Myocardial infarction in youth

Introduction to young myocardial infarction Young myocardial infarction refers to acute myocardial infarction in young people under the age of 40. More than 90% of patients have the first onset of 31 to 40 years old, more men than women, the vast majority of patients have no history of angina before the disease, and the typical manifestations of ischemic chest pain. The acute and long-term mortality of young myocardial infarction is low. The condition is stable after discharge and the labor can be recovered. basic knowledge Sickness ratio: 0.5% Susceptible people: young people under 40 years old Mode of infection: non-infectious Complications: heart failure, shock, arrhythmia, sudden death

The cause of young myocardial infarction

(1) Causes of the disease

1. The main cause of myocardial infarction in coronary atherosclerosis is coronary atherosclerosis. It has been found that atherosclerotic lesions exist in children aged 8 years. The autopsy of young myocardial infarction found that about 60% of the two branches existed. Vascular lesions.

2. Non-coronary atherosclerosis is more common in patients with myocardial infarction than in middle-aged and elderly patients. Understanding these causes is very beneficial for the diagnosis and treatment of young myocardial infarction. The cause of non-coronary atherosclerosis can be obtained from the following aspects: analysis.

(1) Coronary arteritis: reported more, can be found in systemic lupus erythematosus, rheumatic heart disease, multiple arteritis, Kawasaki disease.

(2) Coronary artery spasm: It has been determined that coronary artery spasm can participate in or induce acute myocardial infarction. The causes of coronary spasm are smoking, drinking, high-fat meal, drug use (marijuana, cocaine, etc.) and strenuous exercise.

(3) coronary embolism: one of the important causes of myocardial infarction in non-coronary atherosclerotic young patients, embolus often originated from infective endocarditis, atrial fibrillation and other heart disease thrombosis, artificial valve replacement Or mitral and aortic valve calcification.

(4) Trauma: myocardial contusion caused by non-penetrating injury of the chest, the incidence rate is 16% to 76%, and severe cases can cause transmural myocardial infarction.

(5) Coronary artery dissection: Intimal injury of the coronary artery caused by aortic dissection and coronary dissection and dissection of the lumen to the lumen can cause acute myocardial infarction.

(6) vascular malformation: abnormal origin of coronary artery.

(7) Others: severe hypoxia, low perfusion pressure of coronary arteries, severe infection, severe blood loss or bleeding disorders.

(two) pathogenesis

Excessive drinking and coffee

A small amount of alcohol and coffee is not harmful. Excessive drinking and coffee may induce acute myocardial infarction. It is reported in the literature that in young myocardial infarction, many people suffer from myocardial infarction due to severe chest pain after excessive drinking, which is currently among young people in China. Excessive drinking, coffee and smokers are worth a lot of caution.

2. Drug addiction

Drug abuse or intravenous drugs such as marijuana, cocaine, etc., can induce coronary spasm and lead to myocardial infarction. It has been reported that cocaine can block the utilization of endogenous catecholamines, can induce ventricular arrhythmia and sudden death, and can also cause coronary vasoconstriction. In the case of myocardial infarction, a author reported a case of a 21-year-old patient with normal coronary artery structure and myocardial infarction due to cocaine addiction.

3. Oral contraceptives Oral contraceptives can increase the risk of myocardial infarction, so oral contraceptives are an important factor in myocardial infarction in women of childbearing age. Women with pregnancy or oral contraceptives have a higher incidence of myocardial infarction.

4. Strenuous exercise recognizes that appropriate exercise and physical exercise can prevent coronary heart disease, but it should be noted that the intensity of exercise and physical exercise methods should vary from person to person. In recent years, many young people have been struggling due to strenuous exercise and overwork (including emotional excitement). In the case of sudden death and myocardial infarction, strenuous exercise induced young myocardial infarction in the following two cases.

(1) Exercise-induced myocardial infarction with coronary artery disease:

1 coronary atherosclerotic vascular damage is based on moderate coronary stenosis: during vigorous exercise, coronary blood flow is difficult to maintain more than 30min, causing myocardial ischemia, eventually leading to myocardial infarction, but also due to vascular stenosis Myocardial infarction is induced by thrombosis or vasospasm.

2 non-coronary atherosclerotic vascular damage is rare: including the following:

A. Congenital lesions: coronary artery-pulmonary spasm.

B. Abnormal origin of coronary artery.

C. Susceptibility to the coronary artery wall, normal and ectopic coronary arteries can form a dissection aneurysm in the coronary artery.

