non-ST-segment elevation myocardial infarction
Introduction
Introduction to non-ST segment elevation myocardial infarction Unstable angina, non-ST-segment elevation myocardial infarction (MI) and ST-segment elevation Q-wave myocardial infarction are called acute coronary syndrome. The common pathophysiological basis of acute coronary syndrome with non-ST-segment elevation myocardial infarction and ST-segment elevation Q-wave myocardial infarction is plaque rupture. Patients with a history of myocardial infarction and previous angina pectoris were more common than those with ST-segment elevation. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: arrhythmia heart failure
Cause
Non-ST segment elevation myocardial infarction
(1) Causes of the disease
Most myocardial infarctions are caused by coronary vascular occlusion in the original mild or moderate stenotic lesions, unstable angina, non-ST-segment elevation MI and ST-segment elevation Q-wave MI acute coronary The common pathophysiological basis of arterial syndrome is plaque rupture. The dynamic process of plaque rupture can develop to thrombus to completely close the coronary artery. The typical manifestation on the electrocardiogram is ST-segment elevation, which eventually develops into the coronary-related ventricle. The wall is completely or almost completely necrotic (so-called transmural myocardial infarction, which is often produced on the electrocardiogram), and the thrombus that is not completely occluded in the lumen produces unstable angina and non-ST-segment elevation MI, both on the electrocardiogram. Typical manifestations are ST-segment depression and T-wave inversion, if transient vasospasm caused by thromboxane A2 and serotonin released by platelet activation is reduced in 20 min, or spontaneous thrombosis in abnormal coronary arteries The anterior blood flow can be recovered, so there is no histological manifestation of necrosis, no biochemical markers of myocardial necrosis, and corresponding electrocardiograms continue to change. A typical result of unstable angina pectoris, a longer and more severe plaque rupture than unstable angina, is the release of necrotic biochemical markers (troponin T or I), but the type of necrotic expansion is more than ST-segment elevation. High myocardial infarction is mild. When clinical evidence of myocardial necrosis is detected, it can be diagnosed as a non-ST-segmented myocardial infarction (there is often no pathological Q wave on the ECG).
(two) pathogenesis
Non-ST-segment elevation MI is more severe than incomplete obstruction of diseased arteries in patients with unstable angina, longer time, resulting in temporary reduction of myocardial blood flow and MI, non-ST-segment elevation MI and ST-segment elevation Compared with MI, the blood flow in the ischemic area of the former is often rebuilt within a few minutes to a few hours after the onset of the disease. This is due to the early dissolution of the completely blocked thrombus; the original plaque ruptures faster; the vasospasm is relieved; There is extensive collateral circulation in complete obstruction; the total thrombus load is low, and the anterior blood flow never disappears. These mechanisms cause myocardial necrosis to stop earlier and limit the development of infarction, which can be considered as non-ST segment elevation. Myocardial infarction is intermediate between ST-segment elevation myocardial infarction and unstable angina. Myocardial necrosis in non-ST-segment elevation myocardial infarction often shows less myocardial necrosis at the site, more concentrated in The inner third of the myocardial wall, because the blood flow is restored and/or the formed collateral circulation can prevent the necrotic area from spanning the entire ventricular wall thickness.
Prevention
Non-ST-segment elevation myocardial infarction prevention
Epidemiological studies have shown that coronary heart disease is a disease that is affected by many factors. Even studies have listed 246 influencing factors. Many epidemiologists divide the main risk factors affecting the onset of coronary heart disease into:
1 factors causing atherosclerosis, including hypertension, hyperglycemia, disorders of fat metabolism, and elevated fibrinogen,
2 Some lifestyle habits that are predisposed to coronary heart disease include excessive eating, lack of physical activity, smoking, and type A personality.
3 Clinical indications for coronary artery involvement, including electrocardiographic abnormalities during rest, exercise, or monitoring, and myocardial perfusion, which are not risk factors for coronary artery disease, but may indicate a considerable degree of coronary artery disease.
4 other congenital factors, such as the family history of early coronary heart disease.
Because epidemiological data show that coronary heart disease is one of the most important diseases causing human death, and there is still no radical measures in clinical practice, it is of great significance for the active prevention of coronary heart disease. The prevention of coronary heart disease involves In the 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 to prevent disease and reduce the incidence rate. Secondary prevention means Patients with coronary heart disease take medicinal or non-pharmacological measures to prevent recurrence or prevent exacerbations.
1. Primary prevention measures Primary prevention measures for coronary heart disease include two situations:
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. Secondary prevention measures The secondary prevention content of patients with coronary heart disease also includes two aspects. The first aspect includes the content of primary prevention, that is, the risk factors of various coronary heart diseases should be controlled. Validated effective drugs to prevent recurrence of coronary heart disease and exacerbation of the disease, the drugs that have been confirmed to have preventive effects are:
(1) Antiplatelet drugs: A number of clinical trials have confirmed that aspirin can reduce the incidence of myocardial infarction and reinfarction rate. The use of aspirin after acute myocardial infarction can reduce the reinfarction rate by about 25%; if aspirin can not tolerate Or allergic, clopidogrel can be used.
(2) -blockers: as long as there are no contraindications (such as severe heart failure, severe bradycardia or respiratory diseases, etc.), patients with coronary heart disease should use beta blockers, especially in the occurrence of acute coronary After the arterial event; there are data showing that the use of beta blockers in patients with acute myocardial infarction can reduce the mortality and reinfarction rate by 20% to 25%. The drugs available are metoprolol, propranolol, Thiolol and so on.
