Introduction
Stable angina(stable angina pectoris) is the most common type of angina in the clinic. 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.
Cause
(1) Causes of the disease
Causes of angina include: 1 coronary atherosclerosis caused by 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, acne tachycardia; 5 hypotension, increased blood viscosity or slow blood flow; 6 Hypertrophic cardiomyopathy, mitral valve prolapse, etc. Among them, the most important is coronary heart disease, that is, coronary atherosclerotic stenosis and/or coronary artery spasm.
(two) pathogenesis
Angina is a consequence of myocardial ischemia and is caused by an 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.
symptom
Most patients showed that the onset of angina pectoris was stable for a period of time (more than 1 month), and the duration, severity, and threshold of angina pectoris were relatively stable, that is, the amount of physical activity causing angina pectoris was more predictable, and the symptoms of discomfort were rested. Or it can be relieved quickly after 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 may 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:
Grade I: General daily activities do not cause angina, laborious, fast, and 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
Angina should also be differentiated from other diseases that cause chest discomfort.
Esophageal disease
(1) reflux esophagitis: due to the lower esophageal sphincter relaxation, acidic gastric reflux, causing esophageal inflammation, paralysis, manifested as burning pain in the posterior sternum or mid-upper abdomen, sometimes can be radiated to the back and suspected angina. However, the disease usually occurs when the patient is lying down on the meal, and the antacid can relieve it.
(2) esophageal hiatus hernia: often accompanied by acid reflux, the symptoms are similar to esophagitis, often after bending or lying down after a meal, gastrointestinal angiography can be clearly diagnosed.
(3) diffuse esophageal fistula: can also be associated with reflux esophagitis, which can cause a variety of chest pain, taking nitroglycerin is effective, ergometrine can be induced, it is easy to suspect angina pectoris, is atypical angina A common cause of chest pain. According to the patient's history of acid reflux and anorexia, the symptoms often occur when eating or especially cold drinks or after meals, and are not related to fatigue, and dysphagia at the time of onset may be distinguished from angina pectoris. Esophagoscopy and esophageal manometry can confirm the diagnosis.
Clinically, angina and esophageal diseases often coexist, esophageal reflux can reduce the threshold of angina pectoris, esophageal fistula can be induced by ergometrine and relieved by nitroglycerin, so the identification of the two is often difficult. Chest pain is characterized by "burning heart" and is associated with changes in body position and eating. At the same time, dysphagia is a characteristic of esophageal pain; esophageal pain is more often radiated to the back than angina. Accurate diagnosis requires not only careful medical history and physical examination, but sometimes laboratory testing.
2. Lung, mediastinal disease
(1) Pulmonary embolism: The pain suddenly occurs and occurs at rest. Patients with high risk factors (such as heart failure, venous disease, postoperative surgery, etc.) are often accompanied by hemoptysis and shortness of breath. The nature of the pain is typically described as a chest tightness accompanied by or subsequent pleural inflammatory chest pain, ie sharp pain in the side of the chest, which is exacerbated by breathing or coughing. X-ray chest radiograph, pulmonary angiography, and pulmonary radionuclide scan can confirm the diagnosis.
(2) Spontaneous pneumothorax and mediastinal emphysema: Both chest pains occur suddenly. The former is located on the side of the chest and the latter is located in the center of the chest, all accompanied by acute dyspnea. X-ray chest X-ray can be clearly diagnosed.
3. biliary colic This disease often occurs suddenly, the pain is severe and often fixed, lasting 2 to 4 hours, and then can disappear by itself, without any symptoms during the interictal period. It is usually the heaviest in the right upper abdomen, but it can also be located in the upper abdomen or in the anterior region. This discomfort often radiates to the scapula and can travel along the costal ribs to the back, occasionally radiating to the shoulders, suggesting that the diaphragm is stimulated. Often nausea and vomiting, but the relationship between pain and meals is uncertain; the disease often has a history of indigestion, abdominal flatulence, can not tolerate fatty foods, but these symptoms are also common in the general population, the specificity is not strong. Ultrasound imaging is accurate for the diagnosis of gallstones, and can understand the size of the gallbladder, the thickness of the gallbladder wall, and whether there is bile duct dilatation. Oral cholecystography failed to show gallbladder filling, suggesting that the gallbladder is not functional.
