Chronic stable angina

Introduction Stable angina pectoris is the most common type of angina pectoris. It means that the disease is relatively stable for a long period of time (the WHO has a stable course for more than one month in 1979), and the frequency, duration, incentives and mitigation methods of angina pectoris are quite fixed. Causes (1) Causes of angina pectoris include: 1 coronary atherosclerosis-induced stenosis (usually above 75%); 2 coronary artery spasm, such as variant angina; 3 other coronary lesions: such as inflammation , embolism or congenital malformation; 4 non-coronary artery lesions: such as aortic stenosis or aortic regurgitation, syphilitic aortitis, severe anemia, hyperthyroidism, tachycardia tachycardia; 5 hypotension, increased blood viscosity Or slow blood flow; 6 hypertrophic cardiomyopathy, mitral valve prolapse and so on. Among them, the most important is coronary heart disease, that is, coronary atherosclerotic stenosis and/or coronary artery spasm. (B) the pathogenesis of angina is the consequence of myocardial ischemia, is caused by the imbalance between myocardial aerobic and oxygen supply. Increased heart rate, left ventricular wall tension and contractile force can increase oxygen demand; coronary blood flow and oxygen content determine myocardial oxygen supply. 1. Increased myocardial oxygen demand causes angina oxygen supply to be relatively constant, myocardial oxygen demand can cause angina pectoris, this condition is called myocardial oxygen demand increased angina. Increased myocardial oxygen demand is usually caused by the release of norepinephrine from sympathetic nerve endings, a physiological response to fatigue, emotional agitation or mental stress. The speed of myocardial oxygen demand is important in all activities. The hasty action and the forced use of second-handed over-the-head movements are particularly prone to angina pectoris. The effects of emotional agitation on the ratio of oxygen supply to oxygen consumption are complex. Emotional stress increases sympathetic tone, reduces vagal activity, and raises blood pressure; anger can cause contraction of a previously narrow coronary artery, but does not necessarily affect oxygen consumption. Factors such as exercise after eating and increased metabolic needs due to chills, fever, hyperthyroidism, and tachycardia for various reasons can also increase myocardial oxygen demand, thereby causing the onset of angina pectoris in patients with stable stenosis of coronary heart disease (Research confirmed that myocardial oxygen demand increased significantly in the onset of angina pectoris in this type of patients, especially heart rate increased). Unlike patients with unstable angina, patients with stable angina have a significant increase in heart rate before the onset of ischemia, and the likelihood of developing ischemia is proportional to the magnitude and duration of heart rate increase. Myocardial ischemia usually has a fixed coronary stenosis, limited myocardial oxygen supply, fatigue, emotional or fever and other factors that stimulate myocardial oxygen demand can induce myocardial ischemia, resulting in chest discomfort. 2. Temporary oxygen supply reduction caused by angina has been confirmed, the symptoms of unstable angina and chronic stable angina can be caused by temporary myocardial ischemia caused by coronary artery contraction. Some people call it oxygen-deficient angina. Coronary beds have good innervation, and multiple stimuli can alter coronary tension. Non-occlusive intracoronary thrombosis is another cause of decreased oxygen supply and angina pectoris, but often manifests as angina at rest, ie unstable angina, rather than chronic stable angina. The degree of fixed stenosis in patients with typical stable angina is sufficient to cause insufficient coronary blood flow to meet the increased oxygen demand for exercise. On this basis, only a small coronary artery dynamic contraction is enough to cause further deficiency of coronary flow reserve function, so that coronary blood flow drops below the critical level, causing myocardial ischemia. 3. Comparison of fixed threshold and variable threshold angina In patients with chronic angina, the range of angina thresholds can vary widely. In patients with angina pectoris who have a fixed threshold by increasing oxygen demand, there is essentially no change in the kinetic component of vasoconstriction, and the level of physical activity that induces angina is relatively constant, and the patient can predict the amount of physical activity that induces angina. The blood pressure heart rate product that induces angina or ECG ischemic performance is constant or nearly constant when the patient is undergoing exercise testing. Patients with varying angina thresholds, most with fixed coronary stenosis, coronary artery contraction can cause dynamic stenosis of blood vessels, which plays an important role in the mechanism of myocardial ischemia. Typical angina thresholds can vary, and patients can sometimes perform a significant amount of physical activity without symptoms; sometimes mild physical activity causes clinical and/or electrocardiographic myocardial ischemia, and even angina can occur at rest. . If the external environment is cold, angina is prone to attack. This is because the former increases the peripheral vascular resistance during rest or exercise, increases the arterial pressure, reduces the threshold of angina by increasing the oxygen demand, and causes the coronary artery on the other hand. Contraction, which is another cause of a decrease in the angina threshold. 