Introduction: Acute myocardial infarction represents one of the most common cardiovascular diseases and includes different mechanisms. Rapid integration of all datas and the correct classification of the coronary event is a not always easy to achieve priority.

Methods: A 70 yo man, smoker, alcohol consumer, presents with intense, diffuse abdominal pain and vo-miting. The clinical examination and the EKG are wi-thout notable particularities. Biologically, he presents severe lactic metabolic acidosis and renal impairement. The multidisciplinary aproach decides the necessity of an abdominal computer tomography which descri-bes a small anterolateral pneumothorax onlyThe pati-ent is admissed in the intensive care unit. Few hours later, he accuses abrupt restrosternal pain, despite the seemingly biological improvement. It is noticed ante-rolateral ST segment elevation, positive troponin and severe systolic dysfunction (35%) with hypokinezia of the LAD territory walls. An urgent coronarography is performed which describes two LAD significant, non-ulcerative stenosis. Two pharmacological stents are be-eing inserted. After the angioplasty, the pacient impro-ves. Shortly, he accuses intense right hypochondrium pain and severe dyspnoea. He has now tachycardia and hypotension, but no fever and no changes in electrical or echocardiographic aspect.

Results: He is programmed for thoracal tomography but until then, the patient develop cardiac arrest from asystole. He is promptly resuscitated but with the ne-cessity of orotracheal intubation. The tomography re-veals massive right hydropneumothorax because of an eso-pleural fissure. Purulent pleural fluid is drained. Subsequent, multiple superior digestive endoscopies are beeing performed in order to stent the clivage. The evolution is towards sepis and the pacient dies two months later.

Discussions: The patient is initially treated as a type I myocardial infarction complicated to severe systolic dysfunction. The heart failure is incriminated for the postangioplasty worsening. The tomography noti-ce the massive right hydropenumothorax and so, the perspective changes. A type II myocardial infarction is nominated. The conclusion is that an alcohol consumer man develops an eso-pleural fissure because of an old esophagitis. The intrapleural fluid gets infected and the consecutive severe metabolic changes lead to a myo-cardial infarction, although the patient associates athe-rosclerotic stenosis as well. The absence of fever and the leukopenia represent particularities of the case.

Conclusions: There are differences between the mana-gement of a type I and a type II myocardial infarction. An early, complete diagnosis by integrating all the dates improve the prognosis of these patients.