Abstract
Dressler described the cases having body temperature elevation and chest pain, which developed following acute myocardial infarction, accompanied with pericarditis, pleuritis, pneumonia, acceleration of erythrocyte sedimentation rate, leucocytosis, eosinophilia, etc.and named this condition as postmyocardial infarction syndrome (PMIS).Tendency of recurrence of these symptoms were also noted by Dressler and he suggested that autoimmune mechanism might be responsible for these manifestations.Although several reports have been published since that time, its clinical features are not always clear yet and laboratory examinations have not been carried out in detail.Its pathogenesis is not elucidated sufficiently.
The purpose of the present study is to investigate the clinical features of PMIS, using 30 cases.The laboratory studies showed the exudative or bloody pleural fluid in all cases in which fluid was taken by pleuroparacentesis.Leucocytosis more than 10, 000 was found in 10 cases and acceleration of erythrocyte sedimentation rate in 19.CRP titer was significantly higher in PMIS than usual congestive heart failure.These findings indicate that PMIS is of inflammatory nature.
In addition, eosinophilia more than 6% was observed in 16 cases (53.3%).Its count was varied in parallel with increase or decrease of pericardial and pleural effusion and other clinical as well as laboratory findings.Immunoserological studies revealed the significantly higher antibody titer to the intact and infarcted human heart muscle antigens in patients with PMIS than ordinary myocardial infarction without PMIS.At postmortem examination of two cases, histology of myocardium was observed not contradictory to autoimmune disease.These findings suggest the pathogenesis of the PMIS can be ascribed to the autoimmune mechanisms.
PMIS was observed in 3.9% of myocardial infarction.In about a half of the cases, PMIS developed from 2 to 6 weeks after the onset of acute myocardial infarction.Pericarditis, pleuritis and pneumonia were found in 29 cases (96.3%), 25 cases (83.3%) and 6 cases (20.0%), respectively.Recurrence of pericarditis was noted in 13 cases and that of pleuritis in 12. Steroids were effective in all cases in which they were employed, but some cases were observed to improve by use of antibiotics and/or diuretics without steroids.
Key words: myocardial infarction, autoimmune mechanism, pericarditis, pleuritis, eosinophilia
