Myocardial infarction

Introduction Acute myocardial infarction is myocardial necrosis caused by acute, persistent ischemia and hypoxia in the coronary arteries. Clinically, there are many severe and persistent post-sternal pain. Rest and nitrate drugs can not be completely relieved, accompanied by increased serum myocardial enzyme activity and progressive ECG changes, which can be complicated by arrhythmia, shock or heart failure, often life-threatening. The disease is most common in Europe and the United States, and about 1.5 million people experience myocardial infarction each year in the United States. In recent years, China has shown a clear upward trend. At least 500,000 new ones are issued each year, and at least 2 million people are now suffering.

Cause

The majority of patients occur on the basis of coronary atherosclerotic stenosis. Due to some incentives, the coronary atherosclerotic plaque ruptures, and the blood platelets accumulate on the surface of the ruptured plaque, forming a blood clot (thrombus) and suddenly blocking the coronary lumen. Causes myocardial ischemia and necrosis. In addition, a dramatic increase in myocardial oxygen consumption or coronary artery spasm can also induce acute myocardial infarction, the common incentives are as follows:

Overworked

Excessive physical labor, especially weight-bearing upstairs, excessive physical activity, continuous stress, etc., can increase the burden on the heart, sudden increase in myocardial oxygen demand, and the coronary artery of patients with coronary heart disease has hardened, narrowed, and cannot fully expand. And cause myocardial ischemia. Intense physical exertion can also induce plaque rupture, leading to acute myocardial infarction.

Excited

Induced by intense emotional changes such as excitement, nervousness, and anger.

Overeating

Many cases of myocardial infarction occur after overeating. After eating a large amount of food containing high fat and high calorie, the blood lipid concentration suddenly rises, resulting in an increase in blood viscosity and an increase in platelet aggregation. A thrombus is formed on the basis of coronary artery stenosis, causing acute myocardial infarction.

4. Cold stimulation

Sudden cold stimuli may induce acute myocardial infarction. Therefore, patients with coronary heart disease should pay great attention to cold and warm, and the cold season in winter and spring is one of the reasons for the high incidence of acute myocardial infarction.

5. Constipation

Constipation is very common among the elderly. Clinically, it is not uncommon for elderly people with myocardial infarction due to exertion of breath during constipation. It is necessary to give the elderly enough attention and keep the stool smooth.

6. Smoking, heavy drinking

Smoking and heavy drinking can induce acute myocardial infarction by inducing coronary artery spasm and increased myocardial oxygen consumption.

an examination

Related inspection

Cardiovascular troponin electrocardiogram selective angiography resting imaging

Electrocardiogram

The characteristic changes are the newly emerging Q wave and ST segment elevation and ST-T dynamic evolution.

2. Elevated myocardial necrosis serum biomarkers

Elevated creatine kinase isoenzyme (CK-MB) and troponin (T or I) are important indicators for the diagnosis of acute myocardial infarction. It can start to increase after 3 to 6 hours of onset, CK-MB returns to normal after 3 to 4 days, and troponin returns to normal after 11 to 14 days. GOT and LDH have poor diagnostic specificity and are rarely used.

3. Detection of myocardial necrosis serum biomarkers

The rapid diagnostic reagent using cardiac troponin I/myoglobin/creatine kinase isoenzyme (CK-MB) can be used as a rapid auxiliary diagnosis in the onset of myocardial infarction and is being used more and more.

4. Other

The number of white blood cells increased, the number of neutrophils increased, the number of eosinophils decreased or disappeared, the erythrocyte sedimentation rate accelerated, and the serum myosin light chain increased.

Differential diagnosis

Myocardial hypoxia:

The heart is deprived of oxygen due to insufficient blood supply. Mainly manifested as: palpitations, heart discomfort, sometimes heart pain or radioactive colic. Shortness of breath, exercise, fullness or agitation is more serious, and the body is weak. In severe cases, it can be short-term shock.

Myocardial abscess:

Myocardial edema is one of the main clinical symptoms of dilated cardiomyopathy. Myocardial gray and relaxation is a type of myocardial damage, which may be related to immune myocardial damage after viral infection, and is generally seen in ultrasonography of dilated cardiomyopathy. Can be used as a differential diagnosis with other cardiomyopathy. Myocardial stunning, also known as myocardial dysfunction after ischemia, means that myocardial transient ischemia has not caused myocardial necrosis, but mechanical resilience after reperfusion returns to normal blood flow requires hours, days or weeks. The phenomenon of complete recovery.

Cardiac hypertrophy: This is a slower but more effective compensatory function, mainly in the case of long-term stress overload, increased myocardial volume, increased contractility, allowing the heart to maintain a normal blood circulation, and at the same time Reserve power. However, this compensatory function also has its disadvantages, mainly because of hypertrophic myocardial aerobic increase, and the coronary blood supply is often unable to be met, resulting in myocardial ischemia, which will eventually lead to a decline in myocardial contractility. Hypertrophic cardiomyopathy is characterized by cardiac hypertrophy. It is characterized by ventricular muscle hypertrophy, typically in the left ventricle, with interventricular septum, occasionally concentric hypertrophy.

Systemic symptoms of myocardial infarction: fever, increased white blood cells, increased erythrocyte sedimentation rate, gastrointestinal symptoms: more common in patients with inferior wall infarction. Arrhythmia: seen in 75% to 95% of patients, occurring within 1 to 2 weeks of onset, but more common within 24 hours, anterior wall myocardial infarction prone to ventricular arrhythmia, inferior myocardial infarction prone to atrioventricular conduction Blocking. Heart failure: mainly acute left heart failure, occurring in the first few hours of onset, the incidence rate is 32% to 48%, manifested as dyspnea, cough, cyanosis, irritability and other symptoms.

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