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Table of Contents
Year : 2011  |  Volume : 14  |  Issue : 3  |  Page : 197-202
Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques

1 Department of Cardiac Anaesthesia, CN Centre, All India Institute of Medical Sciences, New Delhi, India
2 Department of Cardiothoracic and Vascular Surgery, CN Centre, All India Institute of Medical Sciences, New Delhi, India

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Date of Web Publication20-Aug-2011


Cardiac surgery with aid of cardiopulmonary bypass (CPB) is associated with neurological dysfunction. The presence of cerebrospecific protein S100β in serum is an indicator of cerebral damage. This study was designed to evaluate the influence of three different anesthesia techniques, on S100β levels, in patients undergoing coronary artery bypass grafting on CPB. A total of 180 patients were divided into three groups - each of who received sevoflurane, isoflurane and total intravenous anesthesia as part of the anesthetic technique, respectively. S100 were evaluated from venous sample at following time intervals - prior to induction of anesthesia (T1), after coming off CPB (T2); 12 h after aortic cross clamping (T3) and 24 h after aortic cross clamping (T4). In all three groups, maximal rise in S100β levels occurred after CPB which gradually declined over next 24 h, the levels at 24 h post-AOXC being significantly higher than baseline levels. Significantly low levels of S100β were noted at all postdose hours in the sevoflurane group, as compared to the total intravenous anesthesia (TIVA) group, and at 12 and 24 h postaortic cross clamp, in comparison to the isoflurane group. Comparing the isoflurane group with the TIVA group, the S100 levels were lower in the isoflurane group only at 24 h postaortic cross clamp. It was concluded that maximum rise in S100β levels occurs immediately after CPB with a gradual decline in next 24 h. The rise in S100β levels is significantly less in patients administered sevoflurane in comparison to isoflurane or TIVA. Hemodynamic parameters had no influence on the S100β levels during the first 24 h after surgery.

Keywords: S100β levels, isoflurane, sevoflurane, total intravenous anesthesia

How to cite this article:
Singh SP, Kapoor PM, Chowdhury U, Kiran U. Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques. Ann Card Anaesth 2011;14:197-202

How to cite this URL:
Singh SP, Kapoor PM, Chowdhury U, Kiran U. Comparison of S100β levels, and their correlation with hemodynamic indices in patients undergoing coronary artery bypass grafting with three different anesthetic techniques. Ann Card Anaesth [serial online] 2011 [cited 2021 Oct 25];14:197-202. Available from:

   Introduction Top

Cardiac surgery performed under cardiopulmonary bypass (CPB) may be associated with an increased risk of cerebral complication. Central nervous dysfunction after CPB represents deficits ranging from neurocognitive deficits (with an incidence of 25-80%) to overt stroke (occurring in 1-5% of patients). [1] Usually, the diagnosis of cerebral injury may be diagnosed by clinical neurological examination or radiological imaging. Since neurological imaging in a patient who has undergone cardiac surgery recently may not only be cumbersome but also dangerous, biochemical markers such as S100β might appear to be good surrogates to assess neurological injury.

S100β, a protein specific for cerebral tissue, under normal circumstances does not cross the blood-brain barrier and, its presence in the serum is an indicator of cerebral damage. [2] Its concentration at 24 h after return of spontaneous circulation (ROSC) is highly predictive of neurological outcome at 6 months in patients treated with hypothermia. [3] During cardiac surgery, early release of S100β (immediately after CPB) has not been associated with adverse cerebral outcome. However, late increases in S100β, after 5-48 h of termination of CPB, have been related to perioperative cerebral complications such as stroke, delayed awakening, and confusion. [4],[5],[6] In ischemic stroke, S100 more accurately correlates with the stroke volume, neurological status at admission and functional outcome as compared to neuron-specific enolase (NSE). [7]

Several studies [8],[9],[10],[11] have proved that pretreatment with volatile anesthetics (like sevoflurane and isoflurane) confers prolonged neuroprotection against ischemic cerebral injury. Different mechanisms involving mitochondrial K ATP channels [11] (same as in cardiac preconditioning), ubiquitin-conjugated protein aggregation, [12] and inducible nitric oxide synthase (iNOS) [13] have been proposed for this cerebral preconditioning.