4. Causes of nerves, muscles and bones
(1) Cervical radiculitis: It can manifest as persistent pain and sometimes causes sensory disturbances. Pain may be related to neck activity, as is the painful episode of bursitis caused by shoulder joint activity. The finger is pressed along the back, there is a skin allergic area, suspicious and thoracic radiculitis. Sometimes, the cervical rib compression of the arm and shoulder plexus can produce angina-like pain. Physical examination can also be found in the shoulder joint inflammation and / or shoulder ligament calcification, cervical spondylosis, musculoskeletal diseases similar to angina, bursitis under the shoulders and costal cartilage.
(2) chest rib syndrome: also known as Tietze syndrome. The pain is limited to the swelling of the costal cartilage and rib cage joints, and there is tenderness. The typical clinical manifestations of Tietze syndrome are uncommon, and the costal pain (without swelling) at the junction of the ribs and costal cartilage is relatively common. At the time of examination, tenderness at the junction of the costal cartilage is a common clinical sign. Treatment of costal cartilage is usually done with anti-inflammatory and anti-inflammatory drugs.
(3) Herpes zoster: chest pain may occur in the early stage of rash, and may even resemble myocardial infarction in severe cases. The diagnosis of this disease can be made based on the persistence of pain, the limitation of the distribution of sensory nerve fibers in the skin, the extreme sensitivity of the skin to touch, and the appearance of specific herpes.
(4) Unexplained chest wall pain and tenderness: palpation and chest activity (such as bending, turning or swinging the arm while walking) can cause chest pain. In contrast to angina pectoris, which can last for a few seconds or hours, nitroglycerin does not relieve it immediately. Generally no treatment is needed, and even salicylate is needed.
5. Functional or psychiatric chest pain It is a manifestation of anxiety in neurological circulatory disorders. Pain can be located at the apex of the heart, which is a pain that lasts for several hours. It often aggravates or changes to a sharp scalp pain of the breast under the 1-2 s time limit. It occurs mostly in emotional stress and fatigue, and has little to do with exercise. There is tenderness in the anterior area. Attacks may be accompanied by signs of palpitations, hyperventilation, numbness and tingling of the limbs, sighs, dizziness, difficulty breathing, general weakness, and emotional instability or depression. Other drugs other than analgesics do not relieve it, but can be alleviated by various forms of intervention such as rest, labor, tranquilizers, and placebo. In contrast to myocardial ischemic pain, functional pain is more likely to show different responses to different interventions. Since functional pain often occurs after hyperventilation, the latter can cause increased muscle tone and a diffuse chest tightness. Some so-called functional chest pains may actually have a basis for organic diseases. This is common in chest pain in patients with mitral valve prolapse. The nature of chest pain varies greatly between patients, and it can be similar to typical angina pectoris and chest pain similar to the aforementioned neurological circulatory weakness.
6. Non-coronary atherosclerotic heart and vascular disease
(1) Acute pericarditis: the age of onset is light. Often there is a history of viral upper respiratory tract infection. The pain caused by inflammation is sudden onset, sharper than angina, and the position is leftward rather than in the middle of the chest, often radiating to the neck. The pain is persistent and unrelated to fatigue. Breathing, swallowing, and twisting the body can make it worse, and the pain is relieved when the patient sits up and leans forward. Auscultation has a pericardial friction sound. The diagnosis can be confirmed with the aid of an electrocardiogram.
