In 1956, Dressler (3) described a hitherto unreported syndrome arising as a sequel or complication of myocardial infarction. Many of these cases formerly had been considered examples of pulmonary infarction, recurrent myocardial infarction, or extension of myocardial infarction (2, 4). Although proof is not available, it is believed that the Dressier syndrome is an expression of an autoimmune reaction (5, 14) and is similar to or identical with the group of post-cardiotomy syndromes (14), the traumatic pericarditis syndrome (12, 16), and the idiopathic benign pericarditis syndrome (8, 9). More than 100 cases of the post-myocardial infarction syndrome have been available for clinical studies at Maimonides Hospital, and of this group 52 have had adequate radiographic examinations. In many instances, the roentgen examination has supported or corroborated the clinical impression of the syndrome, and at other times it has suggested the diagnosis when it was not under clinical consideration. The purpose of this report is to present the roentgen findings in these 52 patients with the Dressier syndrome, and at the same time summarize its pertinent clinical elements. General Considerations The essential elements of the syndrome, pericarditis, pleuritis, and pneumonitis, are usually present in combination, but each may occur as a sole manifestation. The illness may be ushered in within a few days of the onset of the myocardial infarction or may be delayed as long as eight weeks. Pain of the pleuropericardial type is typical, together with low-grade fever, leukocytosis, and elevation of the sedimentation rate. A pericardial friction rub is found in about 80 per cent of the cases and is more persistent than the transient rub of pericarditis epistenocardiaca. The tendency toward relapse is a conspicuous feature of the syndrome, and there may be as many as six episodes, each lasting from one to six weeks (2, 7, 9, 10, 15). The prognosis is usually excellent, and the illness pursues a benign course. Even when the symptomatology is severe, dramatic improvement can be expected with the institution of steroid therapy (5, 6). In rare instances, however, there may be severe intensification of the disease process and death (8, 11, 14). Postmortem examinations were obtained in three of these patients: in two during the course of the post-myocardial infarction syndrome and in the third one year subsequent to the initiating infarct and in the course of a second infarct. In the first two cases, there were 700 and 380 ml of hemorrhagic pericardial fluid, respectively, and the visceral and parietal pericardia appeared shaggy and covered with thick granular fibrinous tissue. The infarcts in one case were in the posteroseptal myocardium and in the other in the anteroseptal wall. They were three to five weeks old.