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CLINICAL RESEARCH: ACUTE ISCHEMIA OR INFARCTION

Coagulopathy After Successful Cardiopulmonary Resuscitation Following Cardiac Arrest

Implication of the Protein C Anticoagulant Pathway

Christophe Adrie, MD^_*,_*, Mehran Monchi, MD, Ivan Laurent, MD, Suzan Um, BS, S. Betty Yan, PhD, Marie Thuong, MD^_*, Alain Cariou, MD, Julien Charpentier, MD and Jean François Dhainaut, MD

^_* Intensive Care Unit, Delafontaine Hospital, Saint Denis, France
Intensive Care Unit, Jacques Cartier Hospital, Massy, France
Lilly Research Laboratories, Eli Lilly Company, Indianapolis, Indiana
Medical Intensive Care Medicine, Cochin Hospital, University of Paris V, Paris, France

Manuscript received October 9, 2004; revised manuscript received February 24, 2005, accepted March 15, 2005.

^_* Reprint requests and correspondence: Dr. Christophe Adrie, Service de Réanimation, Hôpital Delafontaine, 2 rue du Dr Delafontaine, Saint Denis, France (Email: christophe.adrie{at}wanadoo.fr).

OBJECTIVES: We investigated coagulation abnormalities in out-of-hospital cardiac arrest (OHCA) patients, with special attention to the protein C anticoagulant pathway.

BACKGROUND: Successfully resuscitated cardiac arrest is followed by a systemic inflammatory response and by activation of coagulation, both of which may contribute to organ failure and neurological dysfunction.

METHODS: Coagulation parameters were measured in all patients admitted after successfully resuscitated OHCA.

RESULTS: At admission, 67 patients had a systemic inflammatory response with increased interleukin-6 and coagulation activity (thrombin-antithrombin complex), reduced anticoagulation (antithrombin, protein C, and protein S), activated fibrinolysis (plasmin-antiplasmin complex), and, in some cases, inhibited fibrinolysis (increased plasminogen activator inhibitor-1 with a peak on day 1). These abnormalities were more severe in patients who died within two days (50 of 67, 75%) and were most severe in patients dying from early refractory shock. Protein C and S levels were low compared to healthy volunteers and discriminated OHCA survivors from nonsurvivors. Furthermore, a subgroup of patients had a transient increase in plasma-activated protein C at admission followed by undetectable levels. This, along with an increase in soluble thrombomodulin over time, suggests secondary endothelial injury and dysfunction of the protein C anticoagulant pathway similar to that observed in severe sepsis.

CONCLUSIONS: Major coagulation abnormalities were found after successful resuscitation of cardiac arrest. These abnormalities are consistent with secondary down-regulation of the thrombomodulin-endothelial protein C receptor pathway.

Abbreviations and Acronyms   AT = antithrombin   CPR = cardiopulmonary resuscitation   ICU = intensive care unit   IL = interleukin   LOD = Logistic Organ Dysfunction score   OHCA = out-of-hospital cardiac arrest   PAI = plasminogen activator inhibitor   PAP = plasmin-antiplasmin complex   SAPS II = Simplified Acute Physiology score   sTM = soluble thrombomodulin   TAT = thrombin-antithrombin complex

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