(3) ACEI: used in patients with severe impairment of left ventricular function or heart failure, many clinical trials (such as SAVE, AIRE, SMILE and TRACE, etc.) have confirmed that ACEI reduces 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 captopril, enalapril, benazepril and blessing Simplice and so on.
(4) statin lipid-lowering drugs: the results of studies from 4S, CARE and recent HPS 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 requires coronary intervention The number of patients with CABG is reduced, which 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, simvastatin, and deforestation. Statins, fluvastatin, and atorvastatin all have this effect.
In addition, coronary angiography has coronary atherosclerotic mild stenotic lesions and clinically no ischemic symptoms, although it is not clearly diagnosed as coronary heart disease, it should be regarded as a high-risk group of coronary heart disease, giving active prevention, Long-dose aspirin can also be given for a long time, and risk factors such as dyslipidemia and hypertension can be eliminated.
Complication
Non-ST segment elevation myocardial infarction complications Complications arrhythmia heart failure
(1) dysfunction of the papillary muscles or rupture of the papillary muscles (mainly the mitral papillary muscles) due to ischemia, necrosis, etc., contraction weakness or rupture, resulting in mitral regurgitation, vocal tract systolic murmur in the apical region, And easy to cause heart failure.
(B) heart rupture is an early rare but serious complication, often occurs within a week of onset, mostly rupture of the ventricular free wall, sudden death due to pericardial hemorrhage and acute pericardial occlusion. Occasionally, the ventricular septal rupture perforation, a loud systolic murmur in the fourth intercostal space on the left sternal border, often accompanied by tremor, can cause heart failure and rapid death.
Symptom
Non-ST-segment elevation myocardial infarction symptoms common symptoms angina pectoris chest pain chest pain arrhythmia
Non-ST-segment elevation myocardial infarction has the following clinical features compared with ST-segment elevation MI:
1. Non-ST-segment elevation MI has a history of MI and previous angina symptoms are more common than ST-segment elevation MI.
2. The complications of AMI are more common in ST-segment elevation MI, less common in non-ST-segment elevation MI.
3. The infarct size of non-ST-segment elevation MI is smaller than the ST-segment elevation MI.
4. The infarct extension of non-ST-segment elevation MI was significantly greater than that of ST-segment elevation.
Infarctory pericarditis is more common in ST-segment elevation MI, less common in non-ST-segment elevation MI.
6. The incidence of post-infarction angina pectoris with non-ST-segment elevation MI is significantly higher than that of ST-segment elevation. It has been reported that the former is 35% to 50%, and the latter is 18% to 30%.
7. The non-ST-segment elevation MI pre-discharge exercise test was 2 times higher than the ST-segment elevation MI.
These characteristics suggest that non-ST-segment elevation MI often has residual endangered myocardium.
Examine
Non-ST-segment elevation myocardial infarction
1. Increased serum myocardial enzymology may lead to abnormal changes such as CK, CK-MB, aspartate aminotransferase, and lactate dehydrogenase.
2. ESR increases.
3. The patient may have blood lipids and the blood sugar concentration increases.
4. Electrocardiogram examination Non-ST-segment elevation MI refers to the absence of pathological Q waves on the electrocardiogram. Only acute ST-T wave evolution of acute myocardial infarction can be classified into 3 types according to the characteristics of acute ECG:
(1) ST segment depression type: ST segment is horizontal or down oblique depression 1mm at the time of onset, T wave can be erect, two-way or lightly inverted.
(2) T wave inversion type: T wave two limbs are symmetric and deeply inverted, but there is no obvious ST segment displacement, and there is a typical infarct T wave evolution.
(3) ST-segment elevation type: ST segment elevation at the time of onset (limb lead elevation 2mm, V1 ~ V4 elevation 3mm), after ST segment recovery, with T wave evolution, in the ST segment depression group, severe The incidence of complications and death is high, and the prognosis of patients with severe ST-segment depression is poor.
5. Radionuclide examination has a lower detection rate of infarct segment and wall motion abnormality than QMI. This is related to non-ST-segment elevation MI early reperfusion, less necrotic myocardium, and less influence on wall motion. It is found that SPECT has a higher sensitivity (95%) for diagnosing NQMI, and positron emission scanning is also a promising method for identifying NQMI.
6. Echocardiography in non-ST-segment elevation MI often seen segmental motor abnormalities, the sensitivity is higher, and NQMI patients have no or less of this phenomenon, using two-dimensional ultrasound to monitor NQMI, once found Segmental motor abnormalities suggest that QMI has evolved.
Diagnosis
Diagnosis and diagnosis of non-ST segment elevation myocardial infarction
Diagnostic points
The diagnostic criteria for non-ST-segment elevation MI are as follows:
The dynamic progression of 1ST-T lasts longer, often over 24 h (ST-T changes in transient myocardial ischemic attacks often recover in a few hours),
2 chest pain lasts for at least half an hour, in line with the characteristics of chest pain in myocardial infarction,
3 serum enzymology changes in accordance with the changes in myocardial infarction and / or serum troponin T or I increased normal value more than 2 times, if there are 1 or 2 and 3 can be diagnosed as non-ST segmental lift High myocardial infarction.
Differential diagnosis
When there is no pathological Q wave on the electrocardiogram, it is easy to be confused with the ECG changes of coronary insufficiency. The ST segment is depressed or raised on the ECG, and both T-wave low-level, bidirectional or inverted changes are observed. In the early stage of clinical onset, it is often difficult to identify, but if you do dynamic observation and comprehensive analysis, you can find that the ECG changes of acute coronary insufficiency are transient, but the electrocardiogram of myocardial infarction without ST-segment elevation is Continuous evolution, combined with clinical symptoms and dynamic changes in enzymology, can often be diagnosed.
