Surgical trauma affects the proinflammatory status after cardiac surgery to a higher degree than cardiopulmonary bypass.
OBJECTIVE
Cytokines contribute to the development of the systemic inflammatory response syndrome or multiple-organ failure frequently observed after cardiopulmonary bypass-supported cardiac surgery. To quantify the contribution of bypass-induced versus trauma-induced inflammatory response after coronary artery bypass grafting, we examined plasma cytokine levels in 120 patients with coronary artery disease who were treated with or without cardiopulmonary bypass-assisted procedures.


METHODS
Patients were treated in accordance with one of the following protocols: (1) elective percutaneous coronary intervention without cardiopulmonary bypass (n = 69), (2) cardiopulmonary bypass-supported percutaneous coronary intervention (cardiopulmonary bypass-percutaneous coronary intervention; n = 10), and (3) cardiopulmonary bypass-supported coronary artery bypass grafting (cardiopulmonary bypass-coronary artery bypass grafting; n = 41). Cytokine levels (picograms/milliliter) were measured by enzyme-linked immunosorbent assay from plasma samples obtained at various time points.


RESULTS
Interleukin-6 was measured in blood samples from all 3 patient populations. The maximum interleukin-6 level was 13.6 +/- 22.3 pg/mL in the percutaneous coronary intervention group, 170.4 +/- 165.4 pg/mL in the cardiopulmonary bypass-percutaneous coronary intervention group, and 640.3 +/- 285.7 pg/mL in the cardiopulmonary bypass-coronary artery bypass grafting group. Interleukin-6 levels were significantly different, and the 95% confidence intervals did not overlap. In the cardiopulmonary bypass-percutaneous coronary intervention group, bypass duration correlated well with interleukin-6 production ( r = 0.915; P < .001), whereas these parameters did not correlate in patients who underwent cardiopulmonary bypass-coronary artery bypass grafting ( r = 0.307; P = .054).


CONCLUSIONS
These findings support the suggestion that surgical trauma and cardiopulmonary bypass contribute to the inflammatory response after cardiac surgery, although trauma may contribute to a higher degree.
Prondzinsky
Roland
R
Department of Medicine III, Martin-Luther-University Halle-Wittenberg, Halle (Salle), Germany. roland.prondzinsky@medizin.uni-halle.de
Knüpfer
Axel
A
Loppnow
Harald
H
Redling
Frank
F
Lehmann
Dirk W
DW
Stabenow
Ina
I
Witthaut
Rochus
R
Unverzagt
Susanne
S
Radke
Joachim
J
Zerkowski
Hans-Reinhard
HR
Werdan
Karl
K
D015906:Angioplasty, Balloon, Coronary; D002315:Cardiopulmonary Bypass; D001026:Coronary Artery Bypass; D003327:Coronary Disease / Q000601:surgery; D016207:Cytokines / Q000097:blood*; D017558:Elective Surgical Procedures; D005260:Female; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood; D012795:Sialoglycoproteins / Q000097:blood; D018746:Systemic Inflammatory Response Syndrome / Q000097:blood
D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D017472:Receptors, Interleukin-1; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D012795:Sialoglycoproteins; D016753:Interleukin-10