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Of 519 coronary-prone middle-aged men participating in the Chicago Coronary Prevention Evaluation Program, 416 reported their self-perceived state as one of no tension or tension at various periodic visits over years in the Program. Group mean serum cholesterol was significantly higher by about 4 mg/dl with tension vs. no tension (slight, moderate, or marked). This relationship was independent of weight change, intercurrent infection, use of medication, and month of year.

Given the very high proportion of deaths that occur too rapidly to bring a physician to the scene or to hospitalize the patient, the only hope for mastering the coronary disease epidemic is primary prevention. Use of existing knowledge to alter the major risk factors before an attack occurs could reduce the premature coronary death toll by 30%. This has already been demonstrated in several pilot studies.

The hearts of 52 patients (aged 61 f 11 years, 34 men) who participated in the Yhrombolysis in Myocardial Infarction (YIMI) Study and dii from 5 hours to 260 days (mediin 2.7 days) after onset of chest pain were studfed. Gne heart became available at cardiac transplantatkn. Gf the 52 patients, 36 received recombinant tissue plasminogen activator @t-PA) not followed by percutaneous transluminal coronary angioplasty (PICA) or coronary artery bypass grafting (CABG). Eight had PYCA, and 6 had CABG. Yhe infarcts were hemorrhagic by gross inspectkn (with histologic confbmatii) in 23 patients, nonhemorrhagic in 20, not vktble 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 ventrkuiar free wall or ventricular septum) [6 (26%) of 23 vs 5 (29%) of 201, cardiogenic shoch [lo (43%) of 23 vs 9 (47%) of 191, and fatal hemorrhage [2 (9%) of 23 vs 2 (10%) of 201; (2) similar percents of necrotic portions of left ventricular wall among patients surviving >18 hours from onset of chest pain (26 f 11 vs 23 f 11 o/o) with the hemorrhage confined to areas of necrotic myocardium in all cases; (3) similar frequencies of thrombi in the infarct-related arteries [7 (32%) VI 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 S-mm segments of the 4 majer (left main, left anterior descending, left circumflex and right) epicardial coronary arteries in 27 patients receiving rt-PA alone between patients with hemorrhagk and nonhemorrhagk infarctsf (5) similar numbers of patients in whom the infarct-related artery was narrowed >75% in cross-sectional area at some point by plaw [21(95%) of 22 vs 16 (64%) of 191, and similar mean percent reduction in crosssectional area by plaque of the infarct-related arteries cakulated by planimetry (67 f 10 vs 99 f 9%); (6) similar frequencies of plaque rupture [ 11 (55%) of 20 vs 12 (75%) of 161 and similar frequencies of hemorrhage into a plaque [13 (6S%) of 20 vs 13 (81%) of 163 in patients without PTCA; (7) fewer right ventricular infarcts in patients with hemotrhagk infarcts (2 of 10 posterior hemorrhagic infarcts VI 6 of 9 posterior nonhemorrhagic infarcts); (8) stmilar percents of plaque with pultaceousdebris(13~ llvsl8f9%), cakificdeposits (14 f 12 vs 20 f 14%) and acellular fibrous tissue (49 f 14 vs 53 l 11%). Thus, hemorrhage eccurs frequently in the infarcts of patients who receive &PA. Hemorrhage into an infarct does not appear to extend the infarct, and patients with hemorrhagii (vs nenhemorrhagic) infarcts have no greater frequency of myocardial rupture or cardiogenk shock, and no signifkant differences in coronary luminal narrowing, plaque rupture or plaque composition. However, those with hemorrhagic infarcts had only nonoccksive thrombi and fewer right ventriilar infarcts. (Am J Cardioi 1990-953~961)