2 English reference variant angina pectoris
Overview of variant angina pectoris (variant? Angina? Angina pectoris is a clinical syndrome characterized by paroxysmal acute myocardial ischemia, but with or without typical angina pectoris and ST segment elevation, and it is an unstable angina pectoris. Because its onset has no obvious relationship with the increase of myocardial oxygen demand, it is induced by the decrease of myocardial oxygen supply caused by coronary artery spasm, which is different from typical fatigue angina pectoris, so it is called variant angina pectoris.
Rare syndrome secondary to myocardial ischemia, first described by Prinzmetal in 1959, almost always occurs at rest, with no physical activity or emotional excitement, often accompanied by st segment elevation of ECG, so it is also called Prinzmetal angina pectoris. Variant angina pectoris is often complicated with acute myocardial infarction and severe arrhythmia, including ventricular tachycardia, ventricular fibrillation and sudden death.
Chest pain in patients with variant angina pectoris occurs at the same time almost every day, especially at midnight and 8 am. More common, most angina pectoris occurs in the early hours of the morning, and it will be very painful when sleeping or waking up. The duration of the attack varies greatly, ranging from tens of seconds to 20 ~ 30 minutes.
Patients should avoid or change bad living habits, such as quitting smoking, paying attention to reasonable diet, proper exercise, maintaining psychological balance, etc., in order to reduce the occurrence of coronary heart disease. For high-risk groups of coronary heart disease, such as hypertension, diabetes, hyperlipidemia, obesity, smoking and family history, active treatment is given.
4 disease name Variant angina pectoris
5 English name variant angina pectoris
6 Variant angina pectoris alias prinz metal angina pectoris; Principle angina pectoris
7 Classification Cardiovascular Medicine > Coronary Atherosclerotic Heart Disease >: Angina Pectoris and Coronary Heart Disease
8 ICD number I20.8
Epidemiological data show that 0.5% ~ 1% of all patients hospitalized for angina pectoris are variant angina pectoris, so its incidence is high and there are serious complications, such as acute myocardial infarction and arrhythmia (ventricular tachycardia or ventricular fibrillation), which should be paid great attention to in clinic.
10 the etiology of variant angina pectoris is the primary decrease of myocardial oxygen supply caused by coronary artery spasm, which is often spontaneous without cause. At present, it is considered that the causes of coronary artery spasm are complicated, which may be related to the following factors:
10. 1 Vascular endothelial dysfunction Coronary artery spasm seems to be the pathological reaction of vascular endothelial dysfunction. Some patients with variant angina pectoris have a great history of smoking, and smoking can damage vascular endothelial cells. When the vascular endothelium is damaged, the vascular intima directly contacts with vasoconstrictive substances (catecholamine, TXA2, endothelin), which makes the vascular smooth muscle contract, resulting in a strong vasoconstrictive effect. At present, it is considered that vascular endothelial dysfunction may be the basic mechanism of coronary artery spasm.
10.2 There are β adrenergic receptors in the coronary artery with autonomic nervous system imbalance, α adrenergic receptors are mainly distributed in the great coronary artery, and β adrenergic receptors exist in both large and small coronary arteries, which can cause coronary artery contraction. When there is coronary atherosclerosis, the sensitivity of blood vessels to vasoconstrictors increases, which is easy to cause vasospasm.
10.3 Variant angina pectoris caused by humoral factors mostly occurs in the middle of the night and early morning, which may be related to low metabolism, decreased hydrogen ion concentration and more calcium ions entering cells to increase coronary artery tension during sleep, which is prone to coronary artery spasm.
10.4 highly reactive atherosclerotic arteries obviously overreact to various vasoconstrictors, and its mechanism may be that cholesterol promotes the influx of extracellular calcium ions into cells and increases the intracellular calcium ion concentration.
1 1 the pathogenesis of variant angina pectoris is coronary artery spasm, which can cause transient, sudden and significant epicardial coronary artery diameter shrinkage, thus leading to myocardial ischemia. There is no inducement to increase myocardial oxygen consumption before onset, such as increased heart rate or elevated blood pressure. Taking nitroglycerin (sometimes in large doses) can relieve spasm.
