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Ann Thorac Surg 2006;82:51-55
© 2006 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Randomized Controlled Trial of Pericardial Blood Processing With a Cell-Saving Device on Neurologic Markers in Elderly Patients Undergoing Coronary Artery Bypass Graft Surgery

¹ Department of Surgery, Biomedical Laboratory, Montreal Heart Institute, Montreal, Quebec, Canada
² Department of Anesthesiology, Biomedical Laboratory, Montreal Heart Institute, Montreal, Quebec, Canada

Accepted for publication February 22, 2006.

^_* Address correspondence to Dr Carrier, Department of Surgery, Montreal Heart Institute, 5000 Belanger St, Montreal, PQ H1T 1C8, Canada (Email: michel.carrier{at}icm-mhi.org).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.

	Abstract

Top Abstract Introduction Patients and Methods Results Comment References

 
BACKGROUND: Processing of pericardial shed blood with a cell-saving device was claimed to prevent lipid microembolization and to protect from neurocognitive dysfunction after cardiopulmonary bypass. The present study tested the hypothesis that processing of pericardial shed blood with a cell-saving device during cardiopulmonary bypass would significantly decrease serum levels of protein S100B, and improve brain oxygen saturation and neurologic outcome, all markers of brain injury in elderly patients.

METHODS: Forty patients, 65 years of age and older, undergoing coronary artery bypass graft with cardiopulmonary bypass, were prospectively randomly assigned to processing of pericardial shed blood with a cell-saving device or to conventional use of a standard closed venous reservoir where cardiotomy blood was collected and reinfused through the arterial circuit (control group). Serum in S100B was measured 30 minutes, 4 hours, 24 hours, and 48 hours after surgery. Near-infrared spectroscopy monitoring was performed during the procedure and the National Institutes of Health stroke scale was measured before surgery and at the time of discharge of the hospital.

RESULTS: Patients in the cell-saving device group averaged 72 ± 3 years of age and underwent 3.1 ± 0.7 coronary artery grafts with a mean of 62 ± 20 minutes of cardiopulmonary bypass time. Patients in the control group averaged 75 ± 4 years of age (p = 0.03) and underwent 3.3 ± 0.6 coronary artery grafts (p = 0.49) with a mean of 75 ± 25 minutes of cardiopulmonary bypass time (p = 0.12). The quantity of blood administered from the cell-saving device averaged 281 ± 162 mL per patient. Serum protein S100B levels averaged 0.06 ± 0.03 before surgery and 0.51 ± 0.23 µg/L 30 minutes after surgery in the cell-saving device patients compared with 0.076 ± 0.04 before surgery (p = 0.32) and 1.48 ± 0.66 (p < 0.0001) in the control patients. The near-infrared spectroscopy baseline mean value of left and right cortical region was 58% ± 12% and 55% ± 7% in the cell-saving device group versus 59% ± 7% and 53% ± 6% in the control group (p = 0.67 and 0.36), and no difference occurred over time in each group. The National Institutes of Health stroke score before and after surgery was similar in the two groups. There was one cerebrovascular complication in the control group (1 of 20, 5%) after surgery.

CONCLUSIONS: The difference between the two groups occurred 30 minutes after surgery, at which time serum levels of protein S100B were significantly higher in the control group compared with cell-saving device patients. Although use of the cell-saving device was not associated with higher brain oxygen saturation nor changes in the National Institutes of Health stroke score, it is associated with lesser release of nonspecific markers of brain injury in elderly patients.

	Introduction

Top Abstract Introduction Patients and Methods Results Comment References

 
Neurologic complications with transitory or permanent deficits remain a significant problem after coronary artery bypass graft (CABG) surgery. The incidence of type 1 neurologic events with stroke and transient or permanent deficit averages 3%, and the rate of type 2 event with deterioration of intellectual function and seizures occurs in a further 3% of patients after elective coronary bypass surgery [1]. Moreover, elderly patients are at higher risk for postoperative neurologic complications [2]. Although several approaches to decrease the incidence of the devastating stroke complications have been proposed, including off-pump surgery, aortic scanning, and single aortic cross-clamping, the rate of neurologic complications remains significant in large studies [3].