(2) Aortic disease: When there is sudden and severe pain in patients with high blood pressure, and the radiation to the back and waist, the possibility of aortic dissection is revealed; the continuous expansion of the thoracic aortic aneurysm can erode the limitation of the vertebral body. Severe drilling-like pain, especially at night; severe aortic stenosis due to insufficient coronary blood supply, angina can occur, systolic murmur in the aortic valve area and echocardiography can be identified.
(3) severe right ventricular hypertension: mitral stenosis, primary pulmonary hypertension and pulmonary heart disease can cause pain. This pain can also occur when the pulmonary artery is depressed, such as severe pulmonary stenosis with right ventricular hypertension. It is currently believed that this type of pain is due to limited cardiac output. In the systolic phase, coronary blood flow is reduced due to right ventricular hypertension, and right ventricular oxygen consumption is increased, resulting in poor myocardial perfusion. Therefore, chest discomfort can be caused by cardiac ischemia. Since this pain can be relieved by itself and lasts for several minutes, the reaction to nitroglycerin is difficult to evaluate. If the pain is caused by activity and can be prevented by nitroglycerin, the pain is most likely due to coronary heart disease. Many patients with pulmonary hypertension have ST-segment shifts on the electrocardiogram during or after exercise.
(4) Chest angiography results of normal chest pain: angina pectoris or chest pain similar to angina with normal coronary angiography syndrome is often called X syndrome, which needs to be distinguished from typical ischemic heart disease caused by coronary heart disease. The etiology is still unclear. Some of these patients have true myocardial ischemia, which is characterized by increased lactate production in the heart during exercise or rapid pacing.
Patients with chest pain and normal coronary angiography are more common in premenopausal women. Most of the symptoms of chest pain are not typical. Chest pain can be induced by fatigue, but the threshold for pain is very variable, sometimes the pain is very severe. The disease can affect the quality of work and quality of the patient. Some patients may have clinical manifestations such as panic, anxiety or mental disorders. Some patients have insulin resistance and hyperinsulinemia. There were no abnormal findings in clinical examinations. Some patients may have non-specific ST-T abnormalities on the electrocardiogram during chest pain. Nearly 20% of patients have a positive exercise test. Exercise nuclide myocardial imaging can be found in some patients with myocardial perfusion abnormalities, but it has no consistent correlation with the extent of the defect, the positive degree of exercise test and exercise tolerance.
Patients with clinical evidence of ischemia can be treated with nitrates and beta-blockers, but the actual treatment is often unsatisfactory. Nitrate does not improve exercise tolerance in patients with syndrome X, and may even reduce exercise tolerance in some patients. Calcium antagonists can reduce the frequency and severity of chest pain in some patients and increase their exercise tolerance. Try to find non-cardiac causes of chest pain during the treatment. For those with gastric-esophageal reflux and esophageal dysfunction, treating these diseases is effective in relieving symptoms. For those who have no evidence of ischemia and/or those who do not respond to ischemic treatment, in addition to providing general supportive care, patiently explain the good prognosis of the disease to the patient, so that it is an important part of the treatment.
complication
Stable angina increases the risk of both cardiac and non-fatal ischemic events.
treatment
(a) treatment
The treatment of angina should include the following four aspects.
1. Correction of risk factors for coronary heart disease, such as active treatment of high blood pressure; control of weight, stop smoking, and patients with diabetes need to reduce elevated blood sugar. If you have anemia, hyperthyroidism, heart failure, or any medication that increases your myocardial oxygen consumption, you should take care to correct or avoid it.
2. Adjust lifestyle to reduce or avoid the onset of myocardial ischemia. For example, the patient's physical activity tolerance is estimated, and daily life and workload are adjusted. Patients should avoid sudden exertion, especially after a long break, such as the study of the onset of angina pectoris, the angina threshold is low in the short time after getting up in the morning, so the activity should be slow after getting up, if necessary Nitroglycerin should be used as a precaution.
3. The drug treatment of angina pectoris is the most basic and most important way to treat coronary heart disease. It can not only relieve acute attacks, but also prevent angina pectoris and improve the quality of life of patients.
