Stable angina pectoris in the elderly
Introduction
Introduction to stable angina pectoris in the elderly Stable angina pectoris is a common kind of angina pectoris in clinical practice. It is mainly caused by myocardial ischemia due to the fact that the blood flow of the diseased coronary artery cannot be compensated to increase to meet the needs of the myocardium during physical activity. There are clear incentives for chest pain attacks. The degree and duration of the attack are relatively fixed. The pain is relieved quickly after rest or nitroglycerin. Basic knowledge Prevalence rate: 0.058% Susceptible population: the elderly Mode of infection: non infectious Complications: acute myocardial infarction, arrhythmia, heart failure
Cause
Etiology of stable angina pectoris in the elderly
（1） Pathogenesis
The vast majority (more than 90%) of angina pectoris is caused by coronary atherosclerotic lesions. When the stenosis caused by atherosclerotic lesions exceeds 50%~75%, when the myocardial oxygen consumption increases and the coronary blood flow cannot increase, myocardial ischemia can occur, causing angina pectoris. Other heart diseases, such as aortic valve stenosis or reflux, can also cause angina pectoris, especially in the elderly, Because the degenerative change of aortic valve can make the valve thickened, stiff or calcified, a few can develop into calcified aortic valve stenosis, which can lead to the reduction of coronary artery blood flow and cause angina pectoris in severe cases, and the congenital bicuspid aortic valve can also form severe calcified main artery valve stenosis in old age, leading to angina pectoris, rheumatic aortic valve stenosis and reflux, Angina pectoris can also be caused in old age. In addition, hypertrophic cardiomyopathy with left ventricular outflow tract stenosis, aortic dissection, syphilitic aortitis, and arteritis invading coronary arteries can also cause angina pectoris. Some extracardiac factors such as severe anemia, hyperthyroidism, obstructive pulmonary diseases can also affect the onset of angina pectoris.
（2） Pathogenesis
1. Occurrence principle of myocardial ischemia
(1) Increased myocardial oxygen consumption: in the resting state, the myocardium absorbs 70%~75% oxygen from the coronary artery blood. Therefore, the increase of myocardial oxygen supply mainly depends on the increase of coronary artery blood flow. Under normal conditions, the coronary circulation has good reserve strength. When the myocardial oxygen consumption increases, the coronary artery expands accordingly, increasing coronary blood flow, In order to meet the needs of the myocardium, for example, during strenuous exercise, the heart rate increases, coronary artery resistance decreases, and coronary blood flow can be increased to 5-6 times of normal.
At rest, the coronary circulation was in a state of low flow and high resistance; During exercise, sympathetic nerve excitation and catecholamine pass through β Adrenergic receptors can dilate blood vessels and increase blood flow; More importantly, when myocardial oxygen tension decreases, adenosine, lactic acid and other metabolites directly expand small arteries to reduce vascular resistance and automatically regulate blood flow. Therefore, during exercise, coronary circulation changes to a state of high flow and low resistance. Coronary artery resistance mainly comes from small arteries. When the stenosis degree of a larger branch of the coronary artery exceeds 50%, the stenosis part will hinder blood flow, The maximum reserve of coronary circulation starts to decline, the metabolic disorder caused by ischemia activates the automatic regulation mechanism, which makes the small arteries expand and the large arteries further narrow. The small arteries need to be expanded accordingly, and the blood flow can still remain normal under the resting state. When the heart is overloaded or the oxygen consumption of its heart muscle increases more than the blood volume provided by the small arteries, There is temporary myocardial ischemia and hypoxia, which causes angina pectoris.
(2) Reduction of myocardial oxygen supply: transient reduction of coronary artery oxygen supply leads to myocardial ischemia, which is another important factor to induce angina pectoris. This primary reduction of blood supply is mainly caused by coronary artery dynamic obstruction. When coronary artery has a fixed obstructive lesion, coronary artery spasm or contraction slightly increases the degree of dynamic obstruction, It can make the coronary blood flow fall below the critical level, thus causing myocardial ischemia and inducing angina pectoris. In some patients, the coronary artery has no obvious stenosis and severe dynamic obstruction (mainly coronary artery spasm). It can also cause myocardial ischemia, leading to variant angina pectoris and non occlusive coronary artery thrombosis, which is also the cause of myocardial ischemia, It often causes unstable angina pectoris.
