Angina pectoris

Introduction to variant angina Variant angina pectoris (variantanginapectoris) is characterized by paroxysmal acute myocardial ischemia, with or without typical angina pectoris, with clinical syndrome of ST-segment elevation, is an unstable angina. Angina pectoris secondary to large vasospasm, characterized by angina pectoris in a quiet state, independent of fatigue and mental stress, can be relieved by bed rest, it can lead to acute myocardial infarction, severe arrhythmia (including ventricular tachycardia, ventricular fibrillation) ) and dying. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute myocardial infarction, arrhythmia, sudden death

Cause of variant angina pectoris

Smoking (30%):

Coronary spasm is a pathological reaction of vascular endothelial dysfunction. Some patients with angina have a history of smoking, and smoking can damage vascular endothelial cells. When the vascular endothelium is damaged, the vascular membrane is directly exposed to vasoconstrictor (catecholamine). , TXA2 and endothelin), vascular smooth muscle contraction and a strong vasoconstriction effect, it is currently believed that vascular endothelial dysfunction may be the basic mechanism of coronary spasm.

Coronary atherosclerosis (30%):

There are adrenergic receptors in the coronary arteries. The receptors are mainly distributed in large coronary arteries. The receptors are present in large and small coronary arteries, which can cause coronary artery contraction. When there is coronary atherosclerosis, the blood vessels are contracted. Increased sensitivity of vascular substances can easily cause paralysis of blood vessels.

Electrolyte disturbance (25%):

Variant angina occurs mostly in the latter half of the night and in the early hours of the morning. It may have lower metabolism during sleep, lower hydrogen ion concentration, and more calcium ions enter the cell to increase coronary tension, which is prone to coronary spasm.

Pathogenesis

1. Pathogenesis: The pathogenesis of this disease is coronary artery spasm, which can cause a transient, sudden, significant reduction in the diameter of the epicardial coronary artery, leading to myocardial ischemia, without any myocardial oxygen consumption before onset. The cause of increased dose, such as increased heart rate or increased blood pressure, taking nitroglycerin (sometimes requiring a larger dose) can relieve sputum.

Coronary artery spasm is often limited to coronary atherosclerotic lesions. Even in patients with variant angina with normal coronary angiography, intracoronary ultrasound can detect atherosclerotic plaque at focal iliac crest. The focal vasospasm is different from the normal contraction of the coronary arteries (such as the normal response of the body after cold stimulation). The latter is usually diffuse, mildly contracted, and patients with variant angina in the entire coronary artery bed. The basic coronary artery tension can be increased, and the segment of the coronary artery fistula not only enhances the response to ergometrine and acetylcholine, but also the entire coronary plexus exhibits high sensitivity to vasoconstriction stimulation. The abnormality of coronary tone may be The formation of coronary atherosclerosis causes an increase in the contractility of the arterial wall. Other pathogenesis includes: vascular endothelium damage, which changes the response of the blood vessel to most dilatation stimuli, such as acetylcholine can make a normal coronary Arteries are significantly dilated by increased release of endothelial-derived relaxing factor (EDRF), but at the site of endothelial damage Tube contraction, it is currently believed that endothelial injury is one of the most important predisposing factors of coronary artery spasm; vascular smooth muscle is highly reactive to vasoconstrictors such as mitogen, leukotriene, serotonin 687 and neovascularization There is a local high concentration of blood-borne vasoconstrictor near the atherosclerotic plaque.

Because coronary artery spasm can occur in the denervated transplanted heart or isolated heart, it is currently believed that the central nervous system does not play a major role in causing coronary artery spasm. The frequency of variant angina is not affected by -adrenergic blockers. , serotonin blockers, inhibition of thromboxane A production and reduction of prostacyclin, acetylcholine can induce coronary artery spasm in patients with variant angina, leading to ischemic attack, but can not induce other coronary heart disease with significant coronary artery stenosis Coronary spasm in patients and other subjects with normal coronary arteries indicates localized sympathetic innervation in patients with variant angina.

Coronary artery spasm in patients with variant angina can induce blood stasis, transform intravascular fibrinogen into fibrin, and increase plasma fibrin peptide A concentration, indicating the formation of fibrin. The concentration of fibrin in plasma is fluctuated within 24 hours. The peak occurs at midnight and early morning, which is consistent with the frequency of myocardial ischemic attacks in patients.

Smoking, hyperinsulinemia and insulin resistance are important risk factors for variant angina. It has been reported that patients with variant angina have magnesium deficiency. Magnesium sulfate can stop the onset of angina induced by cold compression test and prevent further attacks. It can suppress the onset of angina caused by hyperventilation and exercise.

