Circulation, Vol 54, 187-193, Copyright © 1976 by American Heart Association
SA Ahmed, JR Williamson, R Roberts, RE Clark and BE Sobel
To evaluate the concordance between elevated plasma MB CPK and irreversible
myocardial ischemic injury, coronary occlusion was induced for 10 minutes
to 48 hours in 21 open chest dogs and 13 conscious animals. Results of
plasma CPK and MB CPK assayed in samples obtained serially ofr 24 hours
were compared to microscopic changes in hearts from the same animals
examined 48 hours after occlusion. Twelve of the 34 dogs died within two
hours after coronary occlusion. Among the surviving 22 dogs, one failed to
exhibit gross of electrocardiographic evidence of ischemia and was
therefore excluded. Twelve had coronary occlusion maintained for 30 minutes
or longer and in 11 of these peak plasma MB CPK activity exceeded thenormal
range (mean +/- 2 SD) and baseline values by at least 100%. Necrosis was
present in the hearts from each manifested by nuclear pyknosis,
eosinophilia, shrinkage of cytoplasm, and leukocytic infiltration. In the
remaining nine dogs with occlusion for less than 30 minutes, peak plasma MB
CPK activity was not elevated and necrosis was not detected. The close
concordance between plasma MB CPK elevations and myocardial necrosis was
significant (chi2 = 14.5, P less than 0.001), and thus, increased plasma MB
CPK activity reflected irreversible myocardial ischemic injury.
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