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Ann Thorac Surg 1998;65:1639-1644
© 1998 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Significance of Serum S100 Release After Coronary Artery Bypass Grafting

^a Division of Cardiothoracic Surgery, Department of Heart-Lung Diseases, University Hospital MAS, Malmö, Sweden

Accepted for publication January 26, 1998.

Address reprint requests to Dr Johnsson, Division of Cardiothoracic Surgery, Lund University Hospital, SE-221 85 Lund, Sweden
e-mail: (pelle.johnsson{at}medforsk.mas.lu.se)

	Abstract

Top Abstract Introduction Material and methods Results Comment References

 
Background. S100 protein has been suggested to be a serum marker for cerebral complications after cardiac operation and extracorporeal circulation. The aim of this study was to characterize the S100 release pattern after extracorporeal circulation in 515 consecutive patients undergoing coronary artery bypass grafting.

Methods. Clinical variables and outcome were prospectively registered. The cerebral outcome was determined by clinical examination. S100 was measured at the end of extracorporeal circulation, and after 5, 15, and 48 hours.

Results. After operation, 13 patients had stroke, 12 had delayed awakening, and 17 had encephalopathy. Early S100 release, immediately after extracorporeal circulation, was associated with age and perfusion time, but not with cerebral outcome. However, S100 release after 5 to 48 hours was associated with cerebral complications and risk factors for such outcome. Patients with stroke had higher S100 levels after 15 to 48 hours. A subset of patients with renal failure had overall higher S100 levels at 5 hours.

Conclusions. Early and late S100 release indicate different mechanisms for release and emphasizes the potential power of this new biochemical marker for cerebral damage.

	Introduction

Top Abstract Introduction Material and methods Results Comment References

 
Cerebral injury persists as the predominant comorbidity after cardiopulmonary bypass (CPB). The incidence of stroke is 1% to 5% [1–4], and early subtle cognitive dysfunction occurs in up to 70% of patients [5]. The pathogenesis of these problems remains unclear, but may involve both surgical and extracorporeal perfusion techniques [2, 3]. Increasing knowledge of cerebral physiology and mechanisms of cellular damage during CPB has resulted in developments in biocompatibility, oxygenator design, and pump technology, and has increased the surgeon’s awareness of potential hazards such as the atherosclerotic ascending aorta [2, 3]. To date, the diagnosis of cerebral injury has relied on clinical neurologic examination, computed tomography, or magnetic resonance imaging. However, these methods may not be available for patients soon after a cardiac operation. The patient may be unconscious, hemodynamically unstable, sedated, or treated in ventilator, and therefore unable to cooperate in the clinical investigation. Therefore, a biochemical serum marker to assist in the detection of cerebral injury is potentially useful.

S100 protein has been suggested as a promising marker for cerebral injury during cardiac operation [6–10]. The protein is small (21-kD) and calcium binding, and it exists in several isoforms [11]. The S100-ß and -ßß forms are predominantly present in astroglial or microglial cells, and are considered to be highly specific for the brain [11]. The elimination of the protein is considered identical to that of other small proteins like ß₂-microglobulin (eg, through glomerular filtration, reabsorption, and degradation in the proximal tubuli) [12]. S100 protein is normally not present in serum, but appears after stroke, subarachnoidal hemorrhage, head injury, or extracorporeal circulation [7, 8, 13–16]. The purpose of this study was to characterize S100 protein release after coronary artery bypass grafting in a large series of consecutive patients.

	Material and methods

Top Abstract Introduction Material and methods Results Comment References

 
Study design
The patient population comprised 607 consecutive patients who underwent coronary artery bypass grafting during a 21-month period at the University Hospital MAS, Malmö, Sweden.

Blood for analysis of S100 protein levels was taken routinely from each patient at the end of extracorporeal circulation (T0), 5 (T5), 15 (T15), and 48 (T48) hours thereafter. A special protocol was used for the detailed prospective registration of intraoperative clinical observations including a palpatory finding of an arteriosclerotic ascending aorta, duration of perfusion, myocardial ischemia time, and lowest body temperature during extracorporeal circulation. A previous history of stroke, transient ischemic attack, reversible ischemic neurologic disorder, or carotid artery disease was also recorded.