(3) The increase of myocardial oxygen consumption and the decrease of myocardial oxygen supply co-exist: for example, when the sympathetic nerve is excited during exercise or cold, the heart rate is accelerated, and the blood pressure is increased, so that the myocardial oxygen consumption is increased; At the same time, due to α- The adrenergic receptor nerve is excited, which makes the blood vessel contract, leading to the reduction of myocardial oxygen supply. The angina pectoris caused by the joint participation of the two factors is called mixed angina pectoris.
2. The main factor determining myocardial oxygen consumption When the main stenosis degree of the coronary artery exceeds 50%, the myocardial oxygen supply can still be met at rest. The relative blood supply of the coronary artery is insufficient during exercise, causing myocardial ischemia. At this time, the important means of treatment is to reduce myocardial oxygen consumption to improve exercise tolerance. The main factors determining myocardial oxygen consumption during the onset of angina pectoris are as follows.
(1) Ventricular wall tension: it is related to the systolic ventricular pressure, heart size and wall thickness. According to Laplace formula, the ventricular wall tension is directly proportional to the ventricular radius and inversely proportional to the wall thickness. Therefore, when the left ventricular systolic pressure or left ventricular volume increases, the ventricular wall tension increases, leading to an increase in myocardial oxygen consumption.
(2) Duration of myocardial systole: it is usually explained by the total ejection time per minute. The ejection time per stroke of the left ventricle × Heart rate=ejection time per minute. During ejection, the ventricular wall tension is the largest. The longer the ejection time is, the more oxygen consumption is. The ejection time per stroke remains the same. When the heart rate increases, the ejection time per minute increases. Therefore, the myocardial oxygen consumption is related to heart rate and ejection time.
(3) Myocardial contractility: the stronger the myocardial contractility, the greater the myocardial oxygen consumption. Heart rate, blood pressure and ventricular volume load are commonly used to estimate the myocardial oxygen consumption, and "heart rate" can also be used × Systolic blood pressure "is used as a rough indicator to judge myocardial oxygen consumption.".
The myocardial oxygen demand increases with the increase of cardiac work, and the following factors can increase the myocardial oxygen consumption:
① Elevated blood pressure, left ventricular hypertrophy, left ventricular outflow tract stenosis, exposure to cold environment and congestive heart failure mainly increase myocardial systolic tension and increase myocardial oxygen consumption.
② The heart rate increases significantly during exercise and emotional stress, which is the main factor to increase myocardial oxygen consumption.
③ Physical activity or the use of positive inotropic drugs mainly increases oxygen consumption by enhancing myocardial contractility.
Prevention
Prevention of stable angina pectoris in the elderly
1. Proper physical exercise can improve the function of myocardium and promote the formation of coronary collateral circulation.
2. Try to avoid the factors inducing angina pectoris, such as smoking, drinking, emotional excitement, etc.
3. Combine work with rest.
4. Reasonable nutrition and less high-fat food.
5. Prevent and actively treat diseases that induce angina pectoris, such as hypertension, obesity, diabetes, etc.
Complication
Complications of stable angina pectoris in the elderly complication Arrhythmia and heart failure in acute myocardial infarction
Acute attack of senile stable angina pectoris causes sudden coronary occlusion, which can lead to acute myocardial infarction, arrhythmia or heart failure.