Because S100β levels may be used as a surrogate marker for cerebral injury and that volatile anesthetics provide neuroprotection via different mechanisms, this study was designed to evaluate the influence of three different anesthetic techniques on S100β levels in patients undergoing coronary artery bypass surgery. A correlation between S100β levels and hemodynamic indices was also sought for as a secondary objective.

   Materials and Methods Top

This prospective, randomized single-blinded trial was conducted over a period of 2 years beginning from 2008. After approval from the hospital ethics committee and obtaining a written informed consent from the patients, 180 patients having coronary artery disease (CAD) and normal left ventricular (LV) function, scheduled for coronary artery bypass grafting (CABG) with the aid of CPB, were included in this study. After an initial pilot study of 15 patients (5 in each group) power analysis was performed with a two-sided type I error of 5% (α= 0.05) and power at 80%. Assuming the baseline to be the same in all the three groups, with three followups, the sample size was calculated by a method of change (STATA 11.2 software, Stata Corp, Texas, USA) in order to achieve a relative efficiency of 2.5. The minimum number of patients required for a statistically significant result came out to be 57 in each group. Therefore, 60 patients were enrolled in each group.

Patients with age of more than 65 years, preoperative left bundle branch block (LBBB) on electrocardiogram (ECG), acute myocardial infarction, significant valvular dysfunction, insulin-dependent diabetes mellitus with glycosylated hemoglobin >8%, severe uncontrolled hypertension (mean arterial pressure >150 mmHg), liver disease, renal insufficiency (serum creatinine >2 mg%), and respiratory disease (forced vital capacity <50% of expected values) were excluded from the study. Patients undergoing redo CABG, requiring intraaortic counterpulsation balloon (IABP) support, developing atrial fibrillation or those with history of stroke, epilepsy, brain abscess, tumor or on any medication for the same were also excluded from the study.

The patients were randomly allocated into either of the three groups using a computer-generated randomization schedule. Blinding was done using the sequentially numbered opaque-sealed envelope technique. The three groups were as follows:

Group Sevo (n = 60): Patients were administered 1 MAC sevoflurane from the time of skin incision till the aortic cross clamp was applied;

Group Iso (n = 59): Patients were administered 1 MAC isoflurane from the time of skin incision till aortic cross clamp was applied;

Group TIVA (n = 61): Patients who underwent total intravenous anesthesia (TIVA) with fentanyl (4 μg/kg/h) and midazolam (0.1 mg/kg/h) infusion from the time of skin incision till aortic cross clamping.

Preoperatively, as per institutional protocol, all the patients received their cardiac medications 2 h prior to surgery except for angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB). Morphine sulfate (0.1 mg/kg) and promethazine (0.5 mg/kg) were administered, intramuscularly, as premedication 1 h prior to surgery. In the operating room (OR), electrocardiogram (ECG), pulse oximetry, invasive arterial pressure monitoring, and central venous pressure monitoring were obtained. The Flotrac Vigileo system (Edwards Lifesciences, Irvine, CA, USA) connected to the radial artery catheter was used to measure the cardiac index (CI), delivered O 2 index (DO 2 I) and systemic vascular resistance index (SVRI). End tidal carbon dioxide (EtCO 2 ) and temperature monitors were connected once the patient's trachea was intubated. Bispectral Index (BIS) monitor (Aspect Medical Systems, USA) was applied after induction of anesthesia and the value was maintained between 40 and 60.

