CARDIAC MORPHOLOGIC FINDINGS IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION TREATED WITH RECOMBINANT TISSUE PLASMINOGEN-ACTIVATOR

The hearts of 52 patients (aged 61 ± 11 years, 34 men) who participated in the Thrombolysis in Myocardial Infarction (TIMI) Study and died from 5 hours to 260 days (median 2.7 days) after onset of chest pain were studied. One heart became available at cardiac transplantation. Of the 52 patients, 38 received recombinant tissue plasminogen activator (rt-PA) not followed by percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). Eight had PTCA, and 6 had CABG. The infarcts were hemorrhagic by gross inspection (with histologic confirmation) in 23 patients, nonhemorrhagic in 20, not visible grossly in 2 and, in 7, there was no myocardial necrosis by either gross or histologic examination. Comparisons between the 23 patients with hemorrhagic infarcts and the 20 patients with nonhemorrhagic infarcts showed: (1) similar frequencies of myocardial rupture (left ventricular free wall or ventricular septum) [6 (26%) of 23 vs 5 (25%) of 20], cardiogenic shock [10 (43%) of 23 vs 9 (47%) of 19], and fatal hemorrhage [2 (9%) of 23 vs 2 (10%) of 20]; (2) similar percents of necrotic portions of left ventricular wall among patients surviving >18 hours from onset of chest pain (26 ± 11 vs 23 ± 11%) with the hemorrhage confined to areas of necrotic myocardium in all cases; (3) similar frequencies of thrombi in the infant-related arteries [7 (32%) vs 7 (37%)], but all thrombi in patients with hemorrhagic infarcts were nonocclusive, and all thrombi in those with nonhemorrhagic infarcts were occlusive (p = 0.0002); (4) similar degrees of luminal cross-sectional area narrowing over all 5-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries in 27 patients receiving rt-PA alone between patients with hemorrhagic and nonhemorrhagic infarcts; (5) similar numbers of patients in whom the infarct-related artery was narrowed >75% in cross-sectional area at some point by plaque [21 (95%) of 22 vs 16 (84%) of 19], and similar mean percent reduction in crosssectional area by plaque of the infarct-related arteries calculated by planimetry (67 ± 10 vs 68 ± 9%); (6) similar frequencies of plaque rupture [11 (55%) of 20 vs 12 (75%) of 16] and similar frequencies of hemorrhage into a plaque [13 (65%) of 20 vs 13 (81%) of 16] in patients without PTCA; (7) fewer right ventricular infarcts in patients with hemorrhagkic infarcts (2 of 10 posterior hemorrhagic infarcts vs 6 of 9 posterior nonhemorrhagic infarcts); (8) similar percents of plaque with pultaceous debris (13 ± 11 vs 18 ± 9%), calcific deposits (14 ± 12 vs 20 ± 14%) and acellular fibrous tissue (49 ± 14 vs 53 ± 11%). Thus, hemorrhage occurs frequently in the infarcts of patients who receive rt-PA. Hemorrhage into an infarct does not appear to extend the infarct, and patients with hemorrhagic (vs nonhemorrhagic) infarcts have no greater frequency of myocardial rupture or cardiogenic shock, and no significant differences in coronary luminal narrowing, plaque rupture or plaque composition. However, those with hemorrhagic infarcts had only nonocclusive thrombi and fewer right ventricular infarcts. © 1990.