Symptom
Symptoms of stable angina pectoris in the elderly common symptom Pale and weak, anxious, dyspnea, arm pain, forced standing position Systolic murmur Upper abdominal pain Chest pain Hypertension
1. Symptoms
The main clinical manifestation is paroxysmal chest pain, which is mainly located behind the sternum, or to the left or the precordial area. The conscious pain is deep rather than on the body surface. The pain range is one, which can be accompanied by radiating pain. The pain site is relatively fixed each time. The nature of the pain is mostly suffocation or oppression, and occasionally accompanied by a sense of fear of dying. The patient often unconsciously stops moving, Until the symptoms are relieved, the amount of physical activity that causes angina attacks is basically fixed and can be predicted, such as heart rate × When systolic blood pressure is used as a rough indicator of myocardial oxygen consumption, the product value of angina pectoris is close each time. Angina pectoris usually occurs suddenly, lasting for a few minutes to 10 minutes, and rapidly alleviates after rest. Most patients have a good response to nitroglycerin, which can be completely alleviated 1 to 3 minutes after taking it. The elderly are insensitive to pain, The location and nature of angina pectoris are not typical due to labor or emotional excitement. Some patients may not have chest pain, but have left or right arm pain, accompanied by finger numbness, or shoulder or interscapular pain, or upper abdominal pain and other digestive tract symptoms, sometimes only manifested as dyspnea, weakness or fatigue without chest pain, and because the elderly often have emphysema and other organ diseases, Angina pectoris can be induced by other diseases, or easily covered up or confused by other diseases, which makes it difficult to diagnose. In addition, the threshold of stable angina pectoris is not always fixed. On the basis of stable coronary artery stenosis, if there is a slight change in coronary tension, the flow of coronary artery can be significantly reduced, and the exercise endurance can be significantly reduced, There are some special clinical manifestations:
(1) First Effort Angina.
(2) Walking Trough Angina: Angina pectoris occurs when walking. The patient only needs to slow down and continue walking. Angina pectoris can disappear. Later, the original walking speed will be restored and angina pectoris will not occur. This phenomenon is related to the increase of coronary artery tension at the beginning of walking.
(3) Stable exertional angina pectoris: patients are more prone to attack when they are active in cold air. The impact of cold air on the pathogenesis of angina pectoris has two aspects: one is that cold blood vessels contract, the surrounding resistance increases, the pressure load of the left ventricle increases, and the increase of myocardial oxygen consumption induces angina pectoris; the other is that cold can also cause coronary artery contraction, reduce the blood supply of coronary artery and induce angina pectoris.
2. Physical signs
The following signs may appear when angina attacks:
(1) Anxiety, pale face, sweating, high blood pressure and heart rate.
(2) The first heart sound (S1) at the apex is weakened, and an enhanced fourth heart sound (S4) may appear. If the heart rate exceeds 100 beats/min, it is called the galloping rhythm of the fourth heart sound, reflecting the decline of ventricular compliance; Hypertonic third heart sound (S3) may also occur. If the heart rate exceeds 100 beats/min, it is called early diastolic galloping rhythm, reflecting left ventricular systolic dysfunction.
(3) When accompanied with dysfunction of papillary muscles, it indicates acute ischemia of papillary muscles, which may lead to temporary mitral insufficiency. Systolic clicks and (or) mid - and late systolic murmurs can be heard on the medial side of the cardiac apex. The above clicks and systolic murmurs can vary in loudness during the onset of angina pectoris, and can be alleviated or disappeared after angina pectoris is relieved.
3. Classification of angina pectoris
When selecting patients for PTCA or coronary artery bypass grafting (CABG), the grade of angina pectoris is an important factor to consider clinically. If the drug treatment for Grade III and IV angina pectoris is ineffective, coronary angiography should be performed to decide whether to do PTCA or coronary artery bypass grafting (CABG). Angina pectoris Grade III and IV have a history of hypertension, myocardial infarction, and ST segment depression of resting ECG is a high-risk group, with a 6-year mortality rate of 40%, and no risk of 8%, It is suggested that the classification of angina pectoris has certain reference value for prognosis.
In 1972, the Canadian Cardiovascular Association graded the patients according to the activity of inducing angina pectoris, which was more suitable for clinical application, helpful for evaluating the condition, and adopted internationally.
Grade I: ordinary daily activities do not cause angina attacks, but physical activities that are laborious, fast, and long time will cause attacks.
Level II: daily physical activity is restricted, especially after meals, in cold wind and in a hurry.
Grade III: daily physical activity is significantly limited. Under normal conditions, walking at a normal speed for one block or one floor on the ground can cause angina pectoris.
Grade IV: Slight activity can cause angina pectoris, even when resting.
Examine
Examination of stable angina pectoris in the elderly
Cholesterol and triacylglycerol are elevated or normal, or lipid metabolism is abnormal, white blood cells and erythrocyte sedimentation rate are normal, myocardial enzymes, troponin and myosin are normal.
1. Electrocardiogram (ECG) ECG examination is the most common examination method to find myocardial ischemia and diagnose angina pectoris. There are three commonly used types of resting ECG, dynamic ECG (Holter monitoring) and stress ECG.
