Determinants of myocardial hemorrhage after coronary reperfusion in the anesthetized dog.

Abstract

SUMMARY Intramyocardial hemorrhage often occurs with reperfusion in experimental acute myocardial infarction and is thought to be associated with extension of necrosis. To determine if hemorrhage was associated with extension of necrosis, 20 anesthetized dogs were reperfused after 6 hours of circumflex coronary artery occlusion and 10 others had control occlusion with no reperfusion. Fifteen of the 20 reperfused dogs had gross hemorrhage and none of the control dogs did. In 12 reperfused and 10 control dogs, radioactive microspheres were injected after coronary occlusion to quantitate collateral flow and in the reperfusion group microspheres were injected to quantitate reflow. Complete flow data were available in eight reperfused and 10 control dogs. Twenty-four hours after coronary occlusion, 1-g segments of infarct and control regions were analyzed for hemorrhage, collateral flow and creatine kinase activity. Serial microscopic examination was performed in eight additional dogs reperfused after 6 hours to determine if hemorrhage occurs into otherwise microscopically normal myocardium.Pathologic examination indicated that hemorrhage did not occur into otherwise microscopically normal myocardium. In dogs with hemorrhage, the extent of hemorrhage was inversely related to myocardial creatine kinase concentration and collateral flow. Mean collateral flow in 47 hemorrhagic segments was 4.5 ml/100 g (4.2% of control). Mean creatine kinase in 36 hemorrhagic segments was 233 mIU/g (21% of control). No hemorrhage was found in areas with collateral flow more than 21% of control or creatine kinase more than 37% of control. Mean reflow in hemorrhagic segments was 78.5% of control flow. These studies indicate that hemorrhage on reperfusion is associated with severe myocardial necrosis and markedly depressed flow before reperfusion and thus occurs only into myocardium already markedly compromised at the time of reperfusion. There is no evidence for hemorrhage into areas that had normal or even moderately depressed flows before reperfusion.THE BENEFITS of reperfusion after acute coronary occlusion are controversial. Extent of infarction is an important determinant of prognosis after coronary occlusion,' and restitution of flow would appear to provide an effective means of rectifying ischemia and thus limiting infarct size. Jennings et al.2 demonstrated that reperfusion after 20 minutes of occlusion prevented the development of ischemic injury, while other studies using enzyme analysis, histologic examination and functional assessment have shown limitation of infarct size with reperfusion 3 hours after coronary occlusion.'-" Other studies have not substantiated significant improvement after reperfusion. Bresnahan et al.6 demonstrated an increase in infarct size in seven of 16 dogs reperfused 5 hours after coronary occlusion. Other investigators have reported ventricular dysrhythmias7 accelerated morphologic changes of ischemia8 and exacerbation of functional'0 and metabolic measurements of ischemia.9The deleterious consequence...

Temporal Evolution of Myocardial Hemorrhage and Edema in Patients After Acute ST‐Segment Elevation Myocardial Infarction: Pathophysiological Insights and Clinical Implications

“…Myocardial hemorrhage reflects the aggregation and extravasation of erythrocytes4, 20, 45 and is a manifestation of severe microvascular injury. On CMR at day 3, 5 patients without evidence of hemorrhage on T2* imaging had hypointense cores on T2 maps and microvascular obstruction on contrast imaging.…”

The Coronary Circulation as a Target of Cardioprotection

“…Hemorrhage is associated with severe ischemia during coronary occlusion and with severe myocardial necrosis. 117,118 Hemorrhage in reperfused myocardial infarction has received more attention by MRI because the hemoglobin catabolites are paramagnetic and attenuate the T 2 -weighted signal intensity within an otherwise high T 2 -weighted signal area (edema). [119][120][121][122] No-reflow is seen in ≈35% of patients with optimal reperfusion therapy, and its incidence increases with the delay of reperfusion.…”

Acute myocardial infarct extension into a previously preserved subendocardial region at risk in dogs and patients.

“…Recurrence of infarction is frequent in patients with SEMI and has been recently reported to occur at the same site as the initial infarct in 86% of cases by Marmor et al 23 26 Because vascular tissue is more resistant to ischemic injury than myocardium,27 the hemorrhagic necrosis is considered to occur in regions that are predestined, at the time of reperfusion, to show signs of infarction at subsequent histologic examination. Significant hemorrhage was only observed in myocardium in which the blood flow had been reduced to less than 15% of control.…”

“…Significant hemorrhage was only observed in myocardium in which the blood flow had been reduced to less than 15% of control. 26 Recognition of infarct extension from specimens stained with hematoxylin-eosin may underestimate the incidence of infarct extension. For infarct extension to be recognized from human postmortem material, not only must the infarct and its extension be separated by several days, but death must also occur within days of the infarct extension.…”