All patients underwent neurologic assessment preoperatively and in the intensive care unit after operation by experienced cardiac anesthesiologists or in the ward by experienced cardiac surgeons. The assessment started just a few hours after the operation and was repeated during the stay in the ward. The patients were classified as either having a normal outcome, delayed awakening, encephalopathy, or stroke. Delayed awakening was defined as a prolonged unconsciousness that could not be explained by the doses of administered sedatives or opiates. Encephalopathy was defined as prolonged postoperative cerebral dysfunction, including confusion, depression, or other obvious alterations in a patient’s behavior, but without focal neurologic findings. Stroke was defined in accordance with the NINCDS ad hoc committee classification [17], and confirmed with computed tomographic scan or magnetic resonance imaging. The evaluation of each patient allowed allocation to only one category, which would be the most protracted one. For instance, if a patient with delayed awakening also had a stroke, he or she would be assigned to the more serious stroke group.

As renal impairment may delay the elimination of S100 from the circulation, patients with known preoperative renal insufficiency (serum/creatinine level >2.2 mg/dL) were analyzed separately.

S100 protein analysis
Blood samples, both arterial and venous samples, were cooled and centrifuged within 5 hours. All samples were measured by a monoclonal two-site immunoradiometric assay (Sangtec 100; AB Sangtec Medical, Bromma, Sweden). The method is defined by three monoclonal antibodies, SMST 12, SMSK 25, and SMSK 28. The serum samples were diluted with phosphate buffer and incubated with a plastic bead coated with monoclonal S100 antibodies. During incubation S100 is bound to the antibody-coated bead. After 1 hour of incubation these beads were washed and incubated with iodine-125-labeled anti-S100 antibody. After a 2-hour incubation and subsequent washing, the amount of radioactive label bound to immobilized S100 was measured by gamma counter. The precision was 7.0% coefficient of variation and sensitivity was 0.2 µg/L.

Anesthesia
Anesthesia was induced with midazolam (Dormicum; Roche, Basel, Switzerland) or thiopentone (Pentothal; Abbott Laboratories, Abbott Park, IL). Subsequently, it was maintained with either fentanyl (Leptanal; Janssen Pharmaceutica, Beerse, Belgian), midazolam, a combination of propofol (Diprivan; Zeneca Ltd, Cheshire, England) and isoflurane, or sevoflourane (both Abbott Laboratories). Nitrous oxide (Aga Industries, Stockholm, Sweden) was used before extracorporeal circulation but not during or after extracorporeal circulation.

Surgical technique
Distal coronary anastomoses were performed during a single period of aortic cross-clamping. A tangential occluder replaced the cross-clamp during the proximal anastomosis. Antegrade cold St. Thomas crystalloid cardioplegia (Cardioplegi; Pharmacia-Upjohn, Uppsala, Sweden) was used for myocardial protection.

Perfusion technique
Perfusion was performed with roller pump (Cobe Industries, Denver, CO) and a membrane oxygenator (Cobe CML or Duo, both Cobe Industries). All circuits contained a heparin-coated 40-µm arterial filter (Cobe Sence, Cobe Industries). The circuit was primed with 1,000 to 1,500 mL of Ringer’s lactate (Pharmacia-Upjohn), 250 mL of 15% mannitol (Pharmacia-Upjohn), and 75 mmol Addex tromethamine. Perfusion flow was nonpulsatile with a flow rate of 2.4 L · min^-1 · m^-2 at normothermia. Systematic cooling to approximately 32°C was used. Heparin (3 mg/kg body weight) was given before cannulation and reversed with a corresponding dose of protamine sulfate at decannulation. The mean arterial pressure was maintained above 40 to 50 mm Hg with intermittent norepinephrine if needed. Hemofiltration was performed when indicated to avoid congestion.

Statistical analysis
All results were analyzed with Statistica version 5.0 for PC (Statsoft, Tulsa, OK). Results are presented as mean ± one standard deviation, unless otherwise stated. For comparisons of means continuous variables were analyzed with unpaired Student’s t test if the sample was large or had a normal distribution. Otherwise a nonparametric test were used (Mann-Whitney). Regression analysis was performed with the least square method with a case-wise deletion of missing data. Unless otherwise stated results were considered significant if the p value was less than 0.05.

