Pericardial involvement in acute myocardial infarction

The incidence of both early postinfarction pericarditis and post-myocardial infarction (Dressler's syndrome) appears to be declining. Pericardial pain and pericardial friction rub define early postinfarction pericarditis and usually develop on day 2 or 3 after a transmural myocardial infarction. The clinical course is benign, and the prognosis of the patient is not altered by development of this complication. Pericardial effusions have been found in as many as 28% of patients after acute MI. Asymptomatic pericardial effusions do not require specific therapy nor do they absolutely contraindicate the use of anticoagulation as was previously thought. The preferred form of therapy for early postinfarction pericarditis is aspirin. Avoidance of corticosteroids and NSAIDs must be considered carefully because of the reported complications of these agents. The post-myocardial infarction syndrome develops usually during the second or third week after acute MI but may be seen as early as 24 hours and as late as several months after the MI. Whether this syndrome is the result of autosensitization to myocardial antigens released into the circulation during infarction remains uncertain. Alternative hypotheses for the causation of the syndrome include the release of blood in the pericardial space and simply that the syndrome represents a prolonged and exaggerated form of early postinfarction pericarditis. Clinically, post-myocardial infarction syndrome is manifested by fever, malaise, chest pain, and the presence of a pericardial and possibly pleuropericardial friction rub. Pericardial effusion is frequently large, and, rarely, cardiac tamponade may develop and require pericardiocentesis. Treatment consists of aspirin, NSAIDs, or corticosteroids.(ABSTRACT TRUNCATED AT 250 WORDS)