General anesthesia was induced with intravenous midazolam 2 mg, fentanyl 3-5 mg/kg and thiopentone 3-5 mg/kg. Endotracheal intubation was facilitated with intravenously administered rocuronium bromide in a dose of 1 mg/kg in all three groups. The lungs were mechanically ventilated with a tidal volume of 8 mL/kg and a mixture of air and oxygen in the ratio of 50:50. The ventilator parameters were adjusted in such a way to attain a PaCO 2 of 35-40 mmHg. Maintenance of anesthesia (BIS 40-60) was done using additional boluses of fentanyl and midazolam along with the intervention for each group, as per protocol. Intravenous vecuronium bromide 0.1 mg/kg was administered intermittently to maintain neuromuscular blockade.

All patients underwent the same CPB protocol and were cooled to 32 °C. Anesthesia during and after CPB was maintained with bolus doses of fentanyl, midazolam, and vecuronium bromide. At the time of rewarming, intravenous nitroglycerine and dopamine were started in doses of 0.5 and 5 μg/kg/min, respectively, to enable weaning from CPB. All patients were rewarmed gradually to a nasopharyngeal temperature of 36 °C (as per the institutional protocol) and pacing was instituted if the heart rate was less than 80 beats per minute. After surgery patients were transferred to the intensive care unit (ICU). They were weaned from the ventilator as soon as they were normothermic, hemodynamically stable (with no major bleeding) and had achieved adequate level of consciousness. They were transferred to the floor whenever they were fit for transfer.

The quantitative estimation of human S-100β in plasma samples was done by a enzyme-linked immunosorbent assay (ELISA) test based on the sandwich model enzyme-linked immunosorbent assay (Sangtec 100, Byk - Sangtec Diagnostica, Dietzenback, Germany).

S100β levels were evaluated from venous blood drawn at following time intervals: before induction of anesthesia (T1), after coming off CPB (T2); 12 h after aortic cross clamping, AOXC (T3) and 24 h after aortic cross clamping (T4). Hemodynamic indices (CI, SVRI, DO2I and mean arterial pressure,MAP) were measured at the same time intervals and a correlation between the enzyme levels and these indices was sought for as well.

Statistical methods

All the statistical analyses were done using SAS (Statistical Analysis System) software (MIXED version 9.1.3, Cary, North Carolina, USA). Patient characteristics among the groups were compared using one-way ANOVA (analysis of variance). Repeated measure analysis of covariance (ANCOVA) was performed to analyze the S100 levels and hemodynamic parameters (CI, SVRI, MAP and DO2I). Factors in this model included the treatment group (Group Sevo, Iso, and TIVA), time (post-CPB, 12 and 24 h postaortic cross clamp) and the group × time interaction. Preinduction values were considered as a covariate in the model. Due to the presence of overall significant treatment group or time interaction effects, data were analyzed at each point of time using one way ANCOVA. Follow-up group comparisons were done using post hoc Fisher LSD t-test. Significant values at 1% and 5% alpha levels of ANCOVA analyses were annotated in the data summary table with mean and standard deviation [Table 1]. Multiple regression analyses were performed at each time interval within the treatment group to assess the correlation of S100 with hemodynamic parameters.
Table 1: Comparison of hemodynamic indices among three groups

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   Results Top

The mean age, height, weight, body mass index, LV ejection fraction, number of grafts, CPB, and aortic cross clamp time were similar in the three groups [Table 2]. Significant decreases were noted in S100 levels at all postdose hours in the Sevo group, as compared to the TIVA group, and at 12 and 24 h postaortic cross clamp (AOXC), in comparison to the Iso group [Table 3]. Comparing the Iso group with the TIVA group, the S100 levels were lower in the Iso group only at 24 h post-AOXC. At all postdose hours, systemic vascular resistance index (SVRI) values in the Sevo group were significantly less as compared to the group TIVA. Immediately post-CPB and at 12 h post-AOXC SVRI was lowest in the Iso group in comparison to Sevo and TIVA groups [Table 1]. Among all the groups, at 24 h post-AOXC SVRI was lowest in the Sevo group. Significant increases were noted at all postdose hours in both groups (Sevo and Iso) for delivered oxygen index (DO2I), when compared to the TIVA group. No significant difference in DO2I values was noted between Sevo and Iso groups. Cardiac index (CI) was significantly high at 24 h post-AOXC in the Sevo group, as compared to the TIVA group and was significantly less during the period immediately following CPB in comparison to the Iso group. Higher CI values were noted at post-CPB and 24 h post-AOXC in the Iso group as compared to the TIVA group. No significant difference was noted in mean arterial pressures, at all time intervals, among all the three groups [Table 1]. On multiple regression analyses, no correlation was found between S100 levels and any hemodynamic parameter (SVRI, CI, MAP, and DO2I), within individual group.
Table 2: Patients demographic characteristics