2. Pathological anatomy: The coronary artery of typical variant angina pectoris is normal or almost normal, which accounts for 10% to 20% of all patients with variant angina pectoris, and occurs in 50% to 70% of coronary arteries with severely fixed stenosis. CAG shows Single-vessel disease accounted for 39%, multi-vessel disease accounted for 19%. In CAG, the normal coronary artery does not mean that the coronary artery is completely free of lesions. Less than 25% of the stenosis can be found because of the angle of projection. Internal ultrasound examination revealed atherosclerosis of the vessel wall.

Variant angina 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. The prevention of coronary heart disease includes primary prevention and secondary prevention. In one aspect, 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 disease and reduce the incidence rate. Secondary prevention refers to taking drugs for patients who have suffered from coronary heart disease. Or non-pharmacological measures 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., thereby 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 positive treatment, of course, some of these risk factors can be Controlled, such as high blood pressure, high blood fat, diabetes, obesity, smoking, less active lifestyle, etc.; and some can not be changed, such as family history of coronary heart disease, age, gender, etc., treatment methods include the use of appropriate drugs to continuously control blood pressure Correct abnormal blood lipid metabolism, quit smoking and alcohol restriction, appropriate physical activity, control weight, control diabetes, etc.

2. Secondary prevention: The use of drugs that have been validated to prevent the recurrence of coronary heart disease and exacerbation of the 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. The use of aspirin after acute myocardial infarction can reduce the rate of reinfarction by about 25%; if aspirin can not tolerate or allergies, optional Clopidogrel.

(2) -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 show that long-term lipid-lowering therapy for patients with coronary heart disease not only reduces the overall mortality rate, but also improves the survival rate, and the number of patients requiring coronary intervention or CABC is reduced. In addition to lipid-lowering effects of statins, it improves endothelial function, anti-inflammatory effects, affects smooth muscle cell proliferation and interferes with platelet aggregation, coagulation, fibrinolysis, simvastatin, pravastatin, lovastatin and atorvastatin. All have this effect.

(4) ACEI: Mostly used in patients with severe impairment of left ventricular function or heart failure, many clinical trials have confirmed that ACEI reduces mortality after acute myocardial infarction; therefore, after acute myocardial infarction, ejection fraction <40% Or patients with wall motion index 1.2, and no contraindications, should use ACEI, commonly used captopril, enalapril, benazepril and fosinopril.

Variant angina complications Complications, acute myocardial infarction, arrhythmia, sudden death

Variant angina often associated with acute myocardial infarction and severe arrhythmias, including ventricular tachycardia, ventricular fibrillation, and sudden death.

Symptoms of variant angina pectoris common symptoms arrhythmia angina psychiatric pulse shortness myocardial infarction

1. Characteristics of medical history: Variant angina pectoris is earlier than the age of chronic stable angina pectoris and unstable angina pectoris, and most of them have no classic coronary heart disease susceptibility factors except for smoking. In addition, there are still chest pain episodes. The following features:

(1) angina often occurs during rest and general daily activities: no significant relationship with increased myocardial oxygen.

(2) The onset of chest pain is often circadian rhythm: almost at the same time every day, especially between midnight and 8:00 in the morning, and most of the angina occurs in the early hours of the morning, but can also wake up during sleep. Appears when you wake up.

(3) Chest discomfort is usually very serious: it is described by the patient as pain, often accompanied by syncope caused by arrhythmia.

(4) The duration of seizures varies greatly: short tens of seconds, long as long as 20 to 30 minutes. In general, episodes of short episodes are more common.

(5) The cause of induction is usually high ventilation, exercise and exposure to cold conditions.

(6) The onset of variant angina is often periodic: it usually episodes within a short period of weeks and is in a period of remission during a prolonged period of time, during which there is an asymptomatic or asymptomatic ischemic event, in short, There is a period of change in growth and decline.

(7) Patients with variant angina pectoris and other vasospasm diseases: such as migraine and Raynaud's phenomenon.

(8) Sublingual nitroglycerin or nifedipine can quickly relieve symptoms.

2. Signs: In the absence of myocardial ischemia, cardiac examination is usually normal, unless the patient has an old myocardial infarction, myocardial ischemic attack often shows myocardial contractile dyskinesia and left ventricular dysfunction.

The diagnosis of variant angina is based on the ST-segment elevation usually accompanied by transient chest discomfort at rest, and the ST segment recovery when the symptoms disappear. There is no acute myocardial infarction evolution. When CAG shows normal or only non-infarct Plaque, more support for coronary spasm, if there is spontaneous chest pain and ST segment elevation in CAG, the epicardial coronary artery is severely paralyzed. When CAG shows coronary artery obstructive lesion, stenosis coronary artery Increased tension can cause complete coronary occlusion, and acute myocardial infarction can occur when the coronary artery is persistent and severely paralyzed.

