Pericarditis after myocardial infarction

Introduction to pericarditis after myocardial infarction Pericarditis after acute myocardial infarction is divided into three types: early pericarditis, Dressler syndrome, and ventricular free wall rupture. The clinical manifestations are pain in the precordial area and pericardial friction. The pericarditis that occurs early is self-limiting, and the prognosis is good. Symptomatic treatment with non-steroidal anti-inflammatory drugs can be used. Dressler syndrome is an autoimmune response of the body to necrotic myocardial tissue and usually requires short-term use of steroids. The prognosis of patients with ruptured ventricular free wall is extremely poor. basic knowledge The proportion of sickness: 0.01% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute myocardial infarction

Causes of pericarditis after myocardial infarction

(1) Causes of the disease

Acute myocardial infarction involves occasional extensive fibrous pericardial inflammation involving the pericardium. Dressler syndrome is an autoimmune response of the body to necrotic myocardial tissue.

(two) pathogenesis

1. Pericarditis after myocardial infarction is an occasional extensive fibrous pericarditis due to the limitation of acute myocardial infarction involving the pericardium.

2. The mechanism of Dressler syndrome is not completely clear, it may be an autoimmune response of the body to necrotic myocardial tissue, because anti-myocardial antibodies can be detected in the blood of patients with Dressler syndrome; or blood infiltration into the pericardial cavity caused by myocardial infarction Epicardial delayed immune response; may also be due to myocardial infarction trauma to activate static or potential virus in the heart, the pericardium of Dressler syndrome is non-specific inflammatory changes, fibrin deposition, and early pericarditis in early infarction, early pericarditis The pericardial inflammatory changes only cover the local extent of the infarct, and the pathological changes of Dressler syndrome are diffuse.

Prevention of pericarditis after myocardial infarction

Coronary heart disease is a disease that is affected by many factors and is the main cause of human death. It is of great significance for the prevention of coronary heart disease. The fundamental measure to prevent pericarditis after acute myocardial infarction is to prevent the occurrence of coronary heart disease, coronary heart disease. Prevention is divided into primary prevention and secondary prevention.

Primary prevention

It mainly consists of two parts:

1 Health education for the entire population, to avoid and change bad habits, maintain psychological balance, reduce the incidence of coronary heart disease.

2 control risk factors for the disease: for high-risk groups of coronary heart disease, such as high blood pressure, high blood fat, obesity, diabetes, smoking and family history, etc., the treatment methods include: drugs control blood pressure, correct abnormal lipid metabolism , quit smoking and alcohol, appropriate physical activity, weight control, control of diabetes and other risk factors.

2. Secondary prevention

Prevention of recurrence of coronary heart disease and exacerbation of the disease, the use of effective drugs such as: anti-platelet drugs, statins, small doses of aspirin.

Complications of pericarditis after myocardial infarction Complications acute myocardial infarction

Post-myocardial infarction may have complications such as cardiac tamponade, and more common acute myocardial infarctic pericarditis.

Myocardial symptoms after myocardial infarction Common symptoms Angina pectoris Myocardial infarction Dull pain Pleural friction Chest pain Pericarditis Pericardial effusion

Pericarditis after myocardial infarction can take two forms, one is acute myocardial infarction, especially the acute pericardial inflammation often accompanied by invasive wall infarction, called postmyocardial infarction pericarditis (postmyocardial infarction pericarditis), 2h after infarction 5 days, usually appear within 10 days, the main clinical manifestations of pericardial pain and pericardial friction sounds, pericardial friction sounds previously reported as 20%, but if repeated cardiac auscultation, the incidence can reach 2 / 3 or more, the amount of pericardial effusion is often very small; but in thrombolytic or anticoagulant therapy, pericardial effusion can be large or bloody, and even cardiac tamponade, need to puncture and discharge, the lesion is infarcted necrotic area The submucosal inflammatory response, which affects the adjacent pericardium, is a localized fibrinous pericarditis. The disease is self-limiting and can usually be controlled by analgesics or non-steroidal anti-inflammatory drugs.

Examination of pericarditis after myocardial infarction

1. Blood tests for leukocytosis.

2. ESR increases.

3. Anti-myocardial antibodies can be detected in the blood.

4. There may be an increase in serum enzymology of the primary disease of acute myocardial infarction.

5. X-ray heart enlargement, unilateral (usually left) or bilateral pleural effusion, sometimes visible in the lungs.

6. Echocardiography pericardial effusion, a small amount of pericardial effusion occurred in about 4/1 patients after myocardial infarction.

7. ECG has a ST-T change in the original myocardial infarction. Some patients have typical ST-T changes in acute pericarditis. Acute myocardial infarctic pericarditis often does not have extensive ST-segment elevation unless the inflammation is diffuse.

Diagnosis and diagnosis of pericarditis after myocardial infarction

Diagnostic criteria

1. Acute myocardial infarction pericarditis occurs more than 1 week after acute myocardial infarction, with pericardial pain and pericardial friction sounds of pericardial inflammation, the amount of pericardial effusion is often very small, the disease is self-limiting, generally with painkillers or Non-steroidal anti-inflammatory drugs can control symptoms.

2.Dressler syndrome after acute myocardial infarction within a few weeks to several months after occasional onset, recurrent, acute onset, common symptoms are fever, general malaise, precordial pain and chest pain, the nature and extent of pain sometimes It is easy to be misdiagnosed and re-infarction angina pectoris, pericardial effusion is small to moderate, a large number of pericardial effusion cardiac tamponade is rare, anti-myocardial antibody is positive, no re-infarction ECG changes, CPK-MB no significant increase can be identified with reinfarction.

Differential diagnosis

The clinical manifestations should be differentiated from early pericarditis in acute myocardial infarction, myocardial infarction extension and post-infarction angina pectoris and long-term anticoagulant therapy after myocardial infarction.

1. Early myocardial infarction occurs more than 1 week after infarction, often anterior wall and extensive anterior wall myocardial infarction, extended to the epicardium to cause localized pericarditis, acute periventricular myocardial infarction 48h can hear pericardial friction sound , lasting 2 to 3 days, more than 3 days suggest a poor prognosis.

2. Myocardial infarction extension or reinfarction (Dressler syndrome) 1 has a characteristic "pericardial pain", related to breathing, body position, no response to nitroglycerin treatment; 2 no new Q wave appeared in ECG; 3CK-MB did not increase significantly, Sometimes pericardial inflammation infiltrates the subepicardial myocardium, causing a slight increase in CK-MB.

3. Long-term anticoagulant therapy after myocardial infarction secondary to bloody pericardial effusion X-ray chest radiograph found in pericardial effusion, lung infiltrative shadow, a small number of patients with hemoptysis, but also need to be differentiated from pneumonia and pulmonary infarction.

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