	Results

Top Abstract Introduction Material and methods Results Comment References

 
Of the 607 eligible patients in this study, 92 patients were not included in the analysis due to incomplete sampling, leaving a total of 515 patients for the final evaluation. The excluded patients did not differ with regard to risk factors, outcome, or S100 levels. The mean age of studied patients was 65.9 ± 10 years (range, 31 to 86 years), with a male preponderance of 78% (396 versus 119).

Forty-two patients had a previous history of stroke or transient ischemic attack/reversible ischemic neurologic disorder, and in 53 patients palpation of the ascending aorta revealed arteriosclerosis of the ascending aorta. Mean perfusion time was 76 ± 26 minutes and the aortic cross-clamp time 37 ± 14 minutes.

Patient outcome
Of the 515 patients studied, 473 (92%) had an uneventful recovery without any clinical detectable brain-related complication. Twelve patients (2.3%) had delayed awakening after operation. Seventeen patients (3.3%) had encephalopathy and 13 patients (2.5%) had stroke. Of the patients who developed stroke, 10 were minor and 3 were extensive, with severe neurologic dysfunction. One of the patients with a minor stroke died from cardiac causes, but the other 9 had a good recovery. The overall 30-day mortality was 1.0% (6 of 607 patients). Three groups, based on presence of risk factors, such as arteriosclerotic ascending aorta, or a history of cerebrovascular accident/transient ischemic attack, or both, were formed. The neurologic outcome by preoperative risk group is presented in Figure 1. In the 12 patients with renal insufficiency, 3 had a delayed awakening, and the others had an uneventful outcome.

View larger version (37K): [in this window] [in a new window]   Fig 1. Outcome by preoperative risk. The odds ratio for an adverse cerebral outcome was calculated in patients with risk factors (AAA = arteriosclerotic ascending aorta, history of cerebrovascular accident/transient ischemic attack [CVI/TIA]), and a group consisting of patients with both of these risk factors, compared with patients without such risk factors. Good outcome is defined as the absence of delayed awakening, encephalopathy, or stroke, and bad outcome as the presence of one of these factors. Odds ratios are presented with a 95% confidence interval (CI). (*Statistical significance.)

View larger version (26K): [in this window] [in a new window]   Fig 2. Box plot of the S100 protein release in the "normal population" (ie, patients undergoing coronary artery bypass grafting without clinical signs of cerebral dysfunction postoperatively). Outliers are defined as 1.5 times interquartile range and extreme outliers as three times interquartile range. (T0 = immediately after termination of extracorporeal circulation; T5 = 5 hours after T0; T15 = 15 hours after T0; T48 = 48 hours after T0.)

View larger version (37K): [in this window] [in a new window]   Fig 3. The relation between perfusion time and S100 protein release at the end of extracorporeal circulation in patients without cerebral complications described by a linear regression analysis (r = 0.31; p = 0.0001). Dotted line indicates the 95% confidence interval for the equation.

S100 protein elimination rate
The biological half-life of the S100 protein during the first 5 hours was calculated for each patient using the following formula: . In 86 patients, the S100 protein concentrations were either <0.2 µg/L at both T0 and T5, or increased during this interval, making calculation of T_1/2 meaningless. In the remaining patients the T_1/2 had a wide range (0.7 to 150 hours). The mean T_1/2 in these patients was 7.2 ± 14.9 hours, median was 3.5 hours.

Clinical variables and S100
Patients with a previous history of stroke or transient ischemic attack/reversible ischemic neurologic disorder had higher S100 protein levels at T0 (3.3 ± 2.4 µg/L versus 2.2 ± 1.8 µg/L; p < 0.001), whereas patients with carotid disease did not differ from patients without. Those with an arteriosclerosis of the ascending aorta had increased levels at both T0, T5, and T48 (3.4 ± 2.8 µg/L, 1.8 ± 1.8 µg/L, and 0.5 ± 1.2 µg/L versus 2.1 ± 1.8 µg/L, 1.0 ± 1.1 µg/L, and 0.23 ± 0.18 µg/L, respectively; p > 0.00001). Both older age and prolonged duration of perfusion during CPB correlated with levels of S100 protein at T0, but the correlation was weak (r 0.3) for both variables (Figs 3, 4). When entered into multiple regression analysis, these two variables only accounted for one-sixth of the variation of the S100 protein level (r = 0.39; p < 0.0001). At T5 and T15 correlation between age and S100 protein levels was still significant, however negligible.