4. The term mixed angina is proposed by Maseri to describe many angina between the fixed and variable thresholds. Understanding the relationship between pathophysiology and clinical myocardial ischemia in patients with stable angina is important for the selection of anti-ischemic drugs and the timing of administration. In the imbalance of aerobic and oxygen supply of the myocardium, the greater the proportion of the increase in oxygen demand, the greater the possibility that the beta blocker is effective. Nitrate and calcium antagonists are more effective when treating angina pectoris, the main cause of vasoconstriction. An increase in myocardial oxygen demand before the ischemic attack indicates an aerobic increased angina pectoris, whereby a beta blocker can be selected as the primary therapeutic agent. The pathological basis of stable angina is the stability of coronary atherosclerotic plaque, the surface of the plaque is smooth, and there are no acute factors such as ulcer, hemorrhage and thrombosis. Symptoms Most patients present: the onset of angina pectoris for a period of time (more than 1 month), the duration, severity and threshold of angina is relatively stable, that is, the amount of physical activity causing angina pectoris is more predictable, the symptoms of discomfort It can be relieved quickly after taking a break or taking nitroglycerin. 1. Symptoms Typical angina has the following six characteristics: (1) The nature of angina: For the same patient, the degree of pain in each episode can vary, but the nature of the pain is basically the same. Patients are often described as: "pressive feeling", "squeezing feeling", "suffocation", "narrowing", "up and down" and "burning". Knife-like or acupuncture-like pain is usually not angina. Sometimes when the patient is unclear about the nature of the pain, it is generally referred to as chest discomfort. The patient generally uses his entire palm or fist to indicate the discomfort, and rarely uses one finger. (2) Location and radiation of angina: Most angina is located in the posterior sternum, in the left thoracic region, and in the upper abdomen to the pharynx, as well as in any part of the bilateral anterior line. More than half of the patients have radioactive pain, and the medial part of the upper arm is a common site (this is helpful for the identification of angina and cervical spondylosis, the pain of which is just outside the upper arm), and a small amount of pain starts in the upper arm and then radiates to the front chest. In the same period, the same patient's pain site is fixed, such as enlarged parts and increased radiation sites, indicating that the lesions are aggravated; the position of chest pain does not support angina. The range of angina is as small as a fist, and it is a large piece, even throughout the chest; such as chest pain, it is dotted, linear, and does not support angina. (3) Causes of angina pectoris: The most common predisposing factor for angina pectoris is physical exertion or emotional agitation, such as the most likely to be induced when taking an emergency road, going up stairs or going uphill. This chest pain occurs at the time of fatigue rather than after, and often the symptoms quickly disappear after stopping the activity. Angina often worsens when walking against the wind, walking cold or eating after a meal, and angina is prone to worsening under physical exertion with emotional factors. It should be pointed out that the strength of angina in the same patient to induce it may vary from day to day, but not on the same day. The reason can be explained by careful questioning of medical history, such as meals, weather, and emotional agitation. The threshold for angina is lower at any time of the day than at any time of the day, so patients often find that angina can occur during the first activity in the morning, but not angina during the rest of the day or after the same activity. If the threshold varies widely, regardless of the type of angina, and is significant at rest, consideration should be given to the possibility of coronary artery spasm. Therefore, careful medical history can not only show the cause of pain (such as myocardial ischemia), but also provide clues to the ischemic mechanism [such as coronary artery spasm and/or organic obstruction]. (4) duration of angina pectoris: angina pectoris is a paroxysmal attack, the whole process is generally 3 ~ 5min, severe episodes can reach 10 ~ 15min, more than 30min are rare, should be identified with myocardial infarction. Intermittent chest pain or a jump in pain consistent with a heartbeat, a chest pain that lasts for a few seconds is not like angina; if the pain is a vague, heavy feeling that lasts for days or weeks, it is not like angina; angina is rarely affected by deep breathing. . (5) Methods for relieving angina pectoris: If you stop the activity and stand in the field for a few minutes, you can relieve it. When the angina pectoris occurs, the patient likes to take a standing position or a sitting position, and does not like the lying position. Sublingual administration of nitroglycerin for 1 to 3 minutes can relieve angina pectoris; if angina pectoris occurs 5 to 10 minutes after physical exertion, it is not effective, it is not necessarily the effect of nitroglycerin; severe angina pectoris, nitroglycerin has poor efficacy; oral nitric acid Glycerin can prevent the onset of angina pectoris and increase the exercise tolerance of patients with angina pectoris; in addition, it should be noted that nitroglycerin is placed for more than half a year, and its therapeutic effect is gradually reduced. (6) Accompanying symptoms: angina pectoris may be accompanied by chest tightness, shortness of breath, fatigue and weakness, and sometimes even the symptoms of angina are covered by these non-specific symptoms, which should be taken seriously. Careful collection of the above six aspects of information is very important for the diagnosis of angina pectoris, taking time, patience and skill. Inspiring questions often lead to error diagnosis and should be avoided. In some patients, the angina threshold can vary widely due to the contraction of the coronary arteries on a fixed stenosis basis. Such patients can perform a relatively large amount of physical activity at a certain time or at a certain time of the day, while mild activity at