title: Cardiomyocyte apoptosis and ischemic preconditioning in open heart operations.
abstract: BACKGROUND
  The aim of the present study was to ascertain the percentage of left apical myocardial apoptosis in three-vessel coronary artery bypass grafting patients quantitatively and the impact of ischemic preconditioning.
  
  
  METHODS
  Twenty-one patients with three-vessel disease who had elective coronary artery bypass grafting were randomized in a ratio of 2:1 to ischemic preconditioning (n = 14) or a control group (n = 7). The ischemic preconditioning protocol was established by two cycles of ascending aorta occlusion for 2 minutes followed by 3 minutes of reperfusion. Myocardial samples from the apex of the left ventricle were taken using a Tru-Cut needle before aortic cross-clamping and immediately after declamping. The percentage of apoptosis was analyzed by TUNEL methods. Data on hemodynamics and biochemical markers were collected.
  
  
  RESULTS
  Low levels of myocardial apoptosis were found before the operation (0.01% +/- 0.00%). During the early reperfusion period, the percentage of myocardial apoptotic cells significantly increased (0.15% +/- 0.05%, p = 0.008). Ischemic preconditioning significantly improved cardiac index and right ventricular ejection fraction recovery after the operation (p = 0.036 and 0.001 respectively, repeated measure) but had no effect on myocardial apoptosis before and after the operation (0.01 +/- 0.00 versus 0.01 +/- 0.00, p = 0.658 and 0.12% +/- 0.04% versus 0.23% +/- 0.14%, p = 0.302).
  
  
  CONCLUSIONS
  Cardioplegic myocardial ischemia during open heart operation was associated with induction of cardiomyocyte apoptosis in humans. Attenuation of postoperative cardiac dysfunction by ischemic preconditioning appeared to be independent of apoptosis.
authors.affiliation: Division of Cardiac Surgery, Department of Surgery, Tampere University Hospital, Tampere, Finland.
authors.forename: Zhong-Kai
authors.initials: ZK
authors.lastname: Wu
authors.forename: Jari
authors.initials: J
authors.lastname: Laurikka
authors.forename: Antti
authors.initials: A
authors.lastname: Saraste
authors.forename: Ville
authors.initials: V
authors.lastname: Kytö
authors.forename: Erkki J
authors.initials: EJ
authors.lastname: Pehkonen
authors.forename: Timo
authors.initials: T
authors.lastname: Savunen
authors.forename: Matti R
authors.initials: MR
authors.lastname: Tarkka
mesh_terms: D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D015415:Biomarkers / Q000032:analysis; D002315:Cardiopulmonary Bypass; D001026:Coronary Artery Bypass / Q000379:methods*; D003327:Coronary Disease / Q000601:surgery; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006439:Hemodynamics; D006801:Humans; D020287:In Situ Nick-End Labeling; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008875:Middle Aged; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000166:cytology / Q000473:pathology*; D011300:Preoperative Care / Q000379:methods; D011336:Probability; D012016:Reference Values; D018570:Risk Assessment; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D016277:Ventricular Function, Left
chemical_list: D015415:Biomarkers; D019210:Troponin I; D003402:Creatine Kinase