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Table 3: Comparison of perioperative S100 levels in the three groups

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   Discussion Top

The presence of S100 in serum indicates cellular brain injury and damage to the blood-brain barrier. [14],[15] Astroglial cells are the most common cells found in brain. The test system used in the present study detects the β subunit of S100 (found in astroglial and Schwann cells) and is specific for astroglial injury. Brain specificity is not improved by individual assay of the two dimer subgroups that constitute S100 β, hence in our study only S100 β levels were measured. [16]

Serum S100 β levels have been correlated with the age of patient, duration of CPB, aortic cross clamping time, duration of deep hypothermic circulatory arrest, renal dysfunction, and preoperative cerebrovascular complications. [4] Therefore, these confounding factors were considered and eliminated during the study [Table 2]. Also, patients with LBBB were excluded as there have been occasional case reports of complete heart block after central venous catheterization in patients with pre-existing LBBB. [17] S100 levels may have wide variations among individuals. Johnsson et al.[5] in their study on 607 patients found that 6.9% patients had levels <0.2 μg/L (the detection level for test) and 93.1% patients had elevated levels at the baseline. In our study, the baseline values of S100 at T0 (baseline) were in ranges of 0.04-0.06 μg/L which is consistent with the observation of Johnson and coworkers. However, the standard deviation is more than mean values in all the three groups because of the fact that a wide range of patients aging up to 65 years was included in the cohort. It has been well proven that younger patients (mean age 59.6 ± 12 years vs. 66.1 ± 10 years) having shorter perfusion times (62.1 ± 30 min vs. 76.8 ± 26 min) have less release of S100 in circulation, often the marker going undetected. [5] The similarity of release between on-pump (when a cell saving system is used) and off-pump surgery suggests that CPB per se does not release S100 β. The mean t1/2 of S100 protein, in patients undergoing CABG, has been calculated to be 7.2 ±14.9 h post-CPB. [5] Therefore, the study was structured so as to determine the levels of S100 β at 12 and 24 h after termination of CPB.

Cardiac surgery causes an increase of serum S100 β after less than an hour (i.e. before cannulation), a further increase to maximum blood levels at the end of CPB, and thereafter it rapidly declines, although occasionally with a late rise. [4] In our study, a similar pattern was observed in all the groups where the level of S100 β was maximum just after CPB and which gradually declined over next 24 h [Table 3]. Wang et al.[18] compared patients undergoing off-pump CABG and on-pump CABG and found that serum S-100 β protein was lowest immediately before induction of anesthesia and significantly increased before and after CPB, then declined by the first postoperative day in both groups. On the day after surgery, S-100 β protein levels were similar between groups, but were higher than the baseline within each group. They concluded that these findings may have implications for anesthesiologic care during the total course of cardiac surgery. Similarly, in our study although the levels decreased on the first postoperative day but were higher than baseline levels. The rise in level of S100 β was less in patients who received volatile anesthetics in comparison to patients who underwent TIVA. Also, patients receiving sevoflurane had significantly lower levels of S100 β than those who underwent isoflurane anesthesia at all postdose hours. The less rise of S100 levels with volatile anesthetic agents (much less with sevoflurane) can be explained on the basis of cerebral preconditioning. Neuroprotection secondary to preconditioning with isoflurane has been shown to be dose-dependent and mediated by mitochondrial K ATP channels. [19] Sevoflurane, in contrast to isoflurane, mediates neuronal preconditioning not only with mitochondrial K ATP channels, [11] but also with enhanced phosphorylated cyclic adenosine monophosphate response element binding protein signaling, [20] by downregulating tumor necrosis factor-α, interleukin-1 β protein and messenger RNA expression, [21] and decrease in reactive oxygen species generation during re-oxygenation. [22]