(1) Treatment during an acute attack: When the angina pectoris suddenly occurs, stop the activity immediately and rest. If the symptoms are still not relieved, a faster acting nitrate drug can be used, and nitroglycerin and isosorbide dinitrate are generally preferred.
1 First, sublingual nitroglycerin: 0.3 ~ 0.6mg, because it can be dissolved by saliva, it will start to take effect in 1-2 minutes, and the effect disappears after about half an hour. It is effective in about 92% of patients, and 76% of them are effective within 3 minutes. If it is ineffective or not fully relieved, it can take 0.4mg every 5min; 1.2~1.5mg in 15min, if the symptoms of angina persist for 20min, and can not be relieved by nitroglycerin, you can go to a nearby medical center to exclude acute myocardium. Infarction.
2 isosorbide dinitrate: 5 ~ 10mg under the sublingual, 1 ~ 5min effective, the effect of maintaining 2 ~ 3h. There are sprays of these two drugs on the market that are easier to absorb than tablets.
3 can also include some fast-acting Chinese medicine preparations, such as quick-acting heart-saving pills, compound Danshen dropping pills and so on.
(2) Treatment during remission: nitrates, beta blockers, calcium channel antagonists and antiplatelet drugs can be used.
1 nitrates: The commonly used nitrates in the clinic are mainly nitroglycerin, isosorbide dinitrate (disgusting) and isosorbide mononitrate.
A. Isosorbide mononitrate: isosorbide mononitrate does not need to be metabolized by the liver for the first time compared with isosorbide dinitrate (disgusting), has a 100% bioavailability, and its serum half-life is 4-5 h, which is significantly longer than The serum half-life of Xiaoxintong is a drug that has been applied more in recent years. Among them, 20mg of the dosage form has long-acting heartache, different hormones, Lunan Xinkang and Lizhu Xinle, and the effect lasts for 8h, suitable for 2 times/d. Dosing. 30mg, 40mg, 50mg, 60mg of the dosage form are yumdo (with 30mg and 60mg two dosage forms), Dezheng Ning, long-acting isolidine, Chen Gongjia and Mononor, the efficacy can last 16 ~ 24h Usually 1 piece / d can be.
B. Quick-acting nitroglycerin and isosorbide dinitrate (disintegration) oral spray: It is a improver of nitroglycerin and Xiaoxin isosorbide dinitrate (disintegration). It takes effect after 15~30s after spraying, and takes effect for 3~4min. The peak can be maintained for 1 to 1.5 hours.
C. Long-acting nitroglycerin sustained-release preparation: There are two kinds of 2.5mg and 6.5mg. After oral administration, the former has obvious curative effect for 2-8 hours, while the latter has a longer duration of action.
D. Isosorbide dinitrate (xinxin) skin spray: It takes about 30 to 60 minutes after spraying the skin, and the effect can be maintained for 12 hours.
E. Intravenous dosage forms of nitroglycerin and isosorbide dinitrate (disgusting pain): suitable for acute onset of acute myocardial infarction and unstable angina.
The main side effects of nitrates are headache, dizziness, reflex tachycardia and orthostatic hypotension.
2 calcium channel antagonists: commonly used in 3 categories:
A. Dihydropyridines: such as nifedipine,Amlodipine(Luohuo hi), Bo Yiding, worship the heart and Nikadipine. It is effective for lowering blood pressure and is suitable for patients with coronary heart disease and hypertension. The usual dose of nifedipine is 30 ~ 120mg / d, divided into 3 ~ 4 times orally; amlodipine (Luo Huxi) is 5 ~ 10mg / d, 1 oral; felodipine (Poiding) 2.5 ~ 10mg / d, 1 oral administration; nifedipine (about the same heart) 30mg / d, 1 oral.
