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Are circulating adhesion molecules specifically changed in cardiac surgical patients?
1Department of Anesthesiology and Intensive Care Medicine, Justus-Liebig-University Giessen, Germany.
The Annals of Thoracic Surgery
|April 4, 1998
Summary
Cardiac surgery significantly elevates soluble adhesion molecules, indicating endothelial activation. Other major surgeries did not show this change, suggesting unique inflammatory responses in cardiac procedures.
Area of Science:
- Cardiovascular Surgery
- Inflammation Markers
- Endothelial Function
Background:
- Soluble adhesion molecules are recognized markers of inflammation, endothelial activation, and damage.
- This study investigated specific alterations in adhesion molecules in patients undergoing cardiac surgery.
Purpose of the Study:
- To assess the impact of cardiac surgical procedures on plasma levels of soluble adhesion molecules.
- To compare these changes with those observed in patients undergoing non-cardiac major surgeries.
Main Methods:
- Prospective study of three patient groups (n=20 each): coronary artery bypass grafting, Whipple pancreatoduodenectomy, and pneumonectomy.
- Measurement of plasma levels of soluble endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and granule membrane protein 140 at multiple time points.
Main Results:
- Cardiac surgery patients showed significant increases in soluble endothelial leukocyte adhesion molecule-1, intercellular adhesion molecule-1, and granule membrane protein 140 post-cardiopulmonary bypass.
- Levels returned to baseline by the first postoperative day, except for soluble vascular cell adhesion molecule-1.
- Patients undergoing Whipple or pneumonectomy procedures exhibited no significant changes in adhesion molecule levels.
Conclusions:
- Cardiac operations are associated with increased plasma levels of soluble adhesion molecules, suggesting endothelial activation or dysfunction.
- In contrast, complex abdominal or lung operations did not alter these markers.
- Proinflammatory cascades, ischemia/reperfusion, and microcirculatory dysfunction are potential explanations for the observed differences.