DO2I was significantly higher in patients receiving volatile anesthetic agents than those undergoing TIVA. This might be secondary to decreased SVRI, compared to the TIVA group, observed in volatile anesthetic agent groups thereby leading to enhanced perfusion and better tissue oxygen delivery. Although there was no statistically significant difference in DO2I values between sevoflurane and isoflurane groups still the S100 levels were much less in the sevoflurane group emphasizing that there might be a different mechanism of neuroprotection than mitochondrial K ATP channels. On multiple regression analysis, no correlation was found between S100 levels and any hemodynamic parameter (SVRI, CI, MAP, and DO2I), within individual group. This observation again suggests that S100 β levels may increase even in the presence of normal hemodynamics irrespective of the anesthetic technique.


A wide range of patients aging up to 65 years were included in this study. Therefore, the S100β values were distributed over a wide range and were reflected as standard deviation being more than the mean value of S100β in all three groups.

   Conclusion Top

The increase in the S100β levels is significantly diminished during sevoflurane use in contrast to isoflurane and TIVA. The hemodynamic changes in the first 24 h do not seem to be influenced by these interventions.

   References Top

1.Grocott HP, Stafford-Smith M. Organ protection during cardiopulmonary bypass. In: Kaplan JA, Reich DL, Lake CL, Konstadt SN, editors. Kaplan's Cardiac Anesthesia. 5 th ed. Philadelphia: Elsevier Inc; 2006. p. 985.  Back to cited text no. 1
2.Wandschneider W, Thalmann M, Trampitsch E, Ziervogel G, Kobinia G. Off-Pump coronary bypass operations significantly reduce s100 release: An indicator for less cerebral damage? Ann Thorac Surg 2000;70:1577-9.  Back to cited text no. 2
3.Mörtberg E, Zetterberg H, Nordmark J, Blennow K, Rosengren L, Rubertsson S. S-100B is superior to NSE, BDNF and GFAP in predicting outcome of resuscitation from cardiac arrest with hypothermia treatment. Resuscitation 2011;82:26-31.  Back to cited text no. 3
4.Ali MS, Harmer M, Vaughan R. Serum S100 protein as a marker of cerebral damage during cardiac surgery. Br J Anaesth 2000;85:287-98.  Back to cited text no. 4
5.Jonsson H, Johnsson P, Alling C, Westaby S, Blomquist S. Significance of serum S100 after coronary artery bypass grafting. Ann Thorac Surg 1998;65:1639-44.  Back to cited text no. 5
6.Lemaire SA, Bhama JK, Schmittling ZC, Oberwalder PJ, Köksoy C, Raskin SA, et al. S100ß correlates with neurologic complications after aortic operation using circulatory arrest. Ann Thorac Surg 2001;71:1913-9.  Back to cited text no. 6
7.Kaca-Ory´nska M, Tomasiuk R, Friedman A. Neuron-specific enolase and S 100B protein as predictors of outcome in ischaemic stroke. Neurol Neurochir Pol 2010;44:459-63.  Back to cited text no. 7
8.Wang H, Lu S, Yu Q, Liang W, Gao H, Li P, et al. Sevoflurane preconditioning confers neuroprotection via anti-inflammatory effects. Front Biosci (Elite Ed) 2011;3:604-15.  Back to cited text no. 8
9.McAuliffe JJ, Loepke AW, Miles L, Joseph B, Hughes E, Vorhees CV. Desflurane, isoflurane, and sevoflurane provide limited neuroprotection against neonatal hypoxia-ischemia in a delayed preconditioning paradigm. Anesthesiology 2009;111:533-46.  Back to cited text no. 9