(2) The mechanism of exercise myocardial infarction in normal coronary arteries may be:

1 Coronary artery spasm: may be the coronary artery spasm induced by increased sensitivity of the coronary artery wall to catecholamine or exercise caused by increased catecholamines.

2 coronary artery embolization.

5. Type A behavior Type A behavior type mainly manifests as time urgency (always want to do the most things in a short time), competitive, irritating, etc., studies have shown that type A actors are susceptible to coronary heart disease.

Youth 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 overeating, 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:

(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 reasonable 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., positive treatment, of course, some of these risk factors can be controlled Such as high blood pressure, hyperlipidemia, diabetes, obesity, smoking, less active lifestyle, etc.; and some can not be changed, such as family history of coronary heart disease, age, gender, etc., including the use of appropriate drugs for continuous control Blood pressure, correct abnormal blood lipid metabolism, limit smoking, limit physical activity, control physical activity, control weight, control diabetes, etc.

2. Secondary preventive 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. The second aspect is to use drugs that have been proven effective. To prevent the recurrence of coronary heart disease and the 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.

Young myocardial infarction complications Complications, heart failure, shock, arrhythmia, sudden death

Common complications of myocardial infarction, such as heart failure, shock, arrhythmia, sudden death, ventricular aneurysm, etc., but the myocardial infarction in young people has relatively good cardiac function, and generally less complications, as long as early diagnosis and treatment, rarely There are complications.

Youth myocardial infarction symptoms common symptoms myocardial infarction sudden chest tightness chest pain myocardial necrosis extensive

About 90% of patients have the first onset of 31 to 40 years old, more men than women, the vast majority of patients have no history of angina before the disease, and the typical onset of ischemic chest pain, the majority of patients for the first time with typical ischemia Sexual chest pain and treatment, due to sudden onset, severe symptoms, due to young age, often lack of sufficient understanding of myocardial infarction, which is often caused by misdiagnosis, although young myocardial infarction is more typical of ischemic chest pain, but It is not uncommon to use the pain of the radiation site as the first manifestation. The use of atropine drugs for misdiagnosis often aggravates the infarction. It should also be highly valued. Some young patients with myocardial infarction have sudden death as the first manifestation. The diagnosis of myocardial infarction cannot be confirmed before birth. As a result, the timing of treatment is lost. Therefore, in the case of young people with no history of typical angina or coronary atherosclerosis, once typical ischemic chest pain occurs, they should be highly alert to the possibility of acute myocardial infarction. The suspected cases should be regularly recorded with electrocardiogram and measurement. Myocardial enzymes for early diagnosis.

Examination of young myocardial infarction

1. Increased serum myocardial enzymology In acute atrial myocardial infarction, abnormally elevated CK, CK-MB, aspartate aminotransferase, lactate dehydrogenase and other abnormal changes may occur.

2. ESR increases.

3. The patient may have blood lipids and the blood sugar concentration increases.

4. Electrocardiogram in the corresponding myocardial infarction site, typical pathological Q wave, ST-T changes, etc., can be qualitative, localized diagnosis.

5. Radionuclide use of ischemic myocardial characteristics of radionuclide and its labeled compounds can be selectively ingested, radionuclide myocardial imaging can find infarction, determine the extent and extent of infarction, determine collateral blood flow, myocardial Injury and ventricular function, and can estimate prognosis.

6. Echocardiography can help to establish the infarction site, infarct size and left and right ventricular dysfunction of acute myocardial infarction by measuring ventricular volume, wall motion and left ventricular ejection fraction, and provide prognostic information. Echocardiography showed regional wall motion abnormalities in almost all patients with transmural acute myocardial infarction.

Diagnosis and diagnosis of young myocardial infarction

diagnosis

The diagnosis of general myocardial infarction is based on internationally accepted diagnostic criteria. Based on symptoms, electrocardiogram and enzymatic changes, comprehensive analysis can be performed. Current radionuclide scanning, myocardial visualization, echocardiography, CT, nuclear magnetic resonance, coronary angiography, etc. It is helpful for the diagnosis of some myocardial infarctions without Q-wave youth.

