Liver damage as a potential source of error in the estimation of myocardial infarct size from plasma creatine kinase activity.
The occurrence of liver damage was investigated in patients with uncomplicated acute myocardial infarction (AMI). Cumulative plasma release of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) was compared with release of alanine aminotransferase (ALT). Up to 48 h after AMI, the appearance of ALT could be fully explained by myocardial ALT release. Thereafter additional release of ALT occurred, indicating liver damage. A possible effect of liver function on the rate of elimination of CK from plasma was studied in the dog. Complete temporary arrest of hepatic blood supply was obtained after previous implantation of a portacaval shunt, ligation of secondary inflows and blockade of retrograde perfusion. Neither these preliminary haemodynamic interventions nor the acute arrest of hepatic blood flow had any effect on the disappearance rate of CK from plasma. It is concluded that some liver damage commonly occurs in patients after AMI. However, this phenomenon does not interfere with the estimation of infarct size because the elimination of CK from plasma is unaltered during total hepatic ischaemia.
D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D003402:Creatine Kinase / Q000097:blood*; D004285:Dogs; D005260:Female; D006801:Humans; D006884:Hydroxybutyrate Dehydrogenase / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000503:physiopathology; D008107:Liver Diseases / Q000201:enzymology / Q000209:etiology*; D008297:Male; D009203:Myocardial Infarction / Q000150:complications* / Q000201:enzymology / Q000473:pathology
C035749:2-hydroxybutyrate dehydrogenase; D006884:Hydroxybutyrate Dehydrogenase; D000410:Alanine Transaminase; D003402:Creatine Kinase