another time causes angina. Patients often complain of circadian circadian variation, and angina often occurs in the morning. Low temperature, emotional agitation, and mental stress can induce exertional angina, and sometimes even induce angina at rest. 2. Signs (1) Systemic examination: A detailed physical examination can provide useful diagnostic clues and affirm the patient's risk factors. Examination at the onset of angina or immediately after the onset can increase the value of the diagnosis. The examination should not only target the cardiovascular system, but also pay special attention to the existence of associated diseases that may affect the prognosis of coronary heart disease and the risk and expected effects of coronary revascularization surgery. The corneal arch (arcus corneae) can be found in the eyes, and the skin can be seen as xanthoma. The size of the corneal arch appears to be positively correlated with age, cholesterol, and low-density lipoprotein levels. The formation of xanthomas is associated with an increase in the concentration of triacylglycerol and a relative lack of high density lipoprotein. Some investigations have found that the incidence of yellow tumor and corneal arch increases with age, the highest incidence in patients with type II hyperlipidemia, and the lowest incidence in patients with type IV hyperlipidemia. Retinal arteriole changes are common in patients with coronary heart disease with diabetes or hypertension. Blood pressure can rise slowly or rise sharply during an episode of angina (and heart rate increases). Changes in blood pressure can occur before angina (promoting angina) or after (caused by angina). Other important findings of systemic physical examination are arterial pulsations and abnormalities in the venous system. The relationship between peripheral vascular disease and coronary heart disease is closely and fully affirmed. These relationships are not only seen in patients with symptomatic, clinically significant peripheral vascular disease or carotid disease, but also in asymptomatic patients with early-onset carotid disease who have decreased sputum-arm blood pressure index or confirmed by ultrasound. If palpation and auscultation are found to have carotid and peripheral arterial disease, it may indicate that unexplained chest discomfort may be caused by coronary heart disease. Examination of the patient's venous system, especially for the evaluation of the lower extremity vein, is important for determining which transplantation method to use during coronary artery bypass surgery. (2) Cardiac examination: murmurs of hypertrophic cardiomyopathy or aortic valve disease suggest that angina is not caused by coronary heart disease. Checking the heart during a chest pain episode is often valuable. A physical examination reveals transient left ventricular dysfunction due to cardiac ischemia, such as a third heart sound or a pulmonary voice. During the angina pectoris, the first heart sound mitral valve component caused by ischemic left ventricular dysfunction can be heard; a temporary second heart sound reverse division occurs, which is caused by uncoordinated left and right ventricular contraction and prolonged left ventricular contraction time. Caused by a delayed closure of the aneurysm. If there is no other obvious heart disease, a third heart sound or a loud fourth heart sound appears, suggesting that myocardial ischemia is the cause of chest pain. The 3rd and 4th heart sounds are more common in patients with angina at rest. When these patients do isometric exercise, the frequency of the third heart sound and the fourth heart sound often increases even if angina is not induced. Apical heart lift is common in patients with moderate or severe left ventricular dysfunction. In the left lateral position, the abnormal pulsation of the apex can be touched. These pulsations are related to the location of the dyskinesia and complement the diastolic auscultation results. Short-term apical systolic murmurs are quite common, suggesting papillary muscle dysfunction due to transient myocardial ischemia. Such murmurs persist, suggesting papillary muscle fibrosis, subendocardial myocardial infarction or abnormal local wall motion, resulting in changes in the relative position of the papillary muscles. Systolic murmurs are quite common in patients with severe coronary heart disease, especially those with myocardial infarction and left ventricular dysfunction. Systolic murmurs can be classified into early, late, or full systolic murmurs, and increased murmurs during exercise or angina attacks. During the onset of angina pectoris, a mid-systolic click sound caused by mitral valve prolapse can also be heard, followed by a late systolic murmur. 1. The diagnosis of angina pectoris relies mainly on symptoms, and a typical diagnosis of symptoms can be established. Before the diagnosis of coronary heart disease angina, angina caused by non-coronary diseases must be excluded. 2. Classification of angina pectoris The classification criteria for the amount of physical activity induced by angina pectoris proposed by the Canadian Society of Cardioemia have been widely adopted. This is a modification of the New York Heart Association's functional grading, but it is more specific than the latter. The grading standards are as follows: Level I: General daily activities do not cause angina, laborious, fast, long-term physical activity causes seizures. Level II: Daily physical activity is slightly restricted, and it is more constrained after a meal, cold, and emotional excitement. Level III: The daily physical activity is obviously limited. It can cause angina pectoris by walking 1 mile or upstairs at a general speed under normal conditions. Grade IV: Slight activity can cause angina, even at rest. This grading depends on accurately observing the patient. Because the clinical tolerance of patients is very different, this grading standard also has certain limitations. diagnosis Read more...