Coronary artery spasm is usually confined to coronary atherosclerotic lesions. Even in patients with variant angina pectoris with normal coronary angiography, atherosclerotic plaques can be seen in local spasm through intracoronary ultrasound. This focal severe vasospasm is different from the normal contraction of coronary artery (such as the normal reaction of the body after cold), and is usually a diffuse mild contraction of the whole coronary artery bed. The basic coronary tension of patients with variant angina pectoris can be increased, and the segments of coronary artery spasm not only respond to ergonovine and acetylcholine, but also the whole coronary artery cluster is highly sensitive to vasoconstriction. The abnormal basis of coronary artery tension may be that the formation of coronary atherosclerosis leads to the increase of arterial wall contraction. Other pathogenesis also includes: vascular endothelial injury, which changes the response of blood vessels to most dilation. For example, acetylcholine can significantly dilate normal coronary arteries by increasing the release of endothelial relaxing factor (EDRF), but the blood vessels in the damaged endothelium contract instead. At present, endothelial injury is considered to be one of the most important inducing factors of coronary artery spasm. Vascular smooth muscle is highly reactive to vasoconstrictors such as cytokinin, leukotriene and 5- hydroxytryptamine 687, and there are local high concentrations of vasoconstrictors near atherosclerotic plaques of new blood vessels.
Because coronary artery spasm can occur in denervated transplanted heart or isolated heart, it is considered that the central nervous system does not play a major role in causing coronary artery spasm. α -adrenergic receptor blockers, 5- hydroxytryptamine receptor blockers, inhibition of thromboxane A production and taking prostacyclin can not reduce the incidence of variant angina pectoris. Acetylcholine can induce coronary artery spasm in patients with variant angina pectoris, leading to ischemic attack, but it can not induce coronary artery spasm in other patients with obvious coronary artery stenosis and normal coronary artery, indicating that patients with variant angina pectoris have local sympathetic innervation disorder.
Coronary artery spasm in patients with variant angina pectoris can induce blood stasis, convert fibrinogen into fibrin, and the plasma concentration of fibrinogen peptide Fibrinopeptide A increases, suggesting the formation of fibrin. The concentration of fibrin in plasma fluctuated within 24 hours, and its peak appeared at midnight and early morning, which was consistent with the frequency of myocardial ischemia attacks in patients.
Smoking, hyperinsulinemia and insulin resistance are important risk factors for variant angina pectoris. It is reported that patients with variant angina pectoris have magnesium deficiency. Magnesium sulfate can prevent angina pectoris attack induced by cold compression test, prevent further attack and inhibit angina pectoris attack induced by hyperventilation and exercise.
Pathological anatomy showed that the coronary artery of typical variant angina pectoris was normal or almost normal, accounting for 10% ~ 20% of all patients with variant angina pectoris. Severe fixed coronary artery stenosis accounted for 50% ~ 70%, CAG showed single-vessel lesions accounted for 39%, and multi-vessel lesions accounted for 19%. When CAG shows that the coronary artery is normal, it does not mean that the coronary artery is completely disease-free. Stenosis below 25% can not be found because of the projection angle, and atherosclerosis of blood vessel wall can be found by intracoronary ultrasound examination.
13 clinical manifestations of variant angina pectoris 13. 1 medical history characteristics variant angina pectoris is earlier than chronic stable angina pectoris and unstable angina pectoris, and most of them have no classical risk factors of coronary heart disease except smoking more. In addition, chest pain attacks have the following characteristics:
(1) Angina pectoris mostly occurs during rest and general daily activities: it has no obvious relationship with the increase of myocardial oxygen.
(2) The onset of chest pain is often circadian rhythm: it occurs almost at the same time every day, especially between midnight and 8 am. Most angina pectoris occurs in the early morning, and it can occur when you wake up from sleep or wake up.
(3) Chest discomfort is usually very serious: the pain described by patients is often accompanied by syncope caused by arrhythmia.
