title: Reduced myocardial cellular damage and lipid peroxidation in off-pump versus conventional coronary artery bypass grafting.
abstract: BACKGROUND
  The development of new surgical devices and techniques allows off pump coronary artery bypass grafting (OPCAB) without the use of CPB and cardioplegia. This study tested whether OPCAB reduces myocardial cell damage, lipid peroxidation and systemic endothelin release when compared to conventional coronary artery bypass grafting.
  
  
  METHODS
  Twenty-six patients were assigned to either the OPCAB procedure using a suction device and regular sternotomy (n = 13) or were treated conventionally using extracorporeal circulation, blood cardioplegia and hypothermic arrest (29-31 degrees C; n = 13). Troponin I and creatine kinase - MB were determined for cardiac specific cell damage. Myocardial and systemic malondialdhyde levels were measured to account for oxyradical mediated lipid peroxidation. Systemic big-endothelin levels were determined as a marker for endothelial cell activation.
  
  
  RESULTS
  A significant reduction of the cardiac specific cell damage was observed in the OPCAB group vs. the CABG group over time in the absence of acute myocardial ischemia or infarction. In addition, systemic and myocardial lipid peroxidation as measured by the malondialdehyde (MDA) levels were lower in the OPCAB group when compared to CABG. Finally, plasma levels of big-Endothelin (big-ET) significantly rose in the CABG but not in the OPCAB group.
  
  
  CONCLUSIONS
  The data of the present study indicate that OPCAB revascularization without the use of CPB and cardioplegic arrest reduces myocardial cell damage and lipid peroxidation. It is also associated with a reduced activation of the potent vasoconstrictor peptide endothelin. All of this may contribute to improved myocardial function and faster postoperative recovery from surgical revascularization procedures, particularly in critically ill patients.
authors.affiliation: Department of Cardiac Surgery, Ludwig-Maximilians University, Marchioninistr. 15, D-81377 Munich, Germany. wildhirt@hch.med. uni-muenchen.de.
authors.forename: S M
authors.initials: SM
authors.lastname: Wildhirt
authors.forename: C
authors.initials: C
authors.lastname: Schulze
authors.forename: N
authors.initials: N
authors.lastname: Conrad
authors.forename: N
authors.initials: N
authors.lastname: Sreejayan
authors.forename: H
authors.initials: H
authors.lastname: Reichenspurner
authors.forename: C
authors.initials: C
authors.lastname: von Ritter
authors.forename: B
authors.initials: B
authors.lastname: Reichart
mesh_terms: D000368:Aged; D001026:Coronary Artery Bypass / Q000379:methods*; D003402:Creatine Kinase / Q000097:blood; D019332:Endothelin-1; D016232:Endothelins / Q000097:blood; D005260:Female; D006801:Humans; D007527:Isoenzymes; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood; D013481:Superoxides / Q000097:blood; D019210:Troponin I / Q000097:blood
chemical_list: D019332:Endothelin-1; D016232:Endothelins; D007527:Isoenzymes; D011498:Protein Precursors; D019210:Troponin I; D013481:Superoxides; D008315:Malondialdehyde; D003402:Creatine Kinase