B. Derivatives of milletine: such as verapamil, 160-320 mg/d, orally 3 to 4 times; verapamil sustained release dosage form is 240 mg/tablet, once daily.
C.1.5-Phenothiazine derivatives: such as diltiazem, 90 ~ 240mg / d, divided into 3 to 4 times orally.
The main side effects: dihydropyridines can lower blood pressure, tachycardia, headache, dizziness, fatigue, gastrointestinal discomfort and peripheral edema (common around the ankle joint). The main side effects of verapamil and diltiazem are bradycardia, conduction block, heart failure, headache and fatigue.
3β receptor blockers: clinically used beta blockers havePropranolol(Shen Dean), atenolol (aminoacylamine), metoprolol (Medocal) and bisoprolol (Concor); these beta blockers have no endogenous sympathomimetic activity, except Except for propranolol (the propranolol), the heart selectively acts on the beta receptor, so the propranolol has recently been used less frequently. The application dose of β-blockers is significantly lower than that of foreign countries.
A. Metoprolol (Medocal): Metoprolol (Medocal) is fat-soluble, mainly metabolized by the liver. The dose is 25 ~ 200mgd, divided into 2 to 3 times orally; the dose is less than 100mg / d when there is cardiac selectivity.
B. Atenolol (aminoacylamine) and bisoprolol (Concor): water-soluble, mainly metabolized by the kidney, atenolol (aminoacylamine) 12.5 ~ 100mg / d, divided into 1 or 2 times orally Bisoprolol (Concor) 2.5 ~ 10mg / d, 1 / d orally. When bisoprolol (Concor) 10 mg, it is equivalent to the efficacy of 100 mg of atenolol (aminoacylamine). The serum half-life of atenolol (aminoacylamine) was 6-9 h, and bisoprolol (Concor) was 18-24 h.
4 anti-myocardial ischemic drugs: in the absence of normal myocardial ischemia, 60% to 90% of the energy of cardiac activity comes from fatty acid metabolism in cardiomyocytes. 10% to 40% is provided by glycolysis and lactate oxidation. During myocardial ischemia, free fatty acid mobilization increases, fatty acid oxidation rate increases, glucose oxidation energy supply (glucose aerobic metabolism) ATP share is compressed by 5% to 10%, and the rate of ATP production decreases. For example, when energy is supplied with 1.6 carbon palmitate, 4.3 ATP energy can be generated for each oxygen molecule (O2) consumed; and when glucose is oxidized, 6 ATP energy can be supplied for each oxygen molecule consumed. It can be seen that the same oxygen is consumed, and the energy supply of glucose is 12% to 28% higher than that of free fatty acid oxidation. As the glycolysis and lactic acid production increase, the intracellular pH decreases, affecting the normal function of the ion pump and the transmembrane flow of sodium and potassium ions, and the calcium ions are overloaded in the cells, resulting in a decrease in cardiac function. In moderate myocardial ischemia (coronary blood flow is only 30% to 60% normal), although there is lactic acid accumulation, the myocardium still uses oxygen-consuming fatty acid oxidation as the main source of energy, pyruvate is converted to lactic acid; The function is further affected.
Trimetazidine (Wan Shuangli): an anti-ischemic drug for the optimization of myocardial energy balance. At the mitochondrial level, by selectively inhibiting long-chain 3-ketoacyl-CoA thiolase (3-KAT), it can partially inhibit fatty acid oxidation, increase glucose aerobic metabolism, reduce oxygen consumption by ATP, and accumulate lactic acid H. Reduces cellular acidosis and intracellular Ca2 overload, reducing free radical damage. It ensures the normal function of the ion pump, and the transmembrane flow of sodium and potassium ions, which in turn maintains the cell's own balance. It has direct cardioprotection and has no effect on hemodynamics.