(1) Rest ECG: 50%~83% of patients with typical angina pectoris have normal rest ECG. Possible ECG changes include ST-T changes, abnormal QRS waves, abnormal Q waves, bundle branch block, and various arrhythmias.
The abnormality (Q wave width>0.04s, depth 1/4R) indicates that there has been myocardial infarction in the past, some of which may have no corresponding symptoms, and the infarcted Q wave may or may not be accompanied by ST-T changes. In addition, some angina pectoris attacks have transient abnormal Q waves, and when the attack stops, the Q wave disappears.
The most common ECG abnormality in elderly patients is nonspecific ST-T change, lacking specificity, and the reliability of diagnosing myocardial ischemia is poor. During the onset of angina pectoris, most patients may have ST segment changes due to temporary myocardial ischemia, that is, the horizontal or downward depression of the upper ST segment in the R wave dominated lead is ≥ 0.1mV, and some patients only show T-wave inversion, Or if the original T wave is inverted, the T wave degree is upright (pseudo improvement), which is due to angina caused by ventricular wall movement disorder, and it recovers quickly after remission. This dynamic change of ECG has a high value for the diagnosis of myocardial ischemia.
Complete left bundle branch block (CLBBB) indicates extensive coronary artery disease and left ventricular dysfunction.
Left anterior branch block and left posterior branch block can be seen in coronary heart disease, left ventricular hypertrophy and changes in heart position, and can be seen in the onset of angina pectoris, which is of diagnostic significance.
QRS wave is short and low voltage of QRS wave is a very sensitive index for diagnosing myocardial ischemia, which has high diagnostic value.
But there are also a few patients who have no ECG changes during the attack, so the diagnosis of angina pectoris cannot be ruled out by the normal ECG during the attack of chest pain.
(2) Holter monitoring:
Positive criteria: ST segment is horizontal or downward sloping (0.08s after the J point), with depression ≥ 0.1mV and duration ≥ 1min. The next ST segment depression should occur at least 1min after the previous ST segment depression recovers to the baseline. Upward sloping ST segment, downward movement of J point and changes of T wave cannot be used as indicators of myocardial ischemia. Holter can continuously monitor for 24 to 48h, not only to record patients' daily activities, ECG changes of myocardial ischemia during chest pain attack during rest or sleep, and the ECG changes of asymptomatic myocardial ischemia can be recorded. About 75% of ischemic ST segment depression in daily life of coronary heart disease patients monitored by Holter is asymptomatic, and the average ratio of asymptomatic myocardial ischemia attack to myocardial ischemia attack with angina symptoms is 3 to 4 ∶ 1, The correlation study with coronary angiography showed that the positive rate of coronary heart disease detected by dynamic electrocardiogram was 80%, and the false positive rate was 13%. The elderly patients could not do exercise test due to various reasons. Holter monitoring has certain diagnostic value.
(3) Load ECG exercise test: this test can be performed for those who have no change in resting ECG. At present, multi-stage treadmill or treadmill exercise test is mostly used. Result judgment: positive standard:
① During and (or) after exercise, the ST segment is horizontal or downward inclined (0.08s after the J point), and the depression is ≥ 0.1mV; Or ST segment is horizontally elevated ≥ 0.1mV;
② ST segment depression with ventricular arrhythmia, such as frequent ventricular premature contractions (ventricular premature beats), paired ventricular premature beats, multi-source ventricular premature beats or short bursts of ventricular tachycardia;
③ U wave inversion;
④ Exercise causes labor induced hypotension, and the systolic blood pressure is reduced by ≥ 10 mmHg;
⑤ Typical angina pectoris occurs during exercise. At present, it is believed that only when coronary atherosclerosis causes coronary artery stenosis diameter ≥ 50%, can exercise test produce ECG ischemic changes. According to the comparative study results of a large number of ECG exercise tests and coronary angiography (CAG), the sensitivity of ECG exercise tests for patients with single coronary artery lesions is 37%~60%, and that for patients with two coronary artery lesions is 69%, 86%~100% of the lesions were in the left main trunk or three branches. The positive rate of ECG exercise test was high in patients with anterior descending branch lesions, and false negative was easy to appear in patients with circumflex branch lesions; The positive rate of