When CAG shows normal or only non-obstructive plaque and ST-segment elevation in the onset of symptoms, it can be diagnosed as variant angina and no further examination is necessary. Therefore, it is important to record the ECG at the time of onset. Frequent, 24h dynamic ECG detection may help to establish a diagnosis. When the symptoms are not accompanied by ST-segment elevation, a provocation test may be used to induce coronary spasm. Calcium antagonists and nitrates should be discontinued before the test.

Examination of variant angina

1. Electrocardiogram: The key to the diagnosis of angina pectoris is chest pain with ST-segment elevation. Some patients have ST-segment elevation at the onset, but then ST-segment depression with T-wave changes. ST-segment and T-wave changes are due to myocardial ischemia. As a result of conduction disorders, fatal arrhythmias may be caused. The broadening of R waves may also be associated with ventricular arrhythmias. Painless ST-segment elevation is more common, and ST-segment shifts can occur in each lead. In the inferior wall and anterior wall leads, ST-segment elevation (reflecting extensive myocardial ischemia) is associated with an increased risk of sudden death, and transient conduction block may occur during myocardial ischemic attack. Ventricular ectopic agitation often occurs in longer-lasting In the case of myocardial ischemic attack, it is often associated with ST segment and T wave changes, suggesting a poor prognosis.

In survivors with a history of cardiac arrest and no significant stenosis of the coronary arteries, spontaneous or induced local coronary spasm can cause fatal ventricular arrhythmias, and malignant arrhythmias in some patients are often caused by reperfusion. In order to release a small amount of CK-MB cardiomyocyte injury, chest pain lasts, but there is no continuous ECG ST segment change, but there may be a short Q wave.

Coronary artery spasm can cause acute myocardial infarction, and the infarct site is consistent with the ST-segment elevation in the onset of variant angina.

2. Hemodynamics and coronary angiography: proximal coronary artery spasm can lead to transmural myocardial ischemia and segmental wall motion abnormalities, clinical studies confirmed that this ventricular dysfunction occurs more than angina symptoms and ECG changes Earlier.

Most patients have at least one proximal fixed stenosis of the main coronary artery, which often occurs within 1 cm of the stenotic lesion. The remaining patients have normal coronary angiography without myocardial ischemia, and sputum most often occurs in the right coronary artery. Can occur simultaneously in one or more parts of one or more coronary arteries, patients with variant angina without chest pain, normal coronary angiography, simple non-laboratory angina, ST-segment elevation of related leads during chest pain episodes High, in contrast, patients with variant angina with fixed stenosis of coronary spasm often have fatigue-related angina and associated lead myocardial ischemia, with no or only minimally fixed coronary stenosis The course of the disease is much better than patients with severe coronary artery disease.

3. Clinically commonly used stimulating test: Variant angina can be diagnosed according to the transient elevation of ST segment on the electrocardiogram at the time of onset. If the electrocardiogram at the time of onset is not obtained and the disease is suspected clinically, a provocation test may be performed to assist in the diagnosis.

(1) Ergometine challenge test: ergometrine maleate is an ergot alkaloid that stimulates -adrenergic receptors and serotonin serotonin receptors to directly contract vascular smooth muscle. Induction of coronary artery spasm in patients with variant angina pectoris is a sensitive and specific method of examination. In low-dose and carefully controlled clinical conditions, ergometrine is a safer drug, and the usual intravenous dose range is 0.05-0.40 mg. The dose required to induce a positive result is inversely proportional to the frequency of spontaneous onset of pain. If a prolonged coronary artery spasm is triggered, myocardial infarction can be caused. Due to this risk, ergometrine is only used for coronary angiography. For patients with normal or near-normal coronary arteries, gradually increase from very low doses.

Normal coronary arteries only respond to a decrease in diffuse arterial diameter when a larger dose (0.40 mg) of ergometrine is used. Patients with atypical chest pain without variant angina have multiple intravenous injections of ergometrine. Caused by a progressive diffuse coronary artery diameter reduction, vasoconstriction in patients and coronary intimal irregularities in patients with more obvious, suggesting mild atherosclerosis, this dose-related coronary diffuse contraction Unlike the abnormal response of variant angina, the latter is typically characterized by severe local spasms at very low drug doses, and increased sensitivity to ergometrine testing in patients with active disease (at least once a day) Patients with occasional episodes of variant angina have lower sensitivity.

The challenge test should be performed in the case of coronary angiography. If coronary artery spasm is found, the test should be stopped immediately. Immediately, 0.2-0.3 mg of nitroglycerin should be administered intracoronically, and this dose can be repeated until the sputum is relieved.

(2) Hyperventilation test: hyperventilation can also induce severe angina pectoris, ECG shows ST-segment elevation, ventricular arrhythmia and angiography show obvious coronary spasm, at least once a day, patients with variant angina active period Sensitivity to hyperventilation is 95%, and sensitivity to ergometrine is 100%. However, in patients with a lower frequency of angina pectoris, the sensitivity of hyperventilation test is lower than that of ergometrine, so its diagnostic value is certain. limitation.

