What is Angina?

Angina pectoris (angina pectoris) is a clinical syndrome mainly manifested by episodic chest pain or chest discomfort caused by insufficient temporary blood supply to the coronary arteries and acute transient ischemia and hypoxia of the myocardium. Angina pectoris is the pain felt by the heart's ischemic reflexes on the surface of the body. It is characterized by paroxysmal and compressive pain of the thorax, which can be accompanied by other symptoms. The pain is mainly located in the back of the sternum and can be radiated to the anterior heart area and the left upper limb. Or emotions often occur, each attack lasts 3 to 5 minutes, can be once a few days, can also be several times a day, rest or disappear after using nitrate preparations. This disease is more common in men, most of whom are over 40 years old. Exhaustion, emotional excitement, fullness, cold, rainy weather, and acute circulatory failure are common causes.

Basic Information

English name
angina pectoris
Visiting department
cardiology
Multiple groups
Men over 40
Common locations
Posterior sternum
Common causes
The immediate cause is an absolute or relative lack of blood supply to the heart muscle
Common symptoms
Mostly manifested as anxiety in the area of the heart, squeezing pain, which can be radiated to the neck or only chest tightness

Causes of Angina Pectoris

The direct cause of angina pectoris is the absolute or relative lack of blood supply to the myocardium. Therefore, there are various ways to reduce myocardial blood (blood oxygen) supply (such as intravascular lumen thrombosis and vasospasm) and increase oxygen consumption (such as exercise and faster heart rate). Factors can induce angina. Myocardial insufficiency is mainly due to coronary heart disease. Sometimes, other types of heart disease or uncontrolled hypertension can cause angina.
If fat accumulates in blood vessels, plaques can form. If the plaque occurs in the coronary arteries, it will cause it to narrow, further reducing its blood supply to the heart muscle, and coronary heart disease will be formed. The process of continuous deposition of fat in the coronary arteries to gradually form plaques is called coronary arteriosclerosis. Some plaques are relatively hard and stable, which can cause the coronary arteries to narrow and harden. Other plaques are relatively soft and easily fragment to form blood clots. The accumulation of this plaque on the inner wall of the coronary arteries can cause angina pectoris in two ways: the fixed position of the coronary arteries narrows the lumen, which results in greatly reduced blood flow; the formed blood clot partially or completely blocks the coronary arteries .
It is often induced by physical labor, emotional excitement, full meals, fright and cold. Typical angina pectoris often occurs under similar working conditions, and severe cases can also occur during meals, dressing, defecation, or rest. Pain occurs at the time of labor or excitement, not after a day or a period of exhaustion. Angina pectoris that occurs during quietness is the result of coronary artery spasm.
The mechanism of pain during myocardial ischemia may be caused by certain products in anaerobic metabolism of myocardium (such as lactic acid, pyruvate and other acidic substances or peptides like kallikrein) that stimulate the afferent nerve endings in the heart and often spread. Superficial nerves to the skin of the same spinal cord, causing painful radiation.

Clinical manifestations of angina pectoris

Mostly manifested as tightness, crushing pain, or a feeling of tightness behind the sternum and throat. Some patients have only chest tightness, which can be divided into typical angina and atypical angina:
1. Typical angina symptoms
Sudden squeezing, bloating, or asphyxiating pain that occurs after the upper or middle part of the sternum, may also affect most of the anterior region of the heart, and can radiate to the left shoulder, the anterior medial side of the left upper limb, reaching the ring finger and the little finger, occasionally accompanied by A sense of dying often forces patients to stop activities immediately, and severe cases also sweat. The pain lasted for 1 to 5 minutes, rarely exceeding 15 minutes. After rest or taking nitroglycerin, the pain disappeared within 1 to 2 minutes (rarely more than 5 minutes). It usually occurs during exertion, emotional excitement (anger, anxiety, excessive excitement), cold, fullness, smoking, and can also be induced by anemia, tachycardia, or shock.
2. Atypical angina symptoms
The pain can be located in the lower sternum, the left anterior region of the heart, or the upper abdomen, and radiates to the neck, lower jaw, left scapula, or right forearm. The pain can quickly disappear or only the left forearm is uncomfortable and stuffy. It is common in elderly patients or diabetic patients. .