(4) The duration of seizures varies greatly: as short as tens of seconds, as long as 20 ~ 30 minutes. Generally speaking, short-term seizures are more common than long-term seizures.
(5) The inducing factors are usually high ventilation, exercise and exposure to cold environment.
(6) The attack of variant angina pectoris is often periodic: generally, the attack is concentrated in just a few weeks, but it is in remission for a long time, during which there are no symptoms or asymptomatic ischemic events. In short, there was a period of ups and downs.
(7) Patients with variant angina pectoris are related to other vasospasm diseases, such as migraine and Raynaud's phenomenon.
(8) sublingual administration of nitroglycerin or nifedipine can quickly relieve symptoms.
13.2 when there is no myocardial ischemia, the physical examination of the heart is usually normal unless the patient has old myocardial infarction. Myocardial ischemic attack often manifests as myocardial contraction dysfunction and left ventricular dysfunction.
14 Complications of Variant Angina Pectoris Variant Angina Pectoris is often complicated with acute myocardial infarction and severe arrhythmia, including ventricular tachycardia, ventricular fibrillation and sudden death.
15 auxiliary examination 15. 1 The key to the diagnosis of variant angina pectoris is chest pain with st segment elevation. Some patients have ST segment elevation at the time of attack, but then ST segment depression with T wave changes occurs. The changes of ST segment and T wave are the result of conduction disorder caused by myocardial ischemia, which can cause fatal arrhythmia. The broadening of R wave may also be related to ventricular arrhythmia. Painless ST segment elevation is more common. ST segment displacement can occur in all leads, and patients with ST segment elevation in lower leads and leads (reflecting extensive myocardial ischemia) have an increased risk of sudden death. Transient conduction block can occur during myocardial ischemia attack. Ectopic ventricular excitation often occurs in myocardial ischemic attack with a long duration, which is often related to the changes of ST segment and T wave, suggesting a poor prognosis.
In survivors with a history of cardiac arrest and no obvious coronary stenosis, their spontaneous or induced local coronary spasm can lead to fatal ventricular arrhythmia. Malignant arrhythmia in some patients is often caused by reperfusion, which is characterized by myocardial cell damage caused by releasing a small amount of CKMB, accompanied by persistent chest pain, but there is no persistent st segment change in ECG, and there may be short Q waves.
Coronary artery spasm can cause acute myocardial infarction, and the infarct site is mostly consistent with the lead of ST segment elevation when variant angina occurs.
15.2 Hemodynamics and coronary angiography can lead to transmural myocardial ischemia and segmental wall motion abnormality. Clinical studies have confirmed that this abnormal ventricular function occurs earlier than angina symptoms and ECG changes.
Most patients have at least one fixed proximal coronary artery stenosis, and spasm often occurs within 65438±0cm of the stenosis. The other patients had normal coronary angiography and no myocardial ischemia. Spasm most often occurs in the right coronary artery, but it can also occur in one or more parts of one or more coronary arteries at the same time. The patients with variant angina pectoris and normal coronary angiography without chest pain are simply non-exertion angina pectoris, and the st segment of the related lead is elevated when chest pain occurs. In contrast, patients with variant angina pectoris accompanied by coronary artery spasm and fixed stenosis often have fatigue-related angina pectoris and myocardial ischemia in related leads. The course of disease of patients with no or only mild fixed coronary artery stenosis is much better than that of patients with severe coronary artery stenosis.
15.3 variant angina pectoris commonly used in clinic can be diagnosed according to the transient elevation of st segment on ECG at the time of attack. If you can't get the ECG at the time of attack, it is feasible to diagnose the disease by stimulating test.
(1) ergonovine challenge test: ergonovine maleate is an ergot alkaloid, which can directly contract vascular smooth muscle with α adrenergic receptor and 5- hydroxytryptamine receptor, and is used to induce coronary artery spasm in patients with variant angina pectoris. This is a sensitive and specific examination method. Ergodine is a relatively safe drug under the clinical conditions of low dose and careful control. The dosage range of intravenous administration is 0.05 ~ 0.40 mg. The dose required to cause a positive result is inversely proportional to the frequency of spontaneous pain attacks. If it causes persistent coronary artery spasm, it will lead to myocardial infarction. Because of this danger, ergonovine is only used for patients whose coronary arteries are normal or close to normal by coronary angiography, and the dose is gradually increased from a very low dose.
