Hemorrhagic infarction: A reperfusion injury following prolonged myocardial ischemic anoxia.
Sixteen canine myocardial pedicle preparations were divided into four groups. Group I received 60 minutes of reversible ischemic anoxia, Group II 90 minutes, Group III 120 minutes, and Group IV 180 minutes. Transmural ischemic infarction was present in Group I. With longer periods of anoxia, capillary disruption occurred, first in the subendocardium (90 minutes) and then transmurally (180 minutes). Reperfusion after ischemic, anoxic time periods of 90 minutes or greater produced hemorrhagic necrosis, the extent of which was directly proportional to the duration of the preceding ischemic, anoxic period. One hundred and twenty patients with aortic valve replacement surgery then were analyzed retrospectively. Of the 25 deaths, seven were due to immediate postinfarction, five from subendocardial hemorrhagic necrosis. The common factor in the patients with hemorrhagic infarction was a markedly reduced coronary flow (45 to 55 ml. per minute) for more than 70 minutes during the interval of cardiopulmonary bypass. Although other factors may be involved, it is hypothesized that the main cause is a degree of localized ischemia of sufficient duration to induce capillary disruption and subsequent postbypass hemorrhagic necrosis when normal coronary artery perfusion is resumed.
D000818:Animals; D002196:Capillaries / Q000648:ultrastructure; D003326:Coronary Circulation; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006324:Heart Arrest, Induced / Q000009:adverse effects; D006349:Heart Valve Diseases / Q000601:surgery; D006470:Hemorrhage / Q000209:etiology*; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D007511:Ischemia / Q000503:physiopathology*; D008854:Microscopy, Electron; D009203:Myocardial Infarction / Q000209:etiology; D009206:Myocardium / Q000648:ultrastructure; D013997:Time Factors