title: Lactate release during reperfusion predicts low cardiac output syndrome after coronary bypass surgery.
abstract: BACKGROUND
  Cardioplegic arrest induces anaerobic myocardial metabolism with a net production of lactate from glycolysis. However, persistent lactate release during reperfusion suggests a delayed recovery of normal aerobic metabolism and may lead to depressed myocardial function necessitating inotropic or intraaortic balloon pump support (low output syndrome [LOS]). We examined the relation between perioperative myocardial metabolism and postoperative clinical outcomes in patients undergoing isolated coronary artery bypass surgery (CABG).
  
  
  METHODS
  We reviewed 623 patients who were enrolled in clinical studies evaluating perioperative myocardial metabolism between 1983 and 1996. Arterial and coronary sinus blood samples were obtained intraoperatively to assess myocardial metabolism. Clinical data regarding patient demographics and postoperative outcomes were prospectively collected and entered into our institutional database.
  
  
  RESULTS
  Low output syndrome developed in 36 patients (5.8%). Myocardial lactate release was higher in these patients compared with those who did not develop postoperative LOS. Advanced age and poor preoperative left ventricular function were independent predictors of lactate release during reperfusion. Persistent lactate release after 5 minutes of reperfusion was the only independent predictor of postoperative LOS in this low-risk population.
  
  
  CONCLUSIONS
  Persistent lactate release during reperfusion occurs in a significant proportion of low-risk patients undergoing isolated CABG and is an independent predictor of postoperative low cardiac output syndrome. Persistent lactate release during reperfusion suggests a delayed recovery of aerobic myocardial metabolism and may be related to intraoperative misadventure or inadequate myocardial protection. Myocardial lactate release may be useful as an alternative end-point in clinical trials evaluating perioperative myocardial protection.
authors: Department of Clinical Biochemistry, Toronto General Hospital, University of Toronto, Ontario, Canada.
authors: V
authors: V
authors: Rao
authors: J
authors: J
authors: Ivanov
authors: R D
authors: RD
authors: Weisel
authors: G
authors: G
authors: Cohen
authors: M A
authors: MA
authors: Borger
authors: D A
authors: DA
authors: Mickle
mesh_terms: D000368:Aged; D002303:Cardiac Output, Low / Q000097:blood / Q000175:diagnosis*; D001026:Coronary Artery Bypass; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D019344:Lactic Acid / Q000097:blood*; D008297:Male; D008875:Middle Aged; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000175:diagnosis*; D009206:Myocardium / Q000378:metabolism; D011183:Postoperative Complications / Q000097:blood / Q000175:diagnosis*; D011237:Predictive Value of Tests; D012189:Retrospective Studies
chemical_list: D007527:Isoenzymes; D019344:Lactic Acid; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form