Overview.
Unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI) are collectively referred to as acute coronary syndromes. The common pathophysiologic basis of acute coronary syndromes is plaque rupture. A history of infarction and previous angina symptoms are more common than ST-segment elevation infarction.
Etiology
Most myocardial infarctions are caused by occlusion of coronary blood flow in pre-existing mildly or moderately stenotic lesions. The common pathophysiologic basis of unstable angina, non-ST-segment-elevation infarctions, and acute coronary syndromes with ST-segment-elevation infarctions is plaque rupture. The dynamic course of plaque rupture can progress to complete occlusion of the coronary artery by a thrombus, which is typified by ST-segment elevation on the electrocardiogram, and ultimately to complete or almost complete necrosis of the wall of the coronary-associated ventricle (so-called permeable infarction, which is often accompanied by the generation of Q waves on the electrocardiogram). Thrombi that allow incomplete occlusion of the lumen produce unstable angina and non-ST-segment elevation infarcts, both of which are typified on the ECG by ST-segment depression and T-wave inversion. If, over a 20-minute period, the transient vasospasm caused by thromboxane A2 and serotonin released as a result of platelet activation is attenuated or if the thrombus within the abnormal coronary artery spontaneously dissolves, anterograde flow is restored, and thus there are no histologic manifestations of necrosis, no biochemical markers of myocardial necrosis, and no corresponding persistent changes on the electrocardiogram that would develop into unstable angina pectoris. Longer and more severe episodes of plaque rupture than those that produce unstable angina typically result in the release of biochemical markers of necrosis (troponin T or I), but the type of manifestation of necrotic extension is less severe than in ST-segment elevation infarcts, and a diagnosis of non-ST-segment elevation infarction is made (often with no pathologic Q-waves on the electrocardiogram) when clinical evidence of myocardial necrosis is perceived.
Symptoms
A history of infarction and previous angina symptoms are more common in non-ST-segment elevation infarction than in ST-segment elevation infarction. Complications of infarction are more common in ST-segment elevation infarction and less common in non-ST-segment elevation infarction. The extent of infarction in non-ST-segment elevation infarction is smaller than that in ST-segment elevation infarction, and the extension of infarction in non-ST-segment elevation infarction is significantly more than that in ST-segment elevation infarction. Infarctive pericarditis is more common in ST-segment elevation infarcts and less common in non-ST-segment elevation infarcts. The incidence of post-infarction angina is significantly higher in non-ST-segment elevation infarction than in ST-segment elevation infarction, with 35% to 50% in the former and 18% to 30% in the latter being reported. The pre-discharge exercise test positivity of non-ST-segment elevation infarction was 2 times higher than that of ST-segment elevation infarction.
These characteristics suggest that non-ST-segment elevation infarcts often have residual endangered myocardium.
Examination
1. Cardiac marker examination
Serum troponin T or I is elevated. Increased serum cardiac enzymes may show abnormal changes such as increased CK, CK-MB, glutamate aminotransferase, and lactate dehydrogenase.
2. Electrocardiography
Non-ST-segment elevation infarction refers to acute myocardial infarction without pathologic Q wave on ECG and only ST-T wave evolution, which can be classified into 3 types according to the characteristics of ECG in the acute stage:
(1) ST-segment depression type: At the onset of ST-segment depression of ≥1mm in horizontal or downward sloping type, T-wave may be upright, bidirectional or mildly inverted.
(2) T-wave inversion T-wave is symmetrical in both limbs and deeply inverted at the onset of the attack, without obvious ST-segment displacement, and later there is a typical infarction T-wave evolution.
(3) ST-segment elevation type: ST-segment elevation at the onset (≥2mm in the limb leads and ≥3mm in V1-V4), followed by ST-segment recovery with T-wave evolution. In the ST-segment depression group, the incidence of serious complications and death is higher, and those with severe ST-segment depression in multiple leads have a poor prognosis.
3. Radionuclide examination
The detection rate of infarcted segments and ventricular wall motion abnormalities is lower than that of QMI, which is related to the early reperfusion of non-ST-segment elevation infarction, less necrotic myocardium, and lighter impact on ventricular wall motion. In recent years, it has been found that the sensitivity of single-photon emission computed tomography (SPECT) for diagnosis of NQMI is relatively high, and the positron emission scanning is a promising examination method for identification of NQMI.
4. Echocardiography
Segmental motion abnormalities are often seen in non-ST-segment elevation infarctions with high sensitivity, while NQMI patients do not have this phenomenon or are less likely to have it. 2D ultrasound is used to monitor NQMI, and once a segmental motion abnormality is detected, it suggests that QMI has developed.
Diagnosis
1. the dynamic evolution of the ST-T lasts for a long time, often more than 24 hours (ST-T changes in transient myocardial ischemic episodes often recover within a few hours).
2. Chest pain lasting at least half an hour or more, consistent with the chest pain characteristic of infarction.
3. Changes in serum enzymology are consistent with the pattern of change of infarction and/or serum troponin T or I is elevated ≥ 2 times the normal value.
