title: Ischemic preconditioning reduces apoptosis in open heart surgery.
abstract: BACKGROUND
  This study was performed to assess the role of ischemic preconditioning on cardiomyocyte apoptosis after open heart surgery, based on morphology by transmission electron microscopy, caspase-3 activity, biochemical markers, and cardiac performance.
  
  
  METHODS
  12 piglets were divided into 2 equal groups: an ischemic preconditioning group and a control group. Ventricular muscles were collected to examine apoptotic ultrastructure morphology and caspase-3 activity. Blood samples from the coronary sinus were obtained for measurement of tumor necrosis factor-α, malondialdehyde, and cardiac troponin I. Aortic blood samples were taken for lactate measurements before and after cardiopulmonary bypass. Cardiac performance was measured by echocardiography before and after surgery.
  
  
  RESULTS
  Cardiomyocyte apoptosis occurred postoperatively, as shown by ultrastructure observation. Caspase-3 activity was less in the ischemic preconditioning group than the control group (p < 0.05). Measurements of specific markers of cardiomyocyte injury also showed lower increases in the ischemic preconditioning group, although not significantly different. Clinical outcomes showed that ischemic preconditioning was able to preserve cardiac performance in terms of ejection fraction, cardiac index, and stroke volume index; these were statistically significant, except for lactate concentration.
  
  
  CONCLUSIONS
  Cardiomyocyte apoptosis occurs after open heart surgery. Ischemic preconditioning can reduce cardiomyocyte apoptosis and improve cardiac performance. Laboratory findings showed that ischemic preconditioning prevents injury of cardiomyocytes and reduces lactate concentration, although not statistically significant.
authors.affiliation: Thoracic and Cardiovascular Surgery Division, Department of Surgery, Faculty of Medicine, University of Indonesia, Jakarta, Indonesia.
authors.forename: Jusuf
authors.initials: J
authors.lastname: Rachmat
authors.forename: Sudigdo
authors.initials: S
authors.lastname: Sastroasmoro
authors.forename: Fransiscus D
authors.initials: FD
authors.lastname: Suyatna
authors.forename: Gunanti
authors.initials: G
authors.lastname: Soejono
mesh_terms: D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D006348:Cardiac Surgical Procedures / Q000009:adverse effects*; D053148:Caspase 3 / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D019344:Lactic Acid / Q000097:blood; D008315:Malondialdehyde / Q000097:blood; D046529:Microscopy, Electron, Transmission; D023421:Models, Animal; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D013318:Stroke Volume; D034421:Sus scrofa; D013997:Time Factors; D019210:Troponin I / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D019344:Lactic Acid; D008315:Malondialdehyde; D053148:Caspase 3
keywords: Apoptosis; biological markers; cardiac performance; ischemic preconditioning; reperfusion injury