(3) Acetylcholine test: Intracoronary injection of acetylcholine in patients with variant angina can lead to severe coronary spasm, which should not be confused with the slight diffuse narrowing induced by acetylcholine in patients with abnormal coronary endothelium. Because this method can induce left and right coronary artery spasm, it is useful for understanding whether patients have multivessel disease or sputum. This method is sensitive, safe and reliable, and its sensitivity (95%) and specificity (99%). Similar to ergometrine.

The parasympathetic medicinal drug methacholine (methamphetamine), histamine and dopamine can also induce coronary spasm, similar to ergometrine and acetylcholine, for patients with varicose angina with severe fixed coronary stenosis and no Patients with limited stenosis can cause significant coronary spasm.

4. Radionuclide myocardial perfusion scintigraphy: 201(201Tl) myocardial perfusion scintigraphy can confirm the presence of sputum during arterial angiography, limited myocardial perfusion defect in the perfusion area, reduction of coronary sinus blood flow, support for coronary artery The relationship between sputum, myocardial perfusion and local myocardial ischemia.

5. Coronary angiography (CAG): CAG results in patients with variant angina can be normal or abnormal. Typical patients have normal or non-infarcted coronary arteries, but most patients have at least one major coronary proximal end. Fixed stenosis, coronary artery stenosis has a close relationship with its lesions, and often occurs within 1cm of stenotic lesions. The total incidence of coronary spasm is highest in LAD, followed by RCA, LCX, Dia and RAD, but In patients with no obvious coronary lesions, the incidence of PCA is higher than that of LAD, while women are relatively common. Coronary fistula can occur simultaneously in one or more sites of one or more coronary arteries.

Diagnosis and identification of variant angina pectoris

Combined with a typical medical history, the ECG changes at the time of onset can diagnose the disease. CAG and the results of the challenge test can be helpful for diagnosis.

1. Aortic dissection: Aortic dissection often produces MI-like chest pain, the site of chest pain is often higher, near the exit of the chest; tearing; the onset is often more sudden than AMI; pain quickly peaks and ranges Widely, often reflected to the back, waist, abdomen and calf; pain continues to not relieve, although there may be shock symptoms, but the course is often accompanied by high blood pressure, aortic dissection can produce compression symptoms, resulting in inconsistent blood pressure in the bilateral upper limbs, single Or bilateral pulse, carotid pulsation weakened, X-ray and echocardiography can be found that the aorta is significantly widened, no AMI electrocardiogram and serum enzymological changes, in order to confirm the aortic dissection, often need to do ultrasound examination Arteriography and/or magnetic resonance imaging.

MI can occur when the aortic dissection invades the coronary arteries, but it is rare that approximately 5% to 10% of patients with aortic dissection have no chest pain.

2. Unstable angina: Although the pain site and nature are similar to AMI, the time of angina pectoris usually does not exceed half an hour; more often without nausea, vomiting, shock, etc.; characteristic changes of serum-free enzymology (myocardial muscle calcium) Protein T can be increased); although there are ST segment and T wave changes at the time of attack, but transient, the ST segment is significantly decreased when angina pectoris occurs, or accompanied by T wave inversion, should be noted with non-ST segment elevation MI, In the onset of angina pectoris, the ST segment is elevated significantly, the T wave is erect, and may be associated with ventricular arrhythmia or bradyarrhythmia. The ST segment of the corresponding lead is significantly reduced, similar to the early AMI pattern, but after the remission, the ST segment Returning to the equipotential line very quickly, pathological Q waves are generally not present during the onset of angina pectoris. Dynamic observation of serum enzymology and changes in cardiac troponin T is one of the main points of differential diagnosis.

3. Pulmonary embolism: sudden onset of pulmonary embolism, chest pain, shortness of breath, cyanosis, hemoptysis or shock, such as no hemoptysis sometimes resembles AMI, but the former fever and white blood cell increase occur within 24h; cardiac signs can be The second heart sound was found in the pulmonary valve area; the electrocardiogram of pulmonary embolism was faster and shorter than that of AMI. The electrocardiogram showed acute right axis deviation, right ventricular enlargement and SIQIIITIII, I-wave new S wave, abnormal Q wave in III lead or even The aVF lead is accompanied by a T wave inversion, but the Q lead does not appear Q wave, and there is a significant clockwise transposition; the total serum lactate dehydrogenase can be increased, but its isoenzyme (LDH1) and phosphocreatine kinase are the same. The enzyme enzyme (cPK-MB) is not elevated, and the radionuclide lung perfusion scan is helpful for diagnosis.

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