If 1 or 2 and 3 can be diagnosed as non-ST-segment elevation infarction.
Differential Diagnosis
When pathological Q waves have not yet appeared on the electrocardiogram, it is very easy to be confused with the electrocardiogram changes of coronary artery insufficiency, both of which will show depression or elevation of the ST segment on the electrocardiogram, and both of which will have changes such as low and flat T waves, bidirectional or inverted, etc. It is often difficult to identify them at the early stage of the clinical onset of the disease; however, if dynamic observation is carried out, and a comprehensive and comprehensive analysis is made, it can be found that the electrocardiogram changes of acute coronary artery insufficiency are transitory, and that However, with comprehensive analysis, it can be found that acute coronary insufficiency has transient ECG changes, whereas non-ST-segment elevation myocardial infarction has continuous ECG evolution, and the diagnosis can usually be made by combining the clinical symptoms and the dynamic evolution of enzymology.
Treatment of myocardial infarction
Principles of treatment
The aim of treatment is to provide immediate relief of ischemia and prevent death or myocardial infarction or reinfarction.The treatment of NSTEMI includes anti-ischemic therapy, antithrombotic therapy, and invasive therapy according to the risk stratification.
2.General treatment
Patients should rest in bed, keep the environment quiet, and avoid tension and anxiety. Cardiac monitoring. Oxygen intake, maintain oxygen saturation >90%.
3. Coronary artery revascularization
Coronary revascularization includes percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG).
The decision to perform early invasive therapy should be based on the risk stratification of patients with NSTEMI, and the GRACE scoring system can be used for risk stratification. The GRACE score system can be used for risk stratification, and aggressive early invasive intervention is recommended for patients with high risk stratification.The choice of PCI or CABG for revascularization of patients with NSTEMI is highly dependent on the results of the coronary angiogram and the patient’s personal preference.
4. Drug therapy
(1) Antiplatelet therapy Reduce the incidence of cardiovascular events (death, recurrent fatal or nonfatal myocardial infarction, and stroke) in patients.
① Aspirin Unless there is a contraindication, all NSTEMI patients should use aspirin as early as possible, the first oral non-enteric or chewable enteric formulation of 300 mg, followed by 75 to 100 mg, 1 time / day, long-term maintenance.
② ADP receptor antagonists Combined use of aspirin and ADP receptor antagonists is recommended in patients with NSTEMI for 12 months. Clopidogrel is available as a loading dose of 300-600 mg for the first dose, followed by 75 mg once/day. Newer generation ADP receptor antagonists include prasugrel and tegretol.
(iii) Platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptor antagonists
(2) Anticoagulant therapy Anticoagulant therapy is routinely received on the basis of antiplatelet therapy. Anticoagulant therapy establishes and maintains patency of the infarct-related arteries and prevents deep vein thrombosis, pulmonary embolism, and intracardiac thrombosis. Commonly used anticoagulants include ordinary heparin, low molecular heparin, sodium sulfadiazine and bivalirudin.
(3) Nitrates For patients with persistent chest discomfort, hypertension, large anterior wall myocardial infarction forearm myocardial infarction, and acute left heart failure, the intravenous application of nitroglycerin during the first 24 to 48 hours of treatment is helpful in controlling myocardial ischemic episodes, reducing the infarct size, and lowering short-term or even possibly long-term morbidity and mortality. Currently, it is recommended to apply nitroglycerin intravenously and switch to oral preparations 12 to 24 hours after symptoms disappear.
(4) Beta-blockers Intravenous beta-blockers administered within the first few hours after myocardial infarction may improve the prognosis by reducing the size of the infarct, decreasing the rate of reinfarction, and decreasing the incidence of ventricular fibrillation and the rate of death.
(5) Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) can help to improve myocardial remodeling during the recovery phase, reduce the mortality rate of acute myocardial infarction (AMI), and reduce the incidence of congestive heart failure, especially in patients with anterior wall myocardial infarction, heart failure, or tachycardia. Those who cannot tolerate ACEI can be replaced by ARB.
(6) Lipid-regulating therapy Statins applied in the acute phase can prompt the endothelial cells to release nitric oxide, with nitrate-like effects, and anti-inflammatory and plaque-stabilizing effects in the long term. It can reduce the incidence of death and myocardial infarction. Statins should be started as early as possible (within 24 hours) regardless of baseline lipid levels.
(7) Calcium antagonists Non-dihydroarsenic calcium antagonists used in acute STEMI, in addition to controlling supraventricular arrhythmias, does not help to reduce the extent of infarction or cardiovascular events, it is not recommended to routinely apply non-dihydroarsenic calcium antagonists in patients with STEMI, but non-dihydroarsenic calcium antagonists can be used in patients with persistent myocardial ischemia or atrial fibrillation with ventricular tachypnea even after nitrate and β-blockers. Patients with persistent myocardial ischemia or atrial fibrillation with tachycardia after nitrate and beta-blockers.
4. Antiarrhythmic therapy
5. Antihypotension and cardiogenic shock treatment
6. Anti-heart failure treatment
7. Treatment of complications