proximal stenosis of the same coronary artery disease was higher than that of distal stenosis; Although the coronary artery has severe stenosis, if sufficient collateral circulation is established, the exercise test can be negative. In addition, the above ST changes, such as those occurring in patients with exertional angina pectoris who have low exercise volume (Bruce program level 1 exercise volume in the treadmill exercise test, METS 5.0), if there is multi lead severe ST segment depression (ST segment level or downward slope depression>0.2 mV) and/or blood pressure drop, It is suggested that there are left main coronary artery or three coronary artery lesions, which is of great significance in evaluating the treatment and prognosis of patients with coronary heart disease. Patients with coronary heart disease can show myocardial ischemia in the resting state, and the myocardial oxygen consumption increases during exercise. When the myocardial oxygen consumption exceeds the coronary artery reserve, it can lead to myocardial blood deficiency. Therefore, exercise ECG is helpful in the diagnosis of coronary heart disease, Indications: According to the exercise test standards recommended by the American Heart Association and the American College of Cardiology (AHA/ACC) in 1990, the main indications are:
① Determine the diagnosis of coronary heart disease;
② Differential diagnosis of chest pain;
③ Early detection of occult coronary heart disease;
④ Determine the arrhythmia related to exercise;
⑤ Evaluating cardiac function;
⑥ Evaluate the therapeutic effect of coronary heart disease (drugs, PTCA, CABG, etc.);
⑦ To evaluate the prognosis of patients with myocardial infarction;
⑧ Instruct patients to recover.
Contraindications: With the increase of clinical research fields, the renewal of treatment methods and the accumulation of experience, the application scope of exercise electrocardiogram (EET) has been significantly broadened, and the contraindications have been somewhat relaxed. Recently, the absolute contraindications formulated in the U.S. EET Guidelines include:
① Acute myocardial infarction within 2 days;
② Unstable angina pectoris beyond drug control;
③ Abnormal heart rate with symptoms or uncontrolled hemodynamic disorders;
④ Severe aortic stenosis;
⑤ Uncontrolled symptoms of obvious heart failure;
⑥ Acute pulmonary artery thrombosis or infarction;
⑦ Acute myocarditis or pericarditis;
⑧ Acute aortic dissection.
End point of exercise: the termination of treadmill exercise has symptom limitation and heart rate limitation (currently, 85%~90% of the expected maximum heart rate is often used), and the absolute termination indications defined in the EET Guide are
① Systolic blood pressure drop ≥ 1.33kPa;
② Moderate to severe angina pectoris;
③ Malignant neurological symptoms, such as syncope;
④ Hypoperfusion, such as cyanosis and pallor;
⑤ Persistent ventricular tachycardia;
⑥ ST segment elevation ≥ 1.0mV.
2. Ultrasonic ECG
(1) Two dimensional echocardiography (2DE) exercise test: detection method: take the patients with normal systolic motion of the ventricular wall at rest as the object, and carry out the treadmill exercise test according to the Balke scheme. 2DE is performed immediately (1~2min) after exercise, and the detection standard of coronary heart disease (CHD) is positive if there is temporary abnormal motion of the ventricular wall:
① During the onset of angina pectoris or exercise test, the amplitude of regional ventricular wall contraction movement in the ischemic area decreases, disappears or even reverses (contradictory movement), of which reduction is the most common.
② The mitral valve orifice flow spectrum of Doppler ultrasound showed that the end diastolic spectrum amplitude (A peak)>the early diastolic spectrum amplitude (E peak), and the E/A ratio<1.0 (normal E/A ratio>1.0), indicating that the left ventricular compliance was reduced.
③ The left ventricular ejection fraction (EF) did not increase during exercise, indicating that the left ventricular pump function was reduced. The sensitivity of 2DE exercise test for the diagnosis of coronary heart disease (CHD) was 76% on average, and the specificity was 86% on average, which was higher than that of ECG exercise test.
(2) Drug load: the drug load can be applied to elderly patients or those who are unable to complete the rated exercise volume due to lack of exercise ability, or when the respiratory acceleration caused by exercise affects the image quality. The commonly used drugs are dipyridamole, dobutamine and adenosine, of which dobutamine is more sensitive than dipyridamole, but the specificity of the three drug loads is similar, Dobutamine was used more frequently than dipyridamole in clinical practice.
