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Mediators of Inflammation
Volume 2009 (2009), Article ID 124384, 7 pages
Review Article

Complement Inhibition as a Proposed Neuroprotective Strategy following Cardiac Arrest

Department of Neurological Surgery, Columbia University, 710 W. 168th Street, New York, NY 10032, USA

Received 13 May 2009; Revised 18 October 2009; Accepted 4 November 2009

Academic Editor: Fulvio D'Acquisto

Copyright © 2009 Brad E. Zacharia et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. Emerging preclinical as well as recent human clinical evidence suggests that activation of the complement cascade plays a critical role in the pathogenesis of GCI/R injury following OHCA. In addition, it is well established that complement inhibition improves outcome in both global and focal models of brain ischemia. Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.