Four patients developed an acute respiratory distress syndrome characterised by clinical and radiological signs of pulmonary oedema, a protein-rich oedema, severe hypoxemia refractory to oxygen therapy, contrasting with normal left ventricular filling pressures and indicating increased permeability of the alveolo-capillary membrane, 24 to 72 hours after the onset of acute myocardial infarction. After having excluded the usual causes of the acute respiratory distress syndrome, the authors suggest that acute myocardial infarction, especially when extensive, may cause a lesion of the alveolo-capillary membrane by an unknown mechanism. Treatment consisted in mechanical ventilation with positive expiratory pressures in 3 cases and with continuous positive pressure during spontaneous respiration in the third patient and in relay with controlled ventilation in the other two. These techniques of ventilation improved the hypoxemia and led to complete cure in all cases without evolution to pulmonary fibrosis. In addition to mechanical ventilation, all patients were given systematic antibiotic therapy because of the possibility of an infectious etiology while waiting for the results of microbiological and serological testing and because of the high risk of superinfection which plays an essential part in the outcome of the condition. The immediate response to treatment was favourable in all cases. One patient died suddenly of cardiogenic shock two weeks after this episode. The other patients are still alive 39, 38 and 20 months after infarction. The importance of the diagnosis of the acute respiratory distress syndrome in the acute phase of myocardial infarction resides in its therapeutic implications which are quite different to those of cardiogenic shock.(ABSTRACT TRUNCATED AT 250 WORDS)