(3) Myocardial contrast-enhanced ultrasound (MCE): also known as ultrasonic myocardial contrast, the Department of Cardiology of Pearl River Hospital has initially successfully developed an acoustic contrast agent, which is a glycoprotein microbubble containing fluorocarbon gas (C3F8 glycoprotein acoustic vibration fluid). On the basis of successful animal experiments, it has been initially applied to clinical practice. After intravenous injection of a new type of contrast agent (0.01ml/kg) to 12 volunteers, Satisfactory results were obtained: the normal myocardium produced visible contrast enhancement of ultrasound; Myocardium in ischemic area showed microbubble contrast medium sparse area; Myocardial necrosis area showed segmental filling defect. One female patient had complete left bundle branch block in ECG and normal coronary angiography. Echocardiography showed segmental filling defect in the anterior septum, and then nuclide myocardial perfusion imaging (ECT) confirmed that there was filling defect in the same segment of the anterior septum. All patients with intravenous injection of new contrast agent had no obvious side effects. ECG, There was no change in blood pressure monitoring.
3. Radionuclide myocardial perfusion imaging (ECT) Radionuclide myocardial perfusion imaging methods include resting myocardial perfusion imaging and stress test. The latter is divided into exercise stress test and drug stress test. Foreign scholars believe that radionuclide myocardial perfusion imaging stress test is an accurate, sensitive and non-invasive main inspection method. The indications are:
① Etiological diagnosis of chest pain;
② Assessment of the location, scope and extent of myocardial ischemia;
③ Understand the myocardial blood supply before and after CABG or PTCA;
④ To judge the prognosis of coronary heart disease, 201IL or 99mTc MIBI are commonly used radionuclides clinically for exercise stress test. Normal myocardial imaging is uniform, and the coronary blood flow of ischemic or infarcted myocardium is reduced, resulting in radioactive release area or defect area. Radionuclide exercise loads the heart
Myocardial perfusion imaging is of great value in diagnosing coronary heart disease. Compared with ECG exercise stress test, it is more sensitive and specific, especially for women. A multicenter study including 1042 cases of SPECT myocardial imaging exercise test showed that the total sensitivity of diagnosing coronary heart disease was 90%, and the detection rate of 1, 2 and 3 coronary artery lesions was 83%, 93% and 95%.
The commonly used drugs for radionuclide drug stress test myocardial perfusion imaging are dipyridamole, dobutamine and adenosine. The application of exercise stress test in elderly people is limited due to lung infection, severe myocardial ischemia, lack of exercise and general state. Drug stress test is helpful to detect the myocardial blood flow perfusion of the above patients, He Zuoxiang et al. observed 21 cases of dobutamine 201TL three-dimensional myocardial imaging in 1996, the diagnostic value of coronary heart disease was 92%, and the sensitivity was 96%.
4. The above medical history, clinical symptoms and various non-invasive examination methods of coronary angiography (CAG) and ventriculography are of great value for the diagnosis and assessment of coronary heart disease. However, coronary angiography is still needed for the diagnosis of coronary heart disease, as well as the accurate judgment of the location, shape, severity and prognosis of coronary stenosis, Coronary angiography is an essential means to determine whether patients need coronary revascularization (including PTCA, circumcision, stent implantation, and CABG). Not all patients with coronary heart disease need coronary angiography, but this examination is necessary when there are the following conditions:
(1) The clinical symptoms and non-invasive examination methods can not determine whether there is coronary heart disease, and coronary angiography can make a clear diagnosis.
(2) Clinical symptoms or non-invasive examination methods suggest that it is uncertain whether there is coronary heart disease, and coronary angiography can make a clear diagnosis.
(3) Angina pectoris symptoms are serious, but medical treatment is unsatisfactory, affecting daily life.
The purpose of coronary angiography is to select patients for percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). The comparative study of clinical and coronary angiography has deepened the understanding of coronary heart disease:
① The relationship between the number of coronary artery lesions and exertional angina pectoris: severe exertional angina pectoris (angina pectoris grade Ⅲ, Ⅳ), most of which are left main coronary artery lesions or multi vessel lesions.