When a large dose (≥0.40mg) of ergonovine is used, the normal coronary artery only responds to the diffuse decrease of arterial diameter. Patients with atypical chest pain but no variant angina pectoris were injected with ergonovine several times in a row, resulting in progressive diffuse coronary artery diameter reduction. The vasoconstriction reaction is more obvious in women and patients with irregular coronary intima, suggesting mild atherosclerosis. This dose-related diffuse coronary contraction is different from the abnormal reaction of variant angina pectoris, which is characterized by severe local spasm at very low drug dose. In the active period of the disease (at least 1 time a day), patients are more sensitive to ergonovine test, while patients with variant angina pectoris who occasionally attack are less sensitive to it.
The excitation test should be performed under the condition of coronary angiography. If coronary artery spasm is found, the test should be stopped immediately, and 0.2 ~ 0.3 mg nitroglycerin should be injected into coronary artery immediately, and this dose can be repeated until the spasm is relieved.
(2) Hyperventilation test: Hyperventilation can also induce severe angina pectoris. Electrocardiogram showed ST segment elevation, ventricular arrhythmia, and angiography showed obvious coronary artery spasm. The sensitivity of patients with variant angina pectoris who have at least 1 attack every day is 95% for hyperventilation and 100% for ergonovine. However, in patients with low frequency of angina pectoris, hyperventilation test is less sensitive than ergonovine, so its diagnostic value is limited.
(3) Acetylcholine test: Intracoronary injection of acetylcholine in patients with variant angina pectoris can lead to severe coronary spasm. This spasm should not be confused with mild diffuse constriction induced by acetylcholine in patients with abnormal coronary endothelium, because this method can induce left and right coronary artery spasm respectively, which is useful for understanding whether patients have multi-vessel disease or spasm. This method is sensitive, safe and reliable, and its sensitivity (95%) and specificity (99%) are similar to those of ergonovine.
Parasympathetic drugs such as methacholine, histamine and dopamine can also induce coronary artery spasm, similar to ergonovine and acetylcholine, which can cause obvious coronary artery spasm in patients with variant angina pectoris with severe fixed coronary artery stenosis and patients without localized fixed coronary artery stenosis.
15.4 radionuclide myocardial perfusion scintigraphy 20 1 thallium (20 1Tl) myocardial perfusion scintigraphy can confirm the spasm during arteriography. At the time of attack, there was a localized myocardial perfusion defect, and the coronary sinus blood flow in the perfusion area decreased, which supported the relationship between coronary artery spasm, myocardial perfusion and regional myocardial ischemia.
15.5 The CAG results of patients with variant angina pectoris can be normal or abnormal. Typical patients have normal coronary arteries or non-infarct lesions, but most patients have fixed stenosis at the proximal end of at least one major coronary artery. Coronary artery spasm is closely related to its pathological changes, which often occurs within 65438±0cm of stenosis. The total incidence of coronary artery spasm is the highest in left anterior descending branch, followed by right coronary artery, LCX, diameter artery and right coronary artery. However, in patients without obvious coronary artery disease, the incidence of PCA spasm is higher than LAD, and it is more common in women. Coronary artery spasm can occur at one or more sites of one or more coronary arteries at the same time.
16 is based on the diagnosis of variant angina pectoris: chest discomfort usually appears st segment elevation briefly at rest, and the elevated st segment recovers when the symptoms disappear, and does not evolve into acute myocardial infarction. When CAG showed normal coronary artery or only non-infarcted plaque, coronary artery spasm was more supported. If there is spontaneous chest pain attack and st segment elevation in CAG, severe local spasm of coronary adventitia can be seen. When CAG shows that coronary artery has obstructive lesions, the increase of coronary artery tension at the stenosis can cause complete occlusion of the coronary artery, and acute myocardial infarction can be complicated when the coronary artery is continuously and severely convulsed.
