, infective endocarditis caused by thrombus material falling off the aortic valve or mitral valve, coronary artery embolism caused by entering the coronary artery mouth can all cause sudden death.
Brief introduction of symptoms:
Coronary heart disease is usually short for coronary atherosclerotic heart disease. This disease is caused by coronary atherosclerosis, which leads to stenosis or obstruction of vascular lumen, resulting in myocardial ischemia and hypoxia. Hyperlipidemia, diabetes and hypertension are often related to the occurrence of this disease. Clinically, the disease can have angina pectoris, arrhythmia, heart failure, myocardial infarction and other manifestations, and even sudden death.
Health guide:
1. Regular life: Go to bed early and get up early, avoid staying up late to work, and don't watch scary novels and TV before going to bed.
2. Physical and mental happiness: mental stress and emotional fluctuation can induce angina pectoris. You should avoid anger, panic, overthinking and overjoy. Cultivate good habits such as raising flowers and fish, nourish feelings and adjust emotions.
3. Diet adjustment: Overeating greasy, fat and sugar will promote the deposition of cholesterol on the arterial wall and accelerate arteriosclerosis, so it is not appropriate to overeat. Diet should be light, eat more digestible food, have plenty of vegetables and fruits, eat less and eat more meals, and eat less at dinner. Obese patients should control their food intake to reduce the burden on their hearts.
4. Quit smoking and drink less: Smoking is an important factor causing myocardial infarction and stroke, and you should definitely quit smoking. Drinking a small amount of low-alcohol wine such as beer, yellow wine and wine can promote blood circulation and reconcile qi and blood. Hard liquor is forbidden. Do not drink strong tea or coffee.
5. Combination of work and rest: You should avoid excessive physical labor or sudden exertion, and don't be overworked. Walk slowly, climb the stairs and ride a bike, otherwise it will cause the heart rate to increase, blood pressure to rise, and induce angina pectoris. It is not advisable to exercise after a full meal. Cold will make blood vessels contract, reduce blood supply to myocardium and cause pain, so pay attention to keep warm. Sexual life is highly stimulating, blood circulation is accelerated, the whole body needs more blood, and coronary artery blood supply is relatively insufficient, which is prone to angina pectoris or myocardial infarction, so strict control is appropriate. After the complete recovery of myocardial infarction, sexual intercourse should be controlled at 1 ~ 2 times a month.
6. Proper rest: It is best to lie down and rest for a while when angina pectoris attacks. You can work normally, but don't overwork. After the diagnosis of myocardial infarction is clear, you should lie flat in bed. Within two weeks, all the patients' life activities are completed with the help of others, and it is absolutely forbidden to turn over, because turning over will increase the burden on the heart and lead to rupture of the myocardial infarction or cardiac arrest. It is advisable to urinate in bed to keep urine unobstructed. If there are no serious complications, usually stay in bed for 2 ~ 3 weeks and stay in bed for 3 ~ 4 times a day. If there is no change after a week, you can get out of bed and sit in a chair for about half an hour, three or four times a day. In another week, you can take a walk in the bedroom. Long-term bed rest is not good for heart recovery and requires proper exercise. You can do light manual labor in three months.
7. Physical exercise: Exercise should be chosen according to your physical condition and hobbies, such as playing Tai Ji Chuan, table tennis, aerobics, practicing the Eighteen Methods, etc. Do what you can, make the whole body circulate blood and reduce the burden on the heart.
8. Active treatment: adhere to the necessary drug treatment and control diseases that can aggravate coronary heart disease, such as hypertension, diabetes and hyperlipidemia.
9. First aid for sudden death: When sudden death occurs, you should race against time for first aid, and immediately carry out chest massage and artificial respiration. Lie the patient on his back on a wooden board or the ground, knock the patient's left chest two or three times with his fist, hold the patient's nostril, and blow 1 time from mouth to mouth for 1 second, then press the heel of one hand (the other hand is overlapped on the hand) at the junction of 1/3 and 2/3 under the sternum, straighten your elbows and press down vertically. Artificial respiration 1 time, cardiac compression 5 times, and so on. General artificial respiration every minute 16 ~ 18 times, heart compression 80 ~ 90 times. Need medical staff to the scene to rescue.
Heart disease caused by coronary atherosclerosis and myocardial blood supply disorder is called coronary atherosclerotic heart disease, or coronary heart disease for short.
Patients with mild coronary heart disease or well-established collateral circulation may have no conscious symptoms, and the ECG only shows symptoms of insufficient myocardial blood supply, or the ECG is normal at rest, but the ECG is positive after increasing heart load, such as two-step treadmill exercise test and treadmill exercise test. This is the so-called recessive coronary heart disease. Early detection, prevention and treatment can alleviate the disease, otherwise the disease may develop angina pectoris or myocardial infarction. It's just that a person may suddenly have severe arrhythmia or cardiac arrest and die suddenly.
Angina pectoris is paroxysmal retrosternal pain caused by coronary artery insufficiency and myocardial ischemia and hypoxia. It is a typical paroxysmal pain, which usually occurs when people are physically working or emotionally excited, and when their bodies are cold or full. Pain is located in the upper or middle sternum, which can radiate to the left shoulder and upper limbs, and directly to the little finger and ring finger. The nature of pain is mostly squeezing, suffocating or tightening. Each attack lasts for 1 ~ 6 minutes, and occasionally lasts for 15 minutes. Forced patients to stop activities immediately, rest or use nitrate preparations can be immediately relieved. Severe cases can occur at rest or at night, and the pain may be located in the upper abdomen or back during the attack. In addition, there is also a kind of "variant angina pectoris" attack, which is characterized by chest pain at rest and often recurs in the middle of the night or early morning or at other fixed times. The attack time is longer, reaching 15 ~ 20 minutes; There was no angina pectoris during labor, and there were certain ECG changes during the attack.
Myocardial infarction is myocardial necrosis caused by coronary artery occlusion and severe and persistent myocardial ischemia. Pain is the most prominent early symptom, and its nature is basically the same as angina pectoris, but it is more intense and often lasts for several hours to several days. Although it can't be relieved by rest or nitroglycerin in the mouth, patients tend to be irritable and afraid. A few patients, mainly the elderly, have little or no pain. Severe myocardial infarction can lead to signs of shock, such as decreased blood pressure, pallor and mental retardation. Gastrointestinal symptoms such as arrhythmia, cardiac insufficiency, nausea and vomiting and fever may also occur during myocardial infarction. Electrocardiogram has special manifestations, which is very valuable for diagnosis. Examination of serum enzymes (mainly serum glutamic acid-oxalic acid-acetic transaminase, creatine phosphokinase and lactate dehydrogenase, etc.). ) is also very helpful for the diagnosis of myocardial infarction. Complications such as ventricular dilatation and papillary muscle dysfunction may occur after myocardial infarction, and in severe cases, heart rupture and rapid death may occur.