In patients with stable angina pectoris, the coronary arteries have a fixed fixation stenosis, which can not increase the perfusion of the coronary artery through adaptive expansion of the coronary artery. At the same time, due to the damage of endothelial cell function, the production of NO (nitric oxide) is reduced, resulting in physical exercise. Coronary contraction in emotional or cold climates, so about 30% of patients with stable angina can develop symptoms at rest. As the first 3-KAT inhibitor, “Trimezepine (Wan Shuangli)” helps to optimize myocardial energy metabolism, from fatty acid oxidation to glucose oxidation, restoring the coupling of glycolysis and oxidation, and promoting oxygen consumption. Less ATP production contributes to the recovery of mechanical function of ischemic myocardium.
A special discussion on the progress of the treatment of trimetazidine was conducted at the European Heart Disease Conference (ESC) in Stockholm, Sweden, in September 2001. It is believed that the treatment of stable angina peptidic beta blockers is a first-line drug, but this class of drugs has certain contraindications and is more likely to occur in elderly patients. Nitrate, calcium antagonist, and trimetazidine can be used as second-line drugs when contraindications or poor tolerance of first-line drugs. Studies have shown that in the treatment of stable angina, TMZ has at least equal efficacy compared to hemodynamic drugs, and patients are better tolerated. Some authors applied TMZ 20mg, 3 times / d (71 cases), compared with propranolol (genus) 40mg, 3 times / d (78 cases); the results show that the treatment of angina is equally effective. TMZ is often synergistic with other drugs, such as TMZ and nitrate esters are more effective than beta blockers and nitrates in prolonged exercise to angina pectoris and ST segment depression. Adding TMZ to patients with ineffective treatment with diltiazem can improve symptoms.
There are also reports on the role of TMZ in improving left ventricular function, increasing LVEF, and on endothelial cells, smooth muscle cells and platelets. In short, due to the unique mechanism of action and good safety of TMZ, its clinical application range is expanding, from the simple treatment of stable angina pectoris to multiple myocardial ischemia and ischemic heart dysfunction. protection of.
5 anti-platelet drugs: the main anti-platelet drugs haveaspirin, ticlopidine, clopidogrel,Dipyridamole(Pan Shengding), fish oil and platelet glycoprotein (GPIIb/IIIa - fibrinogen receptor) antagonists.
4. Interventional treatment of angina mainly refers to coronary revascularization therapy. There are two main types of PTCA (percutaneous transluminal coronary angioplasty) and CABG (coronary artery bypass grafting).
(1) PTCA: a cardiac catheter treatment technique that uses a percutaneous puncture method to deliver a balloon catheter and dilate a narrow coronary artery. The therapeutic mechanism is through the mechanical compression of the balloon in the atherosclerotic stenosis segment, the atherosclerotic endocardium is stretched to the outer membrane, the diameter of the blood vessel is enlarged, or the atherosclerotic plaque is torn along the lumen of the vessel. Under physiological pressure and blood flow impact, reshape the skin to create a new smooth lumen, and keep the blood flowing smoothly for a long time.
With the improvement of PTCA technology, the improvement of materials, the introduction of high-quality image enhancement system and the accumulation of PTCA operation experience, its clinical indications are expanding. In clinical practice, drug therapy is ineffective, patients require revascularization therapy; patients with the possibility of successful revascularization may be considered for PTCA.
(2) CABG: It can achieve immediate recovery and/or increase blood flow of ischemic myocardium by effectively bypassing the graft vessel around the coronary stenosis site, effectively reducing the incidence of angina pectoris, alleviating symptoms and improving the heart. Features improve the quality of life.
