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LETTER TO THE EDITOR |
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Division of Cardiothoracic Surgery Prince of Wales Hospital The Chinese University of Hong Kong Shatin, Hong Kong People's Republic of China Department of Cardiac Surgery 1 Department of Intensive Care University Hospital Erasme Free University of Brussels Route de Lennik 808 Brussels B-1070, Belgium |
CPB carries less untoward effects today when compared with its infancy stage half a century ago, due to continued efforts to improve the managing protocol through a better understanding of the pathophysiologic concepts involved.2 From somehow physiological cross-circulation4 to the use of bubble and membrane oxygenators, CPB has been established as a safe procedure and has gained worldwide acceptance among cardiac surgeons. Recently developed therapies aimed at interfering with the inflammatory response have included the administration of pharmacological agents such as corticosteroids, aprotinin, and antioxidants, as well as modification of techniques and equipment by the use of heparin-coated CPB circuits, intraoperative leukocyte depletion, and ultrafiltration.2 These improved management modalities with complete revascularization have resulted in shorter recovery times5,6 as well as improved event-free long-term survival in patients undergoing coronary artery bypass grafting.7 In fact, it has been observed recently that there is no difference in the incidence of cerebral injury in patients undergoing coronary artery bypass grafting with and without CPB.8
The inflammatory reactions occurring during and after CPB are extremely complex. With a much improved knowledge of the pathophysiologic changes during CPB it is still possible to make CPB even less aggressive. For instance, the release of proinflammatory cytokines has been suggested to play a key role in the development of postoperative complications.9 However, an endogenous anti-inflammatory, potentially protective response is also associated with CPB, as reflected in the production of an anti-inflammatory cytokine interleukin-10 (IL-10) as well as a preconditioning effect involving the stimulation of myocardial alpha adrenergic receptors and adenosine receptors.9,10 It has been found that IL-10 may reduce pulmonary ischemia-reperfusion injury.11 Interestingly, neither the heart nor the lung12 but the liver13 is the major source of IL-10 during CPB, and the release of IL-10 is markedly increased in steroid-pretreated patients.9 To enhance IL-10 release in patients undergoing a longer duration of both CPB and cardiopulmonary ischemia, the timing of steroid administration can be crucial.14 Nevertheless, the balance between these proinflammatory and anti-inflammatory responses may be even more important. For example, in combination with the reduction of some other proinflammatory mediators, reduced IL-10 production has also been associated with the use of heparin-coated CPB circuits and, interestingly, this may lead to reduced myocardial injury in patients undergoing heart and heart-lung transplantation. (Authors' unpublished data).
Back to our question if CPB could be less aggressive. The answer is obvious. Therefore, the definition of less invasive cardiac surgery in the future may not be just off-pump but on-a-better-pump with not only enhanced biocompatibility of materials but also improved perioperative management.
REFERENCES
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