② The incidence of 1, 2 and 3 branches of exertional angina pectoris is roughly the same, but the reports are different from each other. The domestic reports of single branch disease are more (36%~48.4%), followed by 2 branches and 3 branches.
③ Left main artery lesions were reported 7%~14% in China and 5%~10% in foreign countries.
④ About 10% of patients with angina pectoris have normal coronary angiography or no important lesions, and some of them have positive ergometrine test, which indicates coronary artery spasm. Those with positive ergometrine test may be caused by small coronary artery diastolic dysfunction, such as syndrome X, left ventriculography: it is the main method for evaluating left ventricular function, and EF value can be calculated, It is of great value to select patients for revascularization to find abnormal regional wall motion (hypokinesia, immobility, and contradictory motion).
Safety of coronary angiography: A large number of data prove that this examination method is safe, with mortality of 0.1%~0.45%, myocardial infarction of 0.61%, and blood embolism complications of 0.23%.
Diagnosis
Diagnosis and differential diagnosis of stable angina pectoris in the elderly
diagnostic criteria
The diagnosis of stable angina pectoris mainly depends on consultation, which can not be replaced by any other diagnostic method. If there are typical symptoms, the diagnosis of angina pectoris can be established. Since labor angina pectoris can also be seen in other diseases, such as hypertrophic cardiomyopathy, aortic stenosis, etc., attention should be paid to the diagnosis of the original disease. After excluding other diseases, It can be considered that exertional angina is caused by coronary heart disease.
Stable angina pectoris should be differentiated from initial exertional angina pectoris. The main difference between the two is that the latter has onset within 1 month and tends to exacerbate, and the symptoms of angina pectoris can be mild. It is not uncommon for exertional angina pectoris to coexist with spontaneous angina pectoris, which is dominated by exertional angina pectoris, but sometimes the onset of angina pectoris has nothing to do with labor, This type should be diagnosed as mixed angina pectoris.
The key point of distinguishing stable angina pectoris from variant angina pectoris is that the attack of the latter has nothing to do with the degree of activity and emotion; The symptoms are serious, lasting for a long time, and rest cannot alleviate the onset of pain; ST segment elevation occurs when angina pectoris attacks, and ST segment returns to normal after the attack.
differential diagnosis
1. Esophageal diseases commonly include reflux esophagitis, hiatal hernia and esophageal spasm, which can cause chest pain and can be easily confused with angina pectoris. According to the history of these diseases, the characteristics of chest pain, the relationship between chest pain and diet, combined with barium meal or gastroscopy, it is not difficult to make a diagnosis.
2. Cholecystitis often starts suddenly, and the pain is more severe in the upper abdomen, accompanied by fever, leukocytosis, etc. Abdominal B-ultrasound can make a clear diagnosis.
3. The location and nature of acute myocardial infarction pain are the same, but the chest pain is severe and lasts for a long time, generally>30min. It is not difficult to distinguish it from angina pectoris by combining the medical history, dynamic observation of ECG, and serum enzyme examination.
4. The main symptom of patients with acute pulmonary infarction is dyspnea, accompanied by chest pain, but the chest pain worsens when inhaled. Pleural friction sounds can be heard by auscultation. X-ray chest film is helpful for diagnosis.
5. Anterior chest wall diseases include costochondritis, chest wall contusion, pectoralis major pain caused by influenza virus, herpes zoster, etc.
6. When cervical or thoracic osteoarthropathy involves the dorsal root of spinal nerve, it can cause severe chest pain, and cervical rib, left shoulder periarthritis can produce angina like symptoms.
7. Chest pain caused by non ischemic angina, such as pericarditis, cardiomyopathy, mitral valve prolapse, mitral valve or active valve disease, etc.
For those whose symptoms of chest pain are ambiguous and can not be sure whether they are angina pectoris, further ECG stress test, echocardiography stress test, radionuclide and other examinations should be carried out, and coronary angiography (CAG) should be carried out when necessary to make a clear diagnosis.
According to the degree, scope and morphological characteristics of coronary artery stenosis, appropriate patients can be selected for PTCA or CABG. When some patients with coronary artery disease have normal CAG results and MCE or ECT has filling defects, microtubule lesions should be considered. At this time, further measurement of coronary artery endothelial cell function is of great significance.
