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Syndrome after myocardial infarction (postinfarction syndrome), also known as Dressler syndrome, the occurrence rate of about 10%, and myocardial infarction occur within a few weeks to several months, can be repeated, showed pericarditis, pleurisy or pneumonia, fever, chest pain, leukocytosis and increased ESR and other symptoms, which may be the body's allergic reaction to necrotic material. 1 Over.1 PMIS is the definition of acute myocardial infarction appear a few days to several weeks to pericarditis, pleurisy, pneumonia and other non-specific inflammation characterized by a syndrome, and recurrent tendency, that is secondary to the concept of disease .1.2 Dressler 1895, the disease has been noted that such .1983 developed in Welinl diagnostic criteria for .1976 of this disease has been reported in China in the beginning. but also to Dressler syndrome syndrome and Welin L, referred to as the incidence of general accounting PMIS.PMIS AMI1% ~ 4%. most of them in 2 to 8 weeks after AMI, a small number of patients in the 1 Zhou Fasheng. occurrence of the disease and myocardial infarction seems no linear relationship between size, there is a tendency to recurrent, ranging from 1 to 7 .2 and dialectical relationship between disease patterns and because of unknown etiology and pathogenesis, so the model hard to know. but is a syndrome, it certainly is a complex PMIS .3 disease pathogenesis and etiology of the current PMIS not quite sure, but more inclined to myocardial infar


ction myocardial necrosis induced after the antigen-antibody reaction theory; and bacteria, viral infection, and adrenal glands - pituitary dysfunction perspective has yet to be excluded. From the information available can be determined PMIS is a myocardial infarction secondary to disease, on the basis that: in the heart infarction based on the emergence of the immune response, in accordance with their own evolution of the immune pathogenesis of myocardial infarction in a more scientific call their own after the immune response. similar to the pericardial incision surgery syndrome .3.1 immune complex theory of the immune response. AMI necrosis after cardiac tissue as an antigen, antigen stimulates the production of anti-myocardial antibodies, antigen-antibody complex formation. In the majority of AMI patients can detect antibodies or immune complexes. necrotic myocardium against myocardial antigen antibody and immune complex formation, with the flow deposition coated heart, pleura, alveolar walls of the capillary endothelial Department, and activate complement, generating biologically active substances, resulting in vascular injury, to increased vascular permeability, fluid leakage, and even rupture, causing pericarditis (fluid ), pleurisy (pleural effusion), pneumonia (aseptic inflammation) and other theories may change .3.2 virus infection is related to MI may also be related to the use of anticoagulants .4 weeks after clinical AMI1 appear fever, chest pain , pericarditis, pleurisy and pleural or pericardial effusion. ESR accelerated leukocytosis. or pericarditis, pleurisy, pneumonia, triple-based levy, or fever, chest pain, erythrocyte sedimentation rate acceleration and differential diagnosis focused .5 Diagnosis 5.1 Diagnostic criteria no uniform standard, the following reference .5.1.1 Welin L: 1983 more than 1 week after myocardial infarction following symptoms occur: pleural pericardial pain; fever above 37.5 ; 40mm / h. If the above two can be diagnosed as PMIS.5.1.2 Dressle: 1985 yes AMI or old myocardial infarction; in 1 ~ 2 weeks after AMI fever, chest pain, breathing difficulties, coughing and so on. with pleurisy, pericarditis , reliable evidence of pneumonia; anti-infective treatment fails, corticosteroids clearly .5.1.3 million Pap results: occurred in more than 1 week after AMI had pericardial friction rub, a clear sign of pericardial effusion, fever, chest pain, heart rate , pneumonia, pleurisy; antibiotic treatment ineffective, and good response to treatment of adrenal cortex hormones; the differential diagnosis of recurrent tendency .5.2 5.2.1 AMI pericarditis after the reaction: occurred transmural myocardial infarction in 24 to 72 hours; pericardial friction rub after more than 36 hours of chest pain occurred, limitations and short duration, an average of 2 days; a small amount of pericardial effusion, cardiac tamponade does not appear; not associated with pleurisy, pneumonia; EKG pericarditis without typical ST-T-like changes in non-specific pericarditis .6 .5.2.2 6.1 disable anticoagulant therapy such as heparin and other drugs of choice .6.2 steroids. began to give short-term prednisone 40 ~ 60mg / d, when the gradual reduction of remission, reduction week 5mg, up to 10 ~ 15mg / d for 4 weeks while maintaining, if not inclined to continue reduction of recurrence to weekly 5mg, for 2 months and then discontinued .6.3 pain aspirin, anti-inflammatory pain.


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