Differential diagnosis

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; the pain quickly reaches a peak and a wide range, often reflected to the back , waist, abdomen and calf; pain does not continue to 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, neck Arterial pulsation weakening, X-ray and echocardiography can be found that the aorta is significantly widened, no AMI electrocardiogram and characteristic changes in serum enzymology, in order to confirm the aortic dissection, often need to do ultrasound examination of aortic angiography and / or Magnetic resonance examination.

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 (cardiac troponin T can be increased); Although ST segment and T wave changes, but transient, angina pectoris significantly decreased ST segment, or accompanied by T wave inversion, should be noted with non-ST segment elevation MI identification, angina pectoris attack, ST The segment is obviously elevated, the T wave is erect, and may be accompanied by ventricular arrhythmia or slow arrhythmia. The ST segment of the corresponding lead is significantly decreased, similar to the early AMI pattern, but after the attack is relieved, the ST segment quickly returns to the equipotential line. On the angina pectoris, there is generally no pathological Q wave. Dynamic observation of serum enzymes and changes in cardiac troponin T is one of the main points of differential diagnosis.

3. Pulmonary embolism

Pulmonary embolism is sudden onset, 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 found in the pulmonary valve area 2 heart sound hyperthyroidism; pulmonary embolism electrocardiogram changes faster and shorter than AMI, its electrocardiogram showed acute right axis deviation, right ventricular enlargement and SIQIIITIII, I lead new S wave, abnormal Q wave in III lead or even aVF lead accompanied T wave is inverted, but there is no Q wave in the II lead, and there is a significant clockwise transposition; the total serum lactate dehydrogenase can be increased, but its isoenzyme (LDH1) and phosphocreatine kinase isoenzyme (cPK- MB) does not rise, and radionuclide lung perfusion scans help to confirm the diagnosis.

4. Acute pericarditis

The disease is often acute, accompanied by more severe and persistent precordial pain and ST-segment elevation, but patients with pericarditis often have fever before or at the same time as chest pain, increased white blood cells, chest pain in cough, and deep breathing. When sitting and leaning forward, the pain in AMI has nothing to do with breathing and body position; the former can hear the pericardial friction sound on the day of onset and even within a few hours, and the pericardial friction sound caused by AMI often appears 2 to 5 days after the onset, sometimes the duration is very high. Short; the electrocardiogram caused by acute pericarditis is the ST-segment of the general lead is raised downward, it does not cause Q wave, low voltage with pericardial effusion; characteristic changes of serum-free enzymology of acute pericarditis; ultrasound Cardiac images can be used to observe the condition of pericardial effusion. There is very little effusion in AMI and pericarditis.

5. Acute abdomen

Acute cholecystitis and cholelithiasis, perforation of ulcer disease, acute pancreatitis, etc. often have upper abdominal pain with nausea, vomiting or shock, easy to be confused with atypical AMI of the pain and cause misdiagnosis, according to medical history, abdominal signs (acute abdomen) Symptoms often have obvious tenderness or rebound tenderness in the upper abdomen), electrocardiogram and (or) serum enzymology to identify, it should be noted that patients with coronary heart disease often have cholelithiasis, when biliary colic attacks, easy to induce angina and Electrocardiogram changes in myocardial ischemia.

6. Esophagus rupture

Perforation or rupture of the esophagus can cause severe chest pain, often resulting in death, emergency surgery can reduce the mortality rate to 30%, 75% of esophageal rupture caused by instrument operation, in addition to foreign body or residual catheter, blunt injury Or puncture wound, gastric ulcer or esophageal cancer caused by oppressive necrosis, vomiting or vomiting after a full meal can also cause automatic esophageal rupture, the patient's pain is mostly under the xiphoid process and reflected to the interscapular region, often accompanied by breathing difficulties. Sweating and cyanosis, followed by pale, tachycardia and shock and signs of mediastinal gas (in the chest wall, neck and clavicle upper fossa). The atrial auscultation can be found in the mediastinum auscultation friction sound, the so-called Hamman sign.

The diagnosis of esophageal rupture is based on the symptoms and signs after vomiting or mechanical operation of the esophagus. Chest X-ray examination of the standing chest can reveal mediastinal gas and pleural effusion. The X-ray examination can confirm the location of the rupture. Sometimes the rupture can be closed and cannot be closed. It was found by X-ray that at this time, the extraction of acidic liquid by thoracentesis can indicate the esophageal rupture.

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