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Eur J Cardiothorac Surg 2004;25:906
© 2004 Elsevier Science NL
Letter to the Editor |
Department of Cardiac Surgery, Royal Liverpool Children's NHS Trust (Alder Hey Hospital), Eaton Road, Liverpool L12 2AP, UK
Received 4 January 2004; accepted 9 February 2004.
* Tel.: +44-151-252-5632/5635; fax: +44-151-252-5643
e-mail: drrajashahzad{at}hotmail.com
Key Words: Coronary artery bypass Off pump Flow cytometry Inflammation Complement Randomised
I read with great interest the article by Wehlin and colleagues [1] in the January issue of EJCTS. They carried out a prospective, randomised study to investigate the influence of extracorporeal circulation on the biological functions of inflammatory cells and concluded that there was less complement activation in low risk OFFCAB patients compared with ONCAB patients. A corollary of their study was that as there was obvious inflammatory response in both groups and a lack of significant differences between groups, therefore, factors other than CPB are responsible for cellular and cytokine activation. Furthermore, they suggest that the dark side of CPB may be overestimated and the surgical trauma could be the more important contributing factor to the enhanced inflammatory response during cardiac surgery. I humbly tend to disagree with the authors in this regard.
Cardiac surgery undoubtedly provokes a vigorous inflammatory response, which has important clinical implications. Although factors influencing incidence, severity, and clinical outcome of the inflammatory response are currently not well understood yet available evidence suggests that CPB specifically activates the inflammatory response via at least three distinct mechanisms. One mechanism involves direct contact activation of the immune system following exposure of blood to the foreign surfaces of the CPB circuit [2]. A second mechanism involves ischemia-reperfusion injury to the brain, heart, lungs, kidney and liver as a result of aortic cross-clamping. Restoration of perfusion on release of the aortic cross-clamp is associated with activation of key indices of the inflammatory response [2]. Finally, splanchnic hypoperfusion, a common finding during and following CPB, may damage the mucosal barrier, allowing gut translocation of endotoxin. The ensuing endotoxemia may indirectly activate the inflammatory cascade [3].
Furthermore, the composition of the priming solution, cardioplegia, presence of pulsatile or nonpulsatile perfusion, type of oxygenator and pump, type of extracorporeal circuit, temperature during CPB and its duration are all important factors influencing the inflammatory response [4]. An additional factor is the development of excessive shear stress during CPB as a result of large pressure changes across the CPB circuit, causing damage to blood constituents and activating the inflammatory response [5]. Shear stress decreases erythrocyte deformability and increases hemolysis. Leukocyte adhesiveness is increased, and mechanical disruption, with neutrophil degranulation and release of cytotoxic products, may be seen at high levels of shear stress. Excess shear stress also increases platelet activation and may contribute to endothelial injury [5].
In short, we must admit that the etiology of inflammatory response after cardiac surgery is probably a composite of unstable peribypass hemodynamics, global myocardial ischemia, suboptimal organ perfusion during CPB, and immune events related to exposure to extracorporeal circulation per se and despite all efforts to improve the design of CPB to make it friendlier the dark side of CPB will always be there.
References
This article has been cited by other articles:
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A. Cannata, P. Biglioli, E. Tremoli, and A. Parolari Biological effects of coronary surgery: role of surgical trauma and CPB Eur. J. Cardiothorac. Surg., September 1, 2004; 26(3): 664 - 664. [Full Text] [PDF] |
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