Angina pectoris

Electrocardiogram
Electrocardiogram is the most commonly used non-invasive test for diagnosing myocardial ischemia. Patients with ECG within normal range at rest may consider dynamic electrocardiogram recording and / or cardiac stress test.
2.X-ray
No abnormal findings were found, and some patients saw changes in heart shadow enlargement, aorta widening, and pulmonary congestion.
3. Radionuclide
The commonly used radionuclides are 201 Tl or 99m Tc-MIBI, which can develop normal myocardium but not the ischemic area.
4. Selective coronary angiography
By injecting a contrast agent into the coronary arteries, obstructive lesions in the left and right coronary arteries and their branches can be displayed. Although it is an invasive test, it is also the most valuable detection method to reflect coronary atherosclerotic lesions.
5. Intravascular ultrasound imaging
The mini-ultrasonic probe is sent to the coronary arteries through a cardiac catheter, and the coronary stenosis and the lesions of the tube wall can be understood at the same time.
6. Angioscopy
Can directly observe the coronary cavity, especially suitable for thrombotic lesions.

Angina Pectoris Diagnosis

According to typical seizure characteristics and signs, remission after taking nitroglycerin, combined with age and susceptibility to coronary heart disease, except for angina caused by other reasons, can generally establish a diagnosis. In the ECG examination during the attack, the ST wave was mainly depressed, and the T wave was flat or inverted (in the case of variant angina, the lead of the ST segment was elevated), and gradually recovered within minutes after the attack. Patients with unchanged ECG may be considered for stress testing.
For patients with atypical seizures, the diagnosis depends on observing the efficacy of nitroglycerin and the changes of the electrocardiogram at the time of the seizure; if the diagnosis is still not confirmed, the electrocardiogram, the electrocardiogram load test or the continuous monitoring of the 24-hour ambulatory electrocardiogram may be repeated, such as a positive change in the electrocardiogram or a stress test A diagnosis can also be made when angina is induced.
Difficulties in diagnosis can be radionuclide examination or selective coronary angiography. Selective coronary angiography is required for those considering surgery. Intracoronary ultrasound may reveal lesions in the tube wall and may be more helpful in diagnosis.

Differential diagnosis of angina pectoris

Acute myocardial infarction
The pain site of this disease is similar to angina pectoris, but it is more severe in nature and lasts for several hours. It is often accompanied by shock, arrhythmia and heart failure, and fever, and nitroglycerin can not relieve it. The ST segment of the lead facing the infarct in the electrocardiogram was elevated with abnormal Q waves. The white blood cell count and creatine phosphokinase, aspartate aminotransferase, lactate dehydrogenase, myoglobin, myosin light chain increased, and the red blood cell sedimentation rate increased.
2.X syndrome
The disease is caused by diastolic systolic dysfunction of small coronary arteries, with recurrent angina pectoris as the main manifestation, and pain can also occur at rest. Electrocardiograms can show myocardial ischemia at the onset or after stress, nuclide myocardial perfusion can show defects, and echocardiography can show segmental wall motion abnormalities. However, this disease is more common in women. The predisposing factors for coronary heart disease are not obvious, the pain symptoms are not typical, the coronary angiography is negative, the left ventricle is not hypertrophic, the ergometrine test is negative, the treatment response is unstable, and the prognosis is good. Heart disease and angina are different.
3. Angina pectoris caused by other diseases
Angina pectoris is caused by severe aortic stenosis or insufficiency, coronary arteritis caused by rheumatic fever or other causes, coronary stenosis or occlusion caused by syphilis aorticitis, hypertrophic cardiomyopathy, and congenital coronary malformations. Differentiation should be based on other clinical manifestations.
4. Intercostal neuralgia ,
This disease often involves 1 or 2 intercostal spaces, but it is not necessarily confined to the front chest. It is tingling or burning, and it is continuous rather than episodic. Coughing, forced breathing and body rotation can make the pain worse. There is tenderness at the nerves, and there is local pain in the pull when the arm is raised, so it is different from angina.
In addition, atypical angina pectoris needs to be distinguished from chest and abdominal pain caused by esophageal lesions, diaphragmatic hernias, ulcers, intestinal diseases, cervical spondylosis, etc.

Angina Pectoris Treatment

1. Treatment at the time of the attack
(1) Rest : Take a rest immediately after the onset. Patients usually relieve their symptoms after stopping their activities.
(2) Drug treatment For severe episodes, fast-acting nitrate preparations can be used. In addition to dilating the coronary arteries, reducing resistance and increasing blood flow, these drugs also reduce peripheral venous blood volume by dilating peripheral blood vessels, reduce ventricular volume, intracardiac pressure, cardiac output and blood pressure, and reduce pre- and post-cardiac load and myocardium. Aerobic, which relieves angina.
Among them, the most commonly used is nitroglycerin tablets, which are taken under the tongue, and take effect in 1 to 2 minutes, and the effect disappears after about half an hour; isosorbide dinitrate can also be used: if taken under the tongue, it takes effect in 2 to 5 minutes; Alternatively, 0.2 ml (1 branch) of isoamyl nitrite can be wrapped with a handkerchief and crushed, and then the volatile gas is inhaled. The advantage is that the effect is fast, but the side effects are large and the smell of ether, so it is rarely used. While applying the above drugs, sedatives can be considered. After the above treatment, the pain cannot be relieved or the seizure is heavier than usual and lasts for a long time. You should consider the possibility of acute myocardial infarction and go to the hospital for treatment in time.
2. Treatment in remission
Try to avoid all incentives. Regulate diet, especially when eating should not be full; never smoke or drink. Adjust daily life and workload to reduce the mental burden; maintain appropriate physical activity, but not to the extent that pain symptoms occur; generally do not need bed rest. The three basic principles of drug therapy in remission are: selective expansion of diseased coronary blood vessels; lowering blood pressure; and improving atherosclerosis.
Patients suspected of having a prelude to myocardial infarction should rest for a period of time and use long-lasting effects. Antianginal drugs to prevent angina pectoris can be used alone, alternately or in combination with the following long-lasting drugs.
(1) Nitrate preparation Isosorbide nitrate. Pentaerythritol tetranitrate. Long-acting nitroglycerin preparation: Taking long-acting tablets makes the nitroglycerin release continuously and slowly. Apply 2% nitroglycerin ointment or patch preparation to the skin on the chest, the effect can be maintained for 12 to 24 hours.
(2) blockers ( blockers) have the ability to block the stimulation of heart rate and cardiac contractility receptors by sympathomimetic amines, slowing heart rate, lowering blood pressure, reducing myocardial contractility and oxygen consumption So as to ease the onset of angina. In addition, it also reduces the blood flow response during exercise, reducing myocardial oxygen consumption at the same level of exercise; shrinking the small arteries (resisting blood vessels) in the ischemic myocardial region, so that more blood passes through the extremely dilated side The branch circulation (transporting blood vessels) flows into the ischemic area. It can be used as the initial treatment drug, and the dose can be adjusted according to the symptoms and heart rate. Adverse reactions include prolonged ventricular ejection time and increased heart volume, which may exacerbate myocardial ischemia or cause heart failure, but its effect of reducing myocardial oxygen consumption far exceeds its adverse effects. Commonly used preparations are: propranolol, increasing the dose gradually; Oxenolol; Aprolol; Indolol; Sotalol; Metoprolol; Atenolol; vinegar dibutrolol; nadorolol and so on.
-blocker can be used in combination with nitrate, but it should be noted that: -blocker has a synergistic effect with nitrate, so the dose should be small, especially at the beginning of the dose should be reduced to avoid adverse reactions such as orthostatic hypotension; -blockers should be gradually reduced when discontinued. Sudden discontinuation may induce myocardial infarction; cardiac insufficiency, bronchial asthma and bradycardia should not be used.
(3) Calcium channel blockers This class of drugs inhibits the entry of calcium ions into cells and also inhibits the use of calcium ions in the excitation-contraction coupling of cardiac muscle cells. Therefore, inhibit myocardial contraction and reduce myocardial oxygen consumption; dilate coronary arteries, relieve coronary spasm, and improve blood supply to the myocardium under the endocardium; dilate peripheral blood vessels, reduce arterial blood pressure, and reduce cardiac load; Improve myocardial microcirculation. Commonly used preparations are: Verapamil Adverse reactions include dizziness, nausea, vomiting, constipation, bradycardia, prolonged PR interval, decreased blood pressure, etc. Nifedipine adverse reactions include headache, dizziness, fatigue, decreased blood pressure, heart rate Increase speed and so on; Diltiazem adverse reactions include headache, dizziness, insomnia and so on. New preparations Nicardipine, Nisoldipine, Amlodipine, Felodipine, Benepridil, etc.
Calcium channel blockers are most effective in treating variant angina pectoris. This class of drugs can be taken with nitrates, of which nifedipine can still be taken with -blockers, but the combination of verapamil and diltiazem with -blockers has the risk of excessive heart inhibition. When stopping this class of drugs, it should also be gradually reduced and then stopped to prevent coronary artery spasm.
(4) Coronary artery dilators can theoretically increase coronary blood flow, improve myocardial blood supply, and relieve angina. However, due to the complex conditions of coronary artery disease in coronary heart disease, some vasodilators such as dipyridamole may expand arteries without lesions or mild lesions more significantly than those with severe lesions, reducing the blood flow in collateral circulation, causing The so-called "coronary artery stealing blood" has increased the blood supply of normal myocardium, and has reduced the blood supply of ischemic myocardium, so it is no longer used to treat angina pectoris. Currently used: Modoming: adverse reactions include headache, facial flushing, gastrointestinal discomfort, etc. Amiodarone: also used to treat tachyarrhythmia, adverse reactions include gastrointestinal reactions, drug rash, corneal pigmentation Calmness, bradycardia, thyroid dysfunction, etc .; ethoxylated flavonoids; carbopolumone; aoxifene; aminophylline; papaverine and so on.
(5) Antioxidant Given that the core cause of atherosclerosis is oxidative stress and inflammatory response. Oxidative stress is caused by the oxidation of low-density lipoprotein LDL to Ox-LDL. Ox-LDL is the starting point of atherosclerosis. Therefore, it is particularly important to prevent LDL from oxidizing to Ox-LDL. Nowadays, a relatively certain therapy is effective. Antioxidants, such as natural antioxidants such as ASTA astaxanthin and anthocyanins, have been selected as the preferred drugs for the prevention and treatment of coronary heart disease in the United States and other countries. Astaxanthin can significantly reduce the inflammatory factor CRP (C-reactive protein) and tissue atherosclerosis Sclerotic thrombosis.
3. Other treatments
Low-molecular dextran or hydroxyethyl starch injection, which is used to improve microcirculation perfusion, can be used for frequent episodes of angina pectoris. Anticoagulants such as heparin, thrombolytic drugs, and antiplatelet drugs can be used to treat unstable angina pectoris. Hyperbaric oxygen treatment can increase the supply of oxygen throughout the body, which can improve stubborn angina, but the effect is not easy to consolidate. Extracorporeal counterpulsation therapy can increase the blood supply to the coronary arteries and may also be considered for application. For those with early heart failure, fast-acting digitalis should be used while treating angina.
4. Surgical treatment
The aorta-coronary artery bypass grafting operation is mainly performed under extracorporeal circulation. The patient's own great saphenous vein is used as the material for bypass grafting. ; Or the free internal mammary artery is anastomosed with the distal end of the diseased coronary artery, and the blood flow of the aorta is introduced to improve the blood flow supply of the myocardium supplied by the diseased coronary artery.