Several authors have suggested that direct reinfusion of shed mediastinal blood during cardiopulmonary bypass (CPB) was associated with lipid microembolization in the brain [4]. Therefore, processing of pericardial shed blood with a cell-saving device during CPB was claimed to prevent lipid microembolization and neurocognitive dysfunction after coronary artery bypass graft surgery [5].

Most studies on neurologic complications after cardiac surgery are based on overall clinical manifestations of neurologic events with a need for large groups of patients to study improvement in neurologic outcomes. Serum protein S100B has been proposed as a marker for brain injury [6] and near-infrared spectroscopy (NIRS) measuring brain oxygen saturation, a novel monitoring approach to cerebral perfusion during cardiac surgery [7] that can be used to detect and prevent neurologic complications after CABG surgery [7–9].

The objective of the present study was to evaluate the effect of pericardial blood processing with a cell-saving device during CPB on serum protein S100B release and cerebral oxygen saturation throughout surgery after elective CABG surgery in elderly patients.

	Patients and Methods

Top Abstract Introduction Patients and Methods Results Comment References

 
Between October 2003 and July 2004, 40 patients, 65 years of age and older undergoing elective CABG with CPB, were recruited for the study. The protocol was reviewed and approved by the Ethics Committee of the Research Center at the Montreal Heart Institute. Patients were prospectively randomly assigned into two groups after informed consent was obtained. Randomization was based on random numbers in a sealed card opened just before surgery by perfusionists.

In the operating room, usual monitoring was installed, including five-lead electrocardiogram, digital pulse oximeter, peripheral venous line, radial arterial line, central venous, pulmonary artery catheter, and transoesophageal echocardiography. Regional cerebral oxygen saturation was monitored using NIRS (INVOS 4100; Somanetics, Troy, Michigan). Near-infrared spectroscopy is based on the absorption of infrared light by biological tissues in a fashion similar to arterial saturometry. The device employs two wavelengths (730 and 805 nm) to measure changes in the oxygenation of hemoglobin. The device uses mathematical algorithms based on the modified Beer-Lambert law [10], subtracting the superficial signal from the total signal to give only the value of the deep signal. In this cortical region, 75% of the blood flow is assumed to be venous blood. Consequently, the final ScO₂ value results from the balance between O₂ supply and consumption. Electrodes are connected to a computerized screen, giving real-time graphical representation of the saturation of both brain hemispheres from data gathered every 10 seconds. The technique has also been validated against many other modalities of brain monitoring such as jugular saturometry [11, 12] and cerebral blood flow measurement [10].

Anesthesia was induced with an intravenous dose of 0.04 mg/kg midazolam and 1 µg/kg sufentanyl, and neuromuscular blockade was achieved with 0.07 mg/kg rocuronium. The patients were endotracheally intubated, and anesthesia was maintained with 1 µg · kg^-1 · h^-1 of sufentanyl, 0.04 mg · kg^-1 · h^-1 of midazolam, and 30 to 50 µg · kg^-1 min^-1 of propofol. Isoflurane was used as needed by the attending anesthesiologist.

Patients in the first group (cell-saving device group) underwent collection of the suctioned blood from the pericardial cavity to a hard-shell cardiotomy reservoir through a 33-µ filter and processing of pericardial blood through a cell-saving device (Cobe Laboratories, BRAT Systems, Lakewood, Colorado). The processed red blood cells were reinjected intravenously immediately after weaning from CPB.

Patients in the second group (control group) were subjected to a standard approach whereby the suctioned pericardial blood was forwarded from the field to a hard-shell reservoir, directly filtered (33-µ filter) to the venous reservoir, and reinfused through the arterial circuit (32-µ filter) throughout surgery. The CPB circuit was composed of nonheparin-coated hard-shell venous reservoir with roller pumps and membrane oxygenators.

