ABSTRACTHemorrhagic acute myocardial infarction (AMI) was studied after selective intracoronary thrombolysis (SICT) in 30 patients undergoing autopsy. Urokinase, 240,000 to 1,200,000 U, was selectively injected into the infarct-related coronary artery at 2 to 9 hr (4 2 hr) after the onset of AMI. The infarct-related coronary artery showed complete occlusion in 21, 99% stenosis in eight, and 90% stenosis in one patient before SICT. After SICT, complete occlusion was seen in only five, 99% stenosis in 22, and 90% stenosis in three patients. Twenty-eight patients had transmural infarction and the other two had subendocardial infarction. Macroscopically and microscopically, the degree of hemorrhage was classified as no, slight, moderate, or marked bleeding and the hemorrhagic infarction was defined as moderate or marked diffuse bleeding in the infarct area. According to the interval from SICT to death, patients were also classified into stage I (early acute stage, 1 to 4 hr after SICT and 4 to 13 hr after the onset of AMI; n = 7), stage IL (late acute stage, 9 hr to 1 1 days after SICT and 15 hr to 1 1 days after the onset of AMI; n = 18), or stage 111 (old infarction stage, over 17 days after AMI and SICT; n = 5). There were no significant differences with respect to the frequency of recanalization, the time from the onset of AMI to SICT, the dose of urokinase, or other clinical parameters among patients at the three stages. Only the hearts of patients in stage LI showed hemorrhagic infarction, and it was found in 15 of 18 of these hearts. Marked diffuse hemorrhage was noted in six hearts, all of which showed recanalization after SICT. However, even in three patients in stage II without recanalization after SICT, moderate diffuse bleeding was evident. In all hearts, the hemorrhagic area was mostly localized within the infarct area. Thus, in most of the patients with AMI treated with SICT, hemorrhage increases gradually after SICT, becomes moderately or markedly diffuse after 4 hr, and is replaced by fibrosis after 3 to 4 weeks. The hemorrhagic infarction is due to the combined effects of reperfusion and large doses of urokinase. The time delay of bleeding seems to depend on the low perfusion pressure in the portion distal to the stenosed, infarct-related coronary artery. It is unlikely that hemorrhage expands the infarct area.