Cardiospecific sevoflurane treatment quenches inflammation but does not attenuate myocardial cell damage markers: a proof-of-concept study in patients.

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Cardiospecific sevoflurane treatment quenches inflammation but does not attenuate myocardial cell damage markers: a proof-of-concept study in patients undergoing mitral valve repair K.A. Kortekaas, A. van der Baan, L.P.H.J. Aarts, M. Palmen, C.M. Cobbaert, J.C.M. Verhagen, F.H.M. Engbers, R.J.M. Klautz, J.H.N. Lindeman British Journal of Anaesthesia Volume 112, Issue 6, Pages 1005-1014 (June 2014) DOI: 10.1093/bja/aet588 Copyright © 2014 The Author(s) Terms and Conditions

Fig 1 Schematic representation of the administration of sevoflurane and the collection of blood samples. Sevoflurane was administered (a) locally by addition of this volatile anaesthetic to the cardioplegia solution or was administered (b) between the two gifts of cardioplegia infusion through the main oxygenator of the CPB. Various blood samples were collected to measure inflammatory mediators and myocardial cell damage markers. A baseline sample was obtained the day before surgery from the brachial vein. Moreover, paired arterial (radial artery) and myocardial venous (coronary sinus) blood samples were collected over the reperfused heart in the early (0, 15, 30, 45, and 60 min after reperfusion) and late reperfusion phase (2, 4, 8, 16, and 24 h after reperfusion). British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions

Fig 2 Attenuation of systemic levels of several cytokines by intramyocardial delivery of sevoflurane. Levels of (a) interleukin (IL)-6, (b) IL-8, (c) IL-16, (d) IL-18, and (e) CXCL10 were already attenuated the moment of reperfusion after intramyocardial delivery of sevoflurane (iSevoflurane). The other seven measured cytokines (IL-1ra, IL-9, IL-10, G-CSF, MCP-1, RANTES, and VEGF) were not attenuated by selective myocardial sevoflurane delivery when compared with levels in patients not receiving sevoflurane treatment and are therefore not shown. *P<0.05 (unpaired t-test using AUCs). Graph error bars represent the median (inter-quartile ranges). British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions

Fig 3 (a) Interleukin (IL)-6 and (b) IL-8 levels the first hour after reperfusion. Concentrations of IL-6 and IL-8 were lower in patients who received sevoflurane intramyocardially (blue empty squares) compared with the reference group (green triangles), (both P=0.001). Controls (pink filled squares) showed the highest levels of both markers. *P<0.05 (unpaired t-test using AUCs). Graph error bars represent the median (inter-quartile ranges). British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions

Fig 4 C-reactive protein (CRP) levels before and after cardiac surgery. CRP levels were attenuated significantly the first day after surgery in patients treated with sevoflurane (blue intramyocardial sevoflurane; green reference group) compared with controls (pink). *P<0.05 (Kruskal–Wallis anova with Mann–Whitney U-tests thereafter if appropriate). The medians and inter-quartile ranges are shown. British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions

Fig 5 Cardiac selective sevoflurane delivery attenuated the myocardial release of interleukin-6 and monocyte chemoattractant protein-1 2–24 h after reperfusion. Arterial (radial artery) and myocardial venous (coronary sinus) blood samples were collected simultaneously over the reperfused heart. Arteriovenous concentration differences were assessed to selectively evaluate the myocardial reperfusion-related inflammatory response. Cardiac selective sevoflurane delivery attenuated the myocardial release of two cytokines in the late reperfusion phase. A cardiac-specific release of interleukin (IL-6, a) was observed in both intramyocardial sevoflurane-treated (P=0.001) and control patients (P=0.004) in the late reperfusion phase (indicated by asterisks), although the arteriovenous difference was smaller in patients treated with sevoflurane. In addition, intramyocardial delivery of sevoflurane attenuated the cardiac-specific release of monocyte chemoattractant protein-1 (MCP-1, b) in the late reperfusion phase, as its release was only observed in controls (P=0.03, indicated by an asterisk). MCP-levels in general seem to be higher in patients treated with sevoflurane with unknown cause. The myocardial release of the other 10 measured cytokines (IL-1ra, IL-8, IL-9, IL-10, IL-16, IL-18, G-CSF, CXCL10, RANTES, and VEGF) was not attenuated by cardiac selective sevoflurane delivery and are therefore not shown. *P<0.05 (paired t-test using AUCs). Graph error bars represent the median (inter-quartile ranges). British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions

Fig 6 Three biomarkers of postoperative myocardial cell damage. Similar myocardial cell damage was observed in patients who received sevoflurane intramyocardially, the reference group, and control patients: (a) high-sensitive cTroponin T (hs cTnT, P=0.87), (b) creatine kinase activity (CK, P=0.38), and (c) creatine kinase-MB subfraction activity (CK-MB, P=0.17, Kruskal–Wallis test). Graph error bars represent the median (inter-quartile ranges). British Journal of Anaesthesia 2014 112, 1005-1014DOI: (10.1093/bja/aet588) Copyright © 2014 The Author(s) Terms and Conditions