When CAG shows normal coronary artery or non-obstructive plaque with only ST-segment elevation at the onset of symptoms, it can be diagnosed as variant angina pectoris without further examination, so it is very important to record ECG at the onset. If the attacks are frequent, 24-hour Holter monitoring may be helpful for the diagnosis. When the symptoms are not accompanied by ST segment elevation, the provocation test can induce coronary artery spasm. Calcium antagonists and nitrates should be stopped before testing.
In a word, the disease can be diagnosed by combining the typical medical history and ECG changes at the time of attack, and the results of CAG and provocation test are helpful to the diagnosis of atypical attack.
17 differential diagnosis 17. 1 aortic dissection often produces chest pain siMIlar to mi. The position of chest pain is often high, close to the chest outlet; Teardrop-shaped; The onset is often more sudden than AMI. Pain quickly reaches its peak and has a wide range, and is often reflected in the back, waist, abdomen and calves. The pain is persistent. Although there may be symptoms of shock, the course of the disease is often accompanied by hypertension. Aortic dissection can produce compression symptoms, resulting in inconsistent blood pressure in both upper limbs and weakened pulse and carotid pulse on one or both sides. X-ray and echocardiography can find that the aorta is obviously widened, and ECG and serum enzymology have no characteristic changes during AMI. In order to diagnose aortic dissection, ultrasound, aortography and/or magnetic resonance imaging are usually needed.
If aortic dissection invades the coronary artery, MI may occur, but it is rare. About 5% ~ 10% of patients with aortic dissection have no chest pain.
17.2 the pain location and nature of unstable angina pectoris are similar to those of AMI, but the onset time of angina pectoris is generally less than half an hour. Most of them were not accompanied by nausea, vomiting and shock. The characteristic changes of serum-free enzymology (cardiac troponin T can be increased); Although there are changes in ST segment and T wave during the attack, they are all transient. When angina pectoris occurs, ST segment is obviously decreased or accompanied by T wave inversion, which should be distinguished from non-ST segment elevation MI. When variant angina pectoris attacks, ST segment is obviously elevated and T wave is upright, which may be accompanied by ventricular arrhythmia or bradycardia. The ST segment of the corresponding lead decreased obviously, similar to the early mode of AMI, but after the onset of remission, the ST segment quickly returned to the equipotential line. There is generally no pathological Q wave when angina pectoris attacks. Dynamic observation of changes in serum enzymology and cardiac troponin T is one of the keys to differential diagnosis.
17.3 pulmonary embolism occurred suddenly, including chest pain, shortness of breath, cyanosis, hemoptysis or shock. If there is no hemoptysis, it is sometimes similar to AMI. But the fever and leukocytosis of the former usually occur within 24 hours. Hyperactivity of the second heart sound in the pulmonary valve area can be seen in cardiac signs; The ECG changes of pulmonary embolism are faster and shorter than those of acute myocardial infarction. Electrocardiogram showed that the acute electric axis shifted to the right, the right ventricle enlarged, new S waves appeared in leads S 1, Q, III, T III and I, abnormal Q waves were accompanied by T wave inversion in lead III or even aVF, but there was no Q wave in lead II, and there was obvious clockwise transposition. The total value of serum lactate dehydrogenase can be increased, but its isoenzymes (LDH 1) and phosphocreatine kinase isoenzymes (cPKMB) are not. Radionuclide lung perfusion scan is helpful for diagnosis.
Treatment of 18 variant angina pectoris 18. 1 can quickly relieve coronary artery spasm. When controlling the acute attack of chest pain, nitroglycerin or nifedipine powder can be taken sublingually, and 0.5mg is appropriate for the first time. If the chest pain is not relieved within 3 ~ 5 minutes, you should take 1 tablet or 2 tablets immediately. Similarly, if nifedipine powder (10 mg) does not relieve within 10 min, it can be repeated. These two drugs can also be used interchangeably. If nitroglycerin is ineffective, nifedipine powder can be used instead, and vice versa. The author can give nitroglycerin continuous intravenous drip in a short time.
