Myocardial infarct extension during reperfusion after coronary artery occlusion: Pathologic evidence

Objectives. The goal of this study was to demonstrate myocardial infarct extension during reperfusion within the same animal. Background. Whether myocardial reperfusion can result in the extension of myocardial necrosis remains controversial. The transformation of reversibly injured myocytes into ir...

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Bibliographic Details
Published in:Journal of the American College of Cardiology 1993-04, Vol.21 (5), p.1245-1253
Main Authors: Farb, Andrew, Kolodgie, Frank D., Jenkins, Marie, Virmani, Renu
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiology. Vascular system
Constriction
Coronary heart disease
Coronary Vessels
Heart
Horseradish Peroxidase
Male
Medical sciences
Microscopy, Electron
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Myocardial Reperfusion Injury - pathology
Myocardial Reperfusion Injury - physiopathology
Myocardium - cytology
Myocardium - pathology
Myocardium - ultrastructure
Necrosis
Rabbits
Time Factors
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Summary:Objectives. The goal of this study was to demonstrate myocardial infarct extension during reperfusion within the same animal. Background. Whether myocardial reperfusion can result in the extension of myocardial necrosis remains controversial. The transformation of reversibly injured myocytes into irreversibly damaged cells after reperfusion has been difficult to demonstrate pathologically. Methods. New Zealand White rabbits (Group I, n = 10) were subjected to 30 min of coronary artery occlusion and 180 min of reperfusion. Horseradish peroxidase, a tracer protein that permeates the sarcolemma of irreversibly injured myocytes, was used to quantitate myocyte necrosis at the beginning of reperfusion. Within the same heart, infarct size was measured after 180 min of reperfusion by triphenyttetrazolium chloride (TTC) staining. In separate experiments to demonstrate the validity of the model, rabbits were subjected to 30 min of coronary occlusion, followed by intravenous infusion of horseradish peroxidase and rapid induction of death (Group II) or 30 min of occlusion, 180 min of reperfusion with horseradish peroxidase administered after 180 min of reperfusion and TTC staining after induced death (Group III). Results. In Group I, infarct size at the onset of reperfusion, delineated by horseradish peroxidase, measured 45.3 ± 2.8% of the area of risk and was significantly less than TTC-delineated infarct size after 189 min of re perfusion (59.8 ± 33%, p = 0.0002). By electron microscopy, border areas within the ischemic bed demonstrated irreversibly injured horseradish peroxidasepositive myocytes adjacent to irreversibly injured horseradish peroxidase-negative myocytes, suggesting that farther cell death occurred during reperfusion. In Group II, infarcts delineated by horseradish peroxidase after 30 min of coronary occlusion were similar in size to infarcts measured by this tracer in Group I. In Group III, infarcts delineated by horseradish peroxidase at 180 min of reperfusion were similar in size to infarcts measured by TTC and similar to TTC-delineated infarcts measured at 180 min of reperfusion in Group I. Conclusions. These results provide evidence that there is a subset of myocytes in border areas within the ischemic region that are viable at the beginning of reperfusion but subsequently progress to irreversible injury during the reperfusion period.
ISSN:0735-1097
1558-3597
DOI:10.1016/0735-1097(93)90253-W