(two) prognosis
The prognosis of patients with stable angina is better than that of patients with unstable angina. The prognosis of stable labor angina is mainly determined by the degree of myocardial ischemia and cardiac function. Some patients with chronic stable angina have some asymptomatic myocardial ischemic attacks. Most reports suggest that Holter's detection of myocardial ischemia in patients with chronic angina has a certain value in assessing the long-term prognosis of patients, but more evidence-based prospective studies are needed. Rocco et al observed 86 patients with stable angina and were positive for electrocardiogram exercise, of which 49 (57%) had myocardial ischemia detected by Holter during daily activities. Follow-up was up to 25 months [mean (12.5 ± 7.8) months]. The follow-up results showed that the number of clinical events (including sudden death, myocardial infarction, unstable angina, CABG) was poorer in the detection of myocardial ischemia in Holter than in non-ischemic, suggesting that both ECG and Holter tests Myocardial ischemia has a poor prognosis.
prevention
Because coronary heart disease is one of the most important diseases causing human death, and there is still no radical treatment in clinical practice, it is of great significance for the active prevention of coronary heart disease. Prevention of coronary heart disease includes both primary prevention and secondary prevention. Primary prevention refers to taking measures to control or reduce the risk factors of coronary heart disease in people who have not suffered from coronary heart disease, in order to prevent illness and reduce the incidence rate. Secondary prevention refers to the use of drugs or non-drugs in patients with coronary heart disease to prevent recurrence or prevent exacerbations.
1. Primary prevention measures include two situations:
(1) Health education: educate the whole population on health knowledge, improve citizens' self-care awareness, avoid or change bad habits, such as quitting smoking, paying attention to proper diet, exercising properly, maintaining psychological balance, etc., thus reducing the incidence of coronary heart disease.
(2) Control high-risk factors: for high-risk groups of coronary heart disease, such as hypertension, diabetes, hyperlipidemia, obesity, smoking, and family history, etc., give active treatment. Of course, some of these risk factors can be controlled, such as high blood pressure, high blood fat, diabetes, obesity, smoking, lifestyle less active, and some can not be changed, such as family history of coronary heart disease, age, gender, etc. . Treatment methods include the selection of appropriate drugs to continuously control blood pressure, correct abnormal blood lipid metabolism, limit smoking, limit physical activity, control body weight, control diabetes, and so on.
2. Secondary prevention uses drugs that have been validated to prevent recurrence and exacerbation of coronary heart disease.
The drugs that have been confirmed to have preventive effects are:
(1) Antiplatelet drugs: Aspirin has been shown to reduce the incidence of myocardial infarction and reinfarction rate,
The use of aspirin after myocardial infarction can reduce the rate of reinfarction by approximately 25%; if aspirin is intolerant or allergic, clopidogrel can be used.
(2) β-blockers: as long as there is no contraindications, patients with coronary heart disease should use beta blockers, especially after acute coronary events; there are data showing that patients with acute myocardial infarction use beta receptors Blocking drugs can reduce the mortality rate and reinfarction rate by 20% to 25%. The drugs that can be used are metoprolol, propranolol, timolol and the like.
(3) statin lipid-lowering drugs: The results of the study showed that long-term lipid-lowering therapy in patients with coronary heart disease not only reduced the overall mortality, increased survival rate, but also reduced the number of patients requiring coronary intervention or CABC. This is due to the improvement of endothelial function, anti-inflammatory effects, effects on smooth muscle cell proliferation and interference with platelet aggregation, blood coagulation, fibrinolysis and other functions in addition to lipid lowering effects of statins. Simvastatin, pravastatin, lovastatin, and atorvastatin all have this effect.
(4) ACEI: It is often used in patients with severe impairment of left ventricular function or heart failure. Many clinical trials have confirmed that ACEI reduces the mortality rate after acute myocardial infarction; therefore, after acute myocardial infarction, patients with ejection fraction <40% or wall motion index ≤ 1.2, and no contraindications, should use ACEI. Commonly used are captopril, enalapril, benazepril and fosinopril.
In addition, coronary angiography has coronary atherosclerotic mild stenosis and clinical symptoms have not yet developed ischemic symptoms, although it is not clear diagnosis of coronary heart disease, it should be regarded as a high-risk group of coronary heart disease, giving active prevention, also Long-term use of low-dose aspirin can be given, and risk factors such as dyslipidemia and hypertension can be eliminated.
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