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Eur J Cardiothorac Surg 2002;22:330-331
© 2002 Elsevier Science NL
Letter to the Editor |
a Division of Congenital Heart Surgery, Michael E. DeBakey Department of Surgery, Texas Children's Hospital/Baylor College of Medicine, Congenital Heart Surgery Service, 6621 Fannin Street, WT 19345-H, Houston, TX 77030-2399, USA
b Congenital Heart Surgery Service, Texas Children's Hospital, 6621 Fannin Street, WT 19345-H, Houston, TX 77030-2399, USA
Received 8 April 2002; received in revised form 10 April 2002; accepted 14 May 2002.
* Corresponding author. Tel.: +1-832-826-1997; fax: +1-832-825-1904
e-mail: aundar{at}bcm.tmc.edu
Key Words: Anti-factor D monoclonal 166-32 • Pulsatile flow • Cardiotomy suction • Cardiopulmonary bypass • Systemic inflammation
We read with great interest the recent review article on cardiopulmonary bypass (CPB) induced inflammation by Paparella and associates [1]. We would like to make several comments based on our own experience with this important topic.
We have clearly documented that alternative complement pathway plays a major role in complement, neutrophil, platelet, and cytokine activation during CPB [2,3]. In addition, it has been suggested that alternative pathway amplifies the classical and lectin pathways. Previously, we showed that anti-factor D monoclonal antibody (Mab) 166-32 significantly inhibits the alternative complement pathway, including the production of Bb, C3a, C5a, and sC5b-9, and upregulation of CD11b on neutrophils and of CD62P on platelets, the release of thrombospondin from platelets, the release of neutrophil-specific elastase and myeloperoxidase, and the production of interleukin 8 in a simulated CPB circuit using human blood. Recently, we also showed that inhibition of complement activation via the alternative pathway by anti-factor D Mab 166-32 significantly reduces leukocyte activation and myocardial ischemia/reperfusion injury in a baboon model of CPB [3] (Ündar et al. Presented at the 38th Annual Meeting of the Society of Thoracic Surgeons, Fort Lauderdale, FL, January 28–30, 2002). Based on these experimental results, we believe that inhibition of the alternative complement pathway may help to minimize complement activation during CPB more than would inhibition of the classical and lectin pathways. The anti-factor D Mab 166-32 targets the factor D because it is a rate-limiting enzyme that is essential for activation and amplification of the alternative complement pathway. In addition, factor D has an extremely low concentration in the blood (approximately 2 µg/ml) compared with other soluble complement components.
As Paparella and associates suggested, there has been no conclusive evidence that pulsatile CPB leads to improved clinical outcomes. We believe that the main reason for this controversy is the lack of definition and quantification of pulsatile and nonpulsatile flow. The precise quantification of pulsatile and nonpulsatile pressure-flow waveforms is a must for a direct and meaningful comparison [4]. The energy equivalent pressure formula should be used for direct comparisons. We have clearly shown that adequate pulsatility improves vital organ blood flow after 60 min of deep hypothermic circulatory arrest or hypothermic CPB [5]. We have also shown that some of the pulsatile pumps could not generate adequate hemodynamic energy for maintaining better tissue perfusion [4]. In addition, it has been shown that pulsatile flow reduces complement (C3a) and neutrophil (CD11b) activation, and S-100ß levels compared to the nonpulsatile flow in high risk patients.
Finally, we also add that the effects of cardiotomy suction on systemic inflammation should be included in Paparella and associates’ manuscript. It has been clearly documented that cardiotomy suction is a major source of systemic inflammation during CPB.
References
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