18.2 calcium antagonist is the first choice to prevent spasm, and nitrate can be used in combination. At present, it is considered that the combination of the two drugs can produce synergistic effect and enhance the curative effect.
Calcium antagonists are the most targeted in the treatment of variant angina pectoris. Nifedipine and diltiazem have a strong effect on dilating coronary arteries. Nifedipine is the first choice for hypertensive patients, and diltiazem is better if the heart rate is fast. When the attack is serious, it can be used together and has synergistic effect to enhance its effect. For right coronary artery spasm, nifedipine is better. For example, diltiazem can slow down the heart rate or aggravate the atrioventricular block when the spasm is not completely controlled. The half-life of nifedipine and diltiazem is 4 ~ 6h (90mg sustained-release tablets, half-life 18 ~ 24h). Isosorbide nitrate has a short half-life, so it should be used 1 time within 4 ~ 6 hours. Because variant angina pectoris usually occurs in the early morning after midnight, we should pay attention to the curative effect after midnight when taking it. Taking long-acting sustained-release calcium antagonists before going to bed has a synergistic effect to control the onset in the second half of the night. Aspirin should be used, and inhibiting TXA2 release is helpful to control vasospasm. Variant angina pectoris occurs all day, mostly because the surface of atherosclerotic plaque festers. In addition to calcium antagonists and aspirin, nitroglycerin should be continuously intravenous drip, combined with heparin anticoagulation or low-dose thrombolysis. If the coronary artery has fixed occlusion, plexus resection should be added during coronary artery bypass grafting (CABG) to prevent coronary artery spasm after operation, or calcium antagonists should be used after operation to prevent vascular spasm.
For the treatment of early variant angina pectoris, we should take a positive attitude, quickly relieve spasm and reduce the incidence of acute myocardial infarction. Drug therapy can often effectively control 80% of variant angina pectoris, and it can be transferred to a longer remission period after 6 ~ 12 months. For patients with coronary artery spasm and severe fixed coronary artery stenosis, PTCA or CABG is feasible when drug treatment can not satisfactorily control the onset of variant angina pectoris. It has been reported abroad that plexus resection is often carried out at the same time, and continuous vasodilation treatment is still needed after operation to reduce the possibility of recurrence of distal spasm of transplanted blood vessels or other coronary arteries.
The prognosis of 19 is generally considered that variant angina pectoris is unstable at the initial stage of onset. After appropriate drug treatment, it can be transferred to a longer remission period after about 6 months. Its prognosis is good. In acute active phase, about 20% patients have myocardial infarction and 10% die. If severe arrhythmia (ventricular tachycardia, ventricular fibrillation, high atrioventricular block or sinus arrest) occurs during the onset of pain, the risk of sudden death will increase. The severity of coronary artery disease is the most important factor affecting prognosis. The more severe the coronary artery stenosis, the higher the risk of persistent angina pectoris, acute myocardial infarction and death. The vast majority of survivors after myocardial infarction or 3 ~ 6 months after onset, with the passage of time, the condition will tend to be stable, and symptoms and cardiac events will decrease. If the ergonovine test result is negative, the variant angina pectoris is relieved, and the dosage of calcium antagonist can be carefully reduced until the drug is finally stopped. There are also patients whose symptoms disappear for a period of time, but the treatment with calcium antagonists and nitrates is still effective.
Prevention of Variant Angina Pectoris Because coronary heart disease is one of the most important diseases leading to human death, there is still no radical treatment in clinic, so it is of great significance to actively prevent coronary heart disease. The prevention of coronary heart disease includes primary prevention and secondary prevention. Primary prevention refers to taking measures to control or reduce the risk factors of coronary heart disease for people who have not yet suffered from coronary heart disease, so as to achieve the purpose of preventing disease and reducing incidence. Secondary prevention means that patients with coronary heart disease take drug or non-drug measures to prevent the recurrence or aggravation of the disease.
