• Marlene Fischer, Anelia Dietmann, Peter Lackner, Ronny Beer, Raimund Helbok, Bettina Pfausler, Markus Reindl, Erich Schmutzhard, and Gregor Broessner.
• Department of Neurology, Neurologic Intensive Care Unit, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
• Neurocrit Care. 2012 Oct 1;17(2):224-30.

BackgroundLittle is known about endothelial activation under the influence of endovascular temperature management. This analysis was designed to measure the endothelial markers Angiopoietin-1 (Ang-1) and -2 (Ang-2) in endovascularly based prophylactic normothermia versus conventional temperature management.MethodsIn this randomized controlled trial patients with spontaneous subarachnoid or spontaneous intracerebral hemorrhage were prospectively enrolled and randomized in two treatment arms: (a) prophylactic normothermia group with target core temperature 36.5°C using endovascular cooling, (b) active control group with conventional stepwise predefined fever management using antipyretic medication and surface cooling. Blood samples were obtained on days 1, 4, and 7. In a substudy Ang-1 and -2 were measured in 63 patients for whom samples on consecutive days were available.ResultsThe median total fever burden during the course of treatment was 0.0°C and 5.9°C h in the endovascular and the conventional group, respectively (P < 0.0001). Angiopoietin serum levels did not yield a statistical difference when comparing the two treatment arms. Ang-1 was significantly lowered, whereas Ang-2 levels were significantly elevated on day 4 compared to baseline levels irrespective of group allocation (P < 0.0001). The application of non-steroidal anti-inflammatory drugs (NSAIDs) was associated with significantly increased Ang-1 (P < 0.05) and lower Ang-2 levels on day 7 (P < 0.05).ConclusionsEndovascular long-term temperature management did not alter Ang-1 and -2 levels compared to the control group indicating that the endovascular cooling technique itself does not lead to additional endothelial impairment. However, application of NSAIDs led to lower Ang-2 serum concentrations in the endovascular group.

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