10.Codaccioni JL, Velly LJ, Moubarik C, Bruder NJ, Pisano PS, Guillet BA. Sevoflurane preconditioning against focal cerebral ischemia: Inhibition of apoptosis in the face of transient improvement of neurological outcome. Anesthesiology 2009;110:1271-8.  Back to cited text no. 10
11.Adamczyk S, Robin E, Simerabet M, Kipnis E, Tavernier B, Vallet B, et al. Sevoflurane pre- and post-conditioning protect the brain via the mitochondrial K ATP channel . Br J Anaesth 2010;104:191-200.  Back to cited text no. 11
12.Zhang HP, Yuan LB, Zhao RN, Tong L, Ma R, Dong HL, Xiong L. Isoflurane preconditioning induces neuroprotection by attenuating ubiquitin-conjugated protein aggregation in a mouse model of transient global cerebral ischemia. Anesth Analg 2010;111:506-14.  Back to cited text no. 12
13.Kapinya KJ, Löwl D, Fütterer C, Maurer M, Waschke KF, Isaev NK, et al. Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent. Stroke 2002;33:1889-98.  Back to cited text no. 13
14.Hu J, Ferreira A, Van Eldik LJ. S100beta induces neuronal cell death through nitric oxide release from astrocytes. J Neurochem 1997;69:2294-301.  Back to cited text no. 14
15.Zimmer DB, Cornwall EH, Landar A, Song W. The S100 protein family: History, function, and expression. Brain Res Bull 1995;37:417-29.  Back to cited text no. 15
16.Anderson RE, Hansson LO, Nilsson O, Liska J, Settergren G, Vaage J. Increase in serum S100A1-B and S100BB during cardiac surgery arises from extracerebral sources. Ann Thorac Surg 2001;71:1512-7.  Back to cited text no. 16
17.Unnikrishnan D, Idris N, Varshneya N. Complete heart block during central venous catheter placement in a patient with pre-existing left bundle branch block. Br J Anaesth 2003;91:747-9.  Back to cited text no. 17
18.Wang K, Wu H, Fang S, Yang Y, Tseng AC. Serum S100b protein during coronary artery bypass graft surgery with or without cardiopulmonary bypass. Ann Thorac Surg 2005;80:1371-4.  Back to cited text no. 18
19.Xiong L, Zheng Y, Wu M, Hou L, Zhu Z, Zhang X, et al. Preconditioning with isoflurane produces dose-dependent neuroprotection via activation of adenosine triphosphate-regulated potassium channels after focal cerebral ischemia in rats. Anesth Analg 2003;96:233-7.   Back to cited text no. 19
20. Luo Y, Ma D, Leong E, Sanders RD, Yu B, Hossain M, et al. Xenon and sevoflurane protect against brain injury in a neonatal asphyxia model. Anesthesiology 2008;109:782-9.  Back to cited text no. 20
21.Ye Z, Guo Q, Wang E, Shi M, Pan Y. Sevoflurane preconditioning induced delayed neuroprotection against focal cerebral ischemia in rats. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2009;34:152-7.  Back to cited text no. 21
22.Canas PT, Velly LJ, Labrande CN, Guillet BA, Sautou-Miranda V, Masmejean FM, et al. Sevoflurane protects rat mixed cerebrocortical neuronal-glial cell cultures against transient oxygen-glucose deprivation; involvement of glutamate uptake and reactive oxygen species. Anesthesiology 2006;105:990-8.  Back to cited text no. 22

Correspondence Address:
Sarvesh Pal Singh
Room No 112, Doctors Hostel, Trauma Center, All India Institute of Medical Sciences, New Delhi - 110029
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.83998

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