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Cardiomyocyte apoptosis and ischemic preconditioning in open heart operations

Zhong-Kai Wu1, Jari Laurikka, Antti Saraste

  • 1Division of Cardiac Surgery, Department of Surgery, Tampere University Hospital, Tampere, Finland.

The Annals of Thoracic Surgery
|August 7, 2003
PubMed

Insights

Coronary artery bypass grafting increases heart cell death (apoptosis). Ischemic preconditioning did not reduce apoptosis but improved recovery after surgery in patients with three-vessel disease.

Area of Science:

  • Cardiology
  • Cardiac Surgery
  • Cell Biology

Background:

  • Coronary artery bypass grafting (CABG) is a common surgical procedure for three-vessel disease.
  • Myocardial apoptosis, or programmed heart cell death, can occur during cardiac surgery.
  • The impact of ischemic preconditioning on myocardial apoptosis in CABG patients requires further investigation.

Purpose of the Study:

  • To quantitatively assess left apical myocardial apoptosis in patients undergoing three-vessel CABG.
  • To determine the effect of ischemic preconditioning on myocardial apoptosis and postoperative cardiac function.

Main Methods:

  • A randomized controlled trial involving 21 patients with three-vessel disease undergoing elective CABG.
  • Patients were assigned to either ischemic preconditioning (n=14) or a control group (n=7).
  • Myocardial samples were analyzed for apoptosis using TUNEL methods before and after aortic cross-clamping.

Main Results:

  • Myocardial apoptosis was low before surgery (0.01%) but significantly increased during early reperfusion (0.15%).
  • Ischemic preconditioning did not significantly alter myocardial apoptosis levels before or after surgery.
  • Ischemic preconditioning significantly improved cardiac index and right ventricular ejection fraction recovery post-operation.

Conclusions:

  • Cardioplegic myocardial ischemia during open-heart surgery induces cardiomyocyte apoptosis in humans.
  • The protective effects of ischemic preconditioning against postoperative cardiac dysfunction appear to be independent of its impact on myocardial apoptosis.
Abstract

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