EJCTS Click here for details of sales representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Shahzad G. Raja
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Raja, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Raja, S. G.
Related Collections
Right arrow Coronary disease
Right arrow Extracorporeal circulation

Eur J Cardiothorac Surg 2004;25:906
© 2004 Elsevier Science NL


Letter to the Editor

The ‘dark side’ of cardiopulmonary bypass

Shahzad G. Raja*

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

  1. Wehlin L., Vedin J., Vaage J., Lundahl J. Activation of complement and leukocyte receptors during on- and off pump coronary artery bypass surgery. Eur J Cardiothorac Surg 2004;25:35-42.[Abstract/Free Full Text]
  2. Picone A.L., Lutz C.J., Finck C., Carney D., Gatto L.A., Paskanik A., Searles B., Snyder K., Nieman G. Multiple sequential insults cause post-pump syndrome. Ann Thorac Surg 1999;67:978-985.[Abstract/Free Full Text]
  3. Martinez-Pellus A.E., Merino P., Bru M., Canovas J., Seller G., Sapina J., Fuentes T., Moro J. Endogenous endotoxemia of intestinal origin during cardiopulmonary bypass. Intensive Care Med 1997;23:1251-1257.[CrossRef][Medline]
  4. Wan S., Yim A.P., Arifi A.A., Lee T.W., DeSmet J.M., LeClerc J.L., Vincent J.L. Can cardioplegia management influence cytokine responses during clinical cardiopulmonary bypass. Ann Thorac Cardiovasc Surg 1999;5:81-85.[Medline]
  5. Biglioli P., Cannata A., Alamanni F., Naliato M., Porqueddu M., Zanobini M., Tremoli E., Parolari A. Biological effects of off-pump vs. on-pump coronary artery surgery: focus on inflammation, hemostasis and oxidative stress. Eur J Cardiothorac Surg 2003;24:260-269.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
Eur. J. Cardiothorac. Surg.Home page
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]


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Shahzad G. Raja
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Raja, S. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Raja, S. G.
Related Collections
Right arrow Coronary disease
Right arrow Extracorporeal circulation


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS