German Clinical Trials Register

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Brief summary in lay language

Despite modern intensive care, prognosis of patients suffering cardiac arrest still remains poor. This high mortality can be attributed to the development of the post-cardiac arrest syndrome, which is thought to be mediated by a systemic inflammatory response. In this prospective observational study the incidence and extent of a systemic inflammatory response will be investigated in blood samples from patients after successful cardiopulmonary resuscitation which will be compared to a control group with coronary artery disease without acute myocardial infarction.

Brief summary in scientific language

Despite improvement in modern intensive care, patients after primarily successful resuscitation still have an impaired prognosis. Intrahospital mortality can be attributed to the development of the post-cardiac arrest syndrome, a unique and complex combination of pathophysiological processes which include anoxic brain injury, myocardial dysfunction, systemic ischemia-reperfusion response and the unresolved pathological condition that caused circulatory arrest [2]. It is thought that whole body ischemia and finally the return of spontaneous circulation after successful cardiopulmonary resuscitation results in generation of reactive oxygen species [3] which lead to induction of a systemic inflammatory response [4] with production of proinflammatory cytokines [5] as well as an endothelial damage with microthrombosis [6, 7]. These processes contribute to microcirculatory disorder and capillary leakage, which finally lead to a “sepsis-like” syndrome [5]. In this prospective observational study the incidence and extent of a systemic inflammatory response will be investigated in blood samples from patients after circulatory arrest, which will be compared to a control group with coronary artery disease without acute myocardial infarction. 1. Peberdy MA, Kaye W, Ornato JP, Larkin GL, Nadkarni V, Mancini ME et al. Cardiopulmonary resuscitation of adults in the hospital: a report of 14720 cardiac arrests from the National Registry of Cardiopulmonary Resuscitation. Resuscitation. 2003;58(3):297-308. 2. Neumar RW, Nolan JP, Adrie C, Aibiki M, Berg RA, Bottiger BW et al. Post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. A consensus statement from the International Liaison Committee on Resuscitation (American Heart Association, Australian and New Zealand Council on Resuscitation, European Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Asia, and the Resuscitation Council of Southern Africa); the American Heart Association Emergency Cardiovascular Care Committee; the Council on Cardiovascular Surgery and Anesthesia; the Council on Cardiopulmonary, Perioperative, and Critical Care; the Council on Clinical Cardiology; and the Stroke Council. Circulation. 2008;118(23):2452-83. 3. Idris AH, Roberts LJ, 2nd, Caruso L, Showstark M, Layon AJ, Becker LB et al. Oxidant injury occurs rapidly after cardiac arrest, cardiopulmonary resuscitation, and reperfusion. Crit Care Med. 2005;33(9):2043-8. 4. Gando S, Nanzaki S, Morimoto Y, Kobayashi S, Kemmotsu O. Out-of-hospital cardiac arrest increases soluble vascular endothelial adhesion molecules and neutrophil elastase associated with endothelial injury. Intensive care medicine. 2000;26(1):38-44. 5. Adrie C, Adib-Conquy M, Laurent I, Monchi M, Vinsonneau C, Fitting C et al. Successful cardiopulmonary resuscitation after cardiac arrest as a "sepsis-like" syndrome. Circulation. 2002;106(5):562-8. 6. Gando S, Nanzaki S, Morimoto Y, Kobayashi S, Kemmotsu O. Alterations of soluble L- and P-selectins during cardiac arrest and CPR. Intensive care medicine. 1999;25(6):588-93. 7. Gando S, Kameue T, Nanzaki S, Nakanishi Y. Massive fibrin formation with consecutive impairment of fibrinolysis in patients with out-of-hospital cardiac arrest. Thromb Haemost. 1997;77(2):278-82.