20. 1 Primary preventive measures Primary preventive measures include two situations:
(1) Health education: educate the whole people about health knowledge, improve citizens' awareness of self-care, and avoid or change bad living habits, such as quitting smoking, paying attention to reasonable diet, exercising properly, and maintaining psychological balance, so as to reduce the occurrence of coronary heart disease.
(2) Control high-risk factors: actively deal with high-risk groups of coronary heart disease, such as hypertension, diabetes, hyperlipidemia, obesity, smoking, family history, etc. Of course, some of the risk factors can be controlled, such as hypertension, hyperlipidemia, diabetes, obesity, smoking, less active lifestyle and so on. Some things can't be changed, such as family history of coronary heart disease, age, gender and so on. Treatment methods include choosing appropriate drugs to continuously control blood pressure, correcting abnormal blood lipid metabolism, quitting smoking and alcohol, proper physical activity, weight control and diabetes control.
20.2 Secondary prevention uses drugs that have been proved to be effective in preventing the recurrence and aggravation of coronary heart disease. At present, the drugs that have been proved to have preventive effects are:
(1) antiplatelet drugs: Aspirin has been proved to reduce the occurrence and reinfarction rate of myocardial infarction, and the reinfarction rate after acute myocardial infarction can be reduced by about 25%; If you are intolerant or allergic to aspirin, you can choose clopidogrel.
(2) Beta blockers: As long as there are no contraindications, patients with coronary heart disease should use beta blockers, especially after acute coronary events; Some data show that the use of beta blockers in patients with acute myocardial infarction can reduce the mortality and reinfarction rate by 20% ~ 25%. Available drugs include metoprolol, Naylor, timolol, etc.
(3) Statins: The results show that long-term lipid-lowering therapy for patients with coronary heart disease not only reduces the overall mortality and improves the survival rate, but also reduces the number of patients who need coronary intervention or CABC. This is due to the effects of statins on improving endothelial function, anti-inflammation, affecting the proliferation of smooth muscle cells and interfering with platelet aggregation, coagulation and fibrinolysis. Simvastatin, pravastatin, lovastatin
Statins and atorvastatin have this effect.
(4)ACEI: mostly used in patients with severe left ventricular dysfunction or heart failure. Many clinical trials have confirmed that ACEI can reduce the mortality 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 shows that coronary atherosclerosis is slightly narrowed and ischemic symptoms have not yet appeared in clinic, so they should be regarded as high-risk groups of coronary heart disease, given active prevention, or given low-dose aspirin for a long time to exclude risk factors such as dyslipidemia and hypertension.
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2 1 Related drugs oxygen, adrenaline, nitroglycerin, glycerin, ergonovine, magnesium sulfate, nifedipine, acetylcholine acetate, histamine, dopamine, diltiazem, diltiazem, isosorbide, sorbitol, aspirin, heparin, clopidogrel, metoprolol, timolol, simvastatin, pravastatin, atorvastatin.
Related examination of catecholamine, endothelin, 5- hydroxytryptamine, fibrinogen, fibrin peptide A and insulin.
Chinese patent medicine Hippophae rhamnoides flavone for treating variant angina pectoris, stable angina pectoris, unstable angina pectoris and myocardial infarction. It is also effective for variant angina pectoris. Can be used for relieving chest distress, palpitation and shortness of breath. ...
More Chinese patent medicines for variant angina pectoris.
Verapamil hydrochloride tablets, a drug related to variant angina pectoris, reduce total peripheral resistance and myocardial oxygen consumption. Can be used for treating variant angina pectoris and unstable angina pectoris. 3. Verapamil reduces calcium influx. ...
Verapamil hydrochloride tablets can reduce total peripheral resistance and myocardial oxygen consumption. Can be used for treating variant angina pectoris and unstable angina pectoris. 3. Verapamil reduces calcium influx. ...
Nifedipine sustained-release capsules alone or in combination with other antihypertensive drugs). (2) angina pectoris, especially variant angina pectoris. Usage and dosage (1) Swallow the whole grain on an empty stomach, and don't chew it up or. ...
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Diltiazem hydrochloride? Sustained release pellets