View larger version (40K): [in this window] [in a new window]   Fig 4. The relation between patient age and S100 protein release at the end of extracorporeal circulation in patients without cerebral complications described by a linear regression analysis (r = 0.29; p = 0.0001). Dotted line indicates the 95% confidence interval for the equation.

View larger version (24K): [in this window] [in a new window]   Fig 5. The median S100 protein release for patients with stroke (dotted line) compared to the patients without any clinical signs of brain dysfunction (ie, "the normal population," solid line). Sampling times are at end of extracorporeal circulation (T0) and 5, 15, and 48 hours thereafter (T5, T15, and T48).

Clinical variables, such as age, duration of perfusion, quality of the ascending aorta, delayed awakening, encephalopathy, stroke, or renal insufficiency, were entered into a multiple regression analysis to determine the association of each with the levels of S100 protein. Predictors of early release of S100 protein were age, duration of perfusion, history of stroke, transient ischemic attack/reversible ischemic neurologic disorder, and arteriosclerotic ascending aorta. Predictors for late release were stroke, delayed awakening, and arteriosclerotic aorta ascendens. Renal insufficiency affected the S100 levels only at T5 (Table 1).

	Comment

Top Abstract Introduction Material and methods Results Comment References

The great variation in S100 levels in patients with an uneventful neurologic outcome can only be explained in part by variables, such as age or perfusion time. Different distribution in age and duration of CPB can also help to explain the contradictory findings in earlier studies by Westaby [7] and Blomquist [10] and their colleagues regarding the association between postoperative S100 levels and perfusion time as these studies were on small groups of patients. Patients with degenerative brain disorders, such as Alzheimer’s disease, are known to have higher intracerebral S100 levels [18]. Preexisting cerebrovascular disease with a past history of stroke or transient ischemic attack/reversible ischemic neurologic disorder, or the presence of an atheromatous aorta, may also be associated with subclinical cerebral pathology, which predisposes to early S100 release. The present study suggests that a susceptible or previously injured brain has a more pronounced S100 release after extracorporeal circulation.

In this series, primary perioperative cerebral injury was not reflected by an early (0 to 5 hours) increase in S100 protein levels. However, patients with perioperative stroke had elevated serum levels of S100 later in the postoperative course (after 15 hours). The spectrum of values in stroke patients probably reflects the differing extent of injured brain in different patients or a considerable temporal variation in the evolution of ischemic brain injury and, therefore, a variation of S100 levels with time. As patients with uneventful clinical outcome occasionally had elevated levels of S100, this may be interpreted as evidence of subclinical cerebral injury. Using magnetic resonance imaging, cerebral pathology has been documented in 30% of patients without clinical signs after coronary artery bypass grafting with CPB [19]. We found elevated serum levels of S100 in 48% of patients at T15 and 13% at T48. This possibly reflects the somewhat alarming magnetic resonance imaging findings recently demonstrated in patients immediately after CPB, in whom we are subsequently unable to detect changes by neurologic examination. In stroke, it is the location rather than the volume of infarcted brain that determines the clinical outcome of a particular lesion.

When considering the nature and significance of S100 protein release, one must also take into account the physiology of the blood–brain barrier. Unless there is an unsuspected pathway for the leak of S100 into the blood, the integrity of the blood–brain barrier must be affected. It is conceivable that early S100 release occurs through "wash out" from the capillaries when pulsatile cerebral blood flow occurs after the return of cardiac action to replace the linear blood flow generated by the roller pump [20].

It is notable that serum S100 protein levels were higher in patients with renal impairment at the 5-hour sampling point. S100 is believed to be eliminated through glomerular filtration and degradation in the proximal tubules. Therefore, patients with impaired renal function may have higher S100 levels through impaired elimination from serum. In particular, this mechanism could provide elevated levels of S100 after prolonged perfusions by further depressing renal function.

Although we did not perform detailed prospective neuropsychologic studies and the sampling times were arbitrarily chosen, it may be concluded that S100 levels were associated to adverse cerebral outcome and to several well-known risk factors for brain injury after CPB. Serial measurements of S100 with identification of an early or late release pattern may provide the opportunity for more accurate diagnosis of cerebral injury after CPB in the future.

	References

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