[Acute myocardial infarction and documented sudden death].

coloring. His blood pressure was 160/100 mmHg, and his heart rate was 90 bpm. His heart rhythm was regular with frequent extrasystoles, and no murmurs could be heard in the carotid arteries. No abnormalities were observed in the remaining physical examination. The patient received 200 mg of ground acetylsalicylic acid, sublingually, and oxygen. Venous access was obtained and continuous electrocardiographic monitoring was installed. Sublingual nitrate provided complete pain relief. The 12-lead electrocardiographic tracings performed before and after nitrate administration, as well as its serial 12-hour recording, showed sinus rhythm with total right bundle-branch block, alteration in the ventricular repolarization of the inferior wall, ventricular extrasystoles, and no dynamic alterations in the ST segment. The levels of myocardial injury markers (troponin-T) were normal. After 24 hours, exercise testing was performed, but no alteration suggesting myocardial ischemia was evidenced. The echocardiogram showed no ventricular dysfunction, and serology for Chagas’ disease was negative. Continuous electrocardiographic 24-h Holter monitoring was performed, because of the complaint of lipothymia. In the 20th hour of Holter monitoring, the patient evolved to witnessed sudden death, immediately received resuscitation measures, but without success. The electrocardiographic recordings showed elevation of the ST segment in the CM5 and D2M leads, which was asymptomatic for 15 minutes, being then followed by complex ventricular arrhythmias that degenerated to ventricular fibrillation refractory to the cardiopulmonary-cerebral resuscitation maneuvers (figs. 1, 2 ,3 , 4, and 5).