Influence of ischemic preconditioning and blood cardioplegia protection on postischemic endothelial activation in coronary bypass surgery |
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Authors: | G Steinhoff MD M Karck J Cremer T Ahnsel D Hollander A Haverich |
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Institution: | (1) Department of Heart and Vascular Surgery, University Kiel, Germany;(2) Department of Thoracic and Cardiovascular Surgery, Medical School Hannover, D-30623 Hannover, Germany |
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Abstract: | Summary
Background Hypothermic ischemia in open heart surgery and cardiopulmonary bypass involve a postischemic in-flammatory reaction caused
by an activation of leukocytes and endothelia with the systemic release of cytokines and adhesion molecules. The present study
addresses the question, if an amelioration of postischemic endothelial activation in the heart could be achieved by means
of cardioplegic protection or ischemic preconditioning. In a randomized prospective study patients underwent a normothermic
preconditioning procedure either followed by crystalloid or blood cardioplegia during coronary bypass surgery.
Methods Patients (n=28) were included and randomized in the study according to defined criteria: Group A received St. Thomas cardioplegia,
group B cold blood cardioplegia. Ischemic precon-ditioning was performed twice at normothermia under a cardiopulmonary bypass
(CPB) for 5 min followed by 10 min of reperfusion before coronary aortic bypass graft (CABG) using St. Thomas (group C) or
blood cardioplegia (group D) hypothermic protection. In coronary sinus blood and arterial blood myocardial (creatine-kinase
myoglobin CK-MB]) and endothelial activation (endothelin, IL-6, IL-8, sE-selectin, soluble vascular adhesion molecule-1 sVCAM-1],
soluble intercellular adhesion molecule-1 sICAM-1]) parameters were investigated 1, 3, 6, 9, 12, and 24 h after coronary
reperfusion.
Results 1) Parameters of myocardial injury (CK-MB, myoglobin) revealed increased levels at 1 h and 9 to 12 h after CABG. Levels at
12 h were lower in group B and D as compared to A and C. 2) Cytokines (IL-6, IL-8) showed increased levels 3 h after reperfusion
with no difference between study groups. 3) Soluble adhesion molecules (E-selectin, VCAM-1, ICAM-1) were found increased in
all groups 6 to 12 h after reperfusion. Lower levels were present in group D for E-selectin and VCAM-1.
Conclusions The results indicate a sequence of cytokine and adhesion molecule release as a potential pathomechanism of myocardial reperfusion
injury. Gradual decrease in the release of endothelial adhesion molecules in late myocardial injury was noted for blood cardioplegia
and ischemic preconditioning. Amelioration of endothelial activation by means of preconditioning and blood cardioplegia may
improve heart muscle recovery in open heart surgery with borderline ischemia time and organ dysfunction.
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Keywords: | Cytokines soluble adhesion molecules reperfusion injury coronary bypass surgery ischemic preconditioning blood cardioplegia |
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