Prognosis of angina pectoris

Most patients can be relieved or disappear after treatment. Myocardial infarction may occur in some of the initial angina pectoris, worsening angina pectoris, lying angina pectoris, variant angina pectoris and intermediate syndrome, so it is also called "pre-infarction angina pectoris".

Angina pectoris prevention

1. Control salt intake
Eat less salt. The main component of salt is sodium chloride. Long-term consumption of sodium chloride will increase blood pressure and damage blood vessel endothelium. Patients with angina pectoris should control their daily salt intake below 6 grams.
2. Control fat intake
Eat less fat and reduce calorie intake. A high-fat diet will increase blood viscosity, increase blood lipids, and hyperlipidemia is the cause of angina pectoris. The amount of edible oil should be reduced as much as possible. Oils are also important substances for fat formation. But you can choose vegetable oil containing unsaturated fatty acids instead of animal oil. The total daily oil consumption should be limited to 5-8 teaspoons.
3. Avoid eating animal gut
Animal organs are rich in fatty alcohols, such as liver, heart, and kidney.
4. Quit smoking and drinking
It is well known that tobacco and alcohol are harmful to the human body. It not only induces angina pectoris, but also induces acute myocardial infarction.
5. Eat more foods rich in vitamins and dietary fiber
Such as fresh vegetables, fruits, coarse grains, etc., eating more marine fish and soybeans is beneficial to the prevention and treatment of coronary heart disease.
6. Eat more foods that improve blood vessels
Such as garlic, onion, hawthorn, black fungus, jujube, bean sprouts, carp, etc.
7. Avoid eating irritating and flatulent foods
Such as strong tea, coffee, pepper, curry and so on.
8. Pay attention to eat less and eat more, avoid overeating
Dinner should not be too full, so as not to induce acute myocardial infarction.

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