A standard Hammersmith full-dose protocol of aprotinin (Bayer, Toronto, Ontario), 2 x 10⁶ kallikrein inhibitor units (KIU) in pump prime, 2 x 10⁶ KIU loading dose, followed by 0.5 x 10⁶ KIU/h was used in all patients of both groups. Each patient received 300 IU/kg porcine heparin to achieve an activated coagulation time (ACT) greater than 750 seconds. The ACT was measured at baseline, after heparinization, and every 30 minutes during CPB. The core temperature was allowed to drift to 33°C to 34°C. Heparin was reversed with 300 mg protamine sulfate and assessed by normalization of the ACT.

Blood samples for the measure of serum protein S100B were obtained immediately before surgery and 30 minutes, 4 hours, 24 hours, and 48 hours after surgery. Protein S100B was measured in the serum using an immunoassay technique (Elecsys S100B Immunoassay; Rocha Diagnostics, Montreal, Quebec). The cerebral oxygen saturation from NIRS was recorded every 30 seconds from the induction of anesthesia to the closure of the thorax. The mean, maximal, and minimal value was recorded for each hemisphere. The area under 50% saturation and the area below 75% of the baseline value was calculated using an Excel program (Microsoft, Seattle, Washington) previously described [9]. This value was selected as a reduction of 25% under the baseline value or saturation below 50% has been proposed as desirable lower limits to justify an intervention [8, 9, 13]. Transoesophageal echocardiography was used to grade atherosclerosis of the aortic arch immediately before surgery. All complications during and after surgery were monitored. The National Institutes of Health (NIH) stroke scale was measured before surgery and at the time of discharge of the hospital [14].

The primary endpoint of the study was the serum level of protein S100B after surgery, which was suggested to decrease from 1.51 ± 0.64 µg/L to 0.9 (one standard deviation) in the cell-saving device group of patients after surgery [15]. Secondary endpoints were cerebral saturation assessed with the NIRS approach and the NIH stroke scale. The analysis was planned with a statistical power of 80% and an alpha level of 5% with a total of 40 patients.

The data are presented as the mean and standard deviation. The difference between groups was analyzed using Student's t test or Fisher's exact test. Analysis of variance with two factors of classification (groups and repeated measures in time) was used to study changes in serum protein S100B after surgery. Statistical significance was established at p values less than 0.05.

	Results

Top Abstract Introduction Patients and Methods Results Comment References

 
Patient Characteristics
Patient's age in the cell-saving device group averaged 72 ± 3 years; they underwent 3.1 ± 0.7 coronary artery grafts with a mean of 62 ± 20 minutes of CPB time. Patient's age in the control group averaged 75 ± 4 years (p = 0.03); they underwent 3.3 ± 0.6 coronary artery grafts (p = 0.49) with a mean of 75 ± 25 minutes of CPB time (p = 0.12; Tables 1 and 2). Seven patients in each group showed grade 4 and 5 atherosclerosis of the aortic arch (p = 0.8).

All blood suctioned from the pericardium was directly filtered to the hard-shell venous reservoir and injected through the arterial line in patients of the control group.

Blood loss after surgery averaged 606 ± 316 mL in the cell-saving device group compared with 862 ± 865 mL in the control group (p = 0.23). A total of 1.4 ± 1.85 unit of packed red blood cells was administered to cell-saving device patients during and after surgery compared with 1.1 ± 1.7 unit in control patients (p = 0.5).

Release of Protein S100B, Cerebral Oximetry, and Neurologic Outcome
Serum protein S100B levels averaged 0.06 ± 0.03 before surgery, 0.51 ± 0.23, 0.27 ± 0.12, 0.19 ± 0.08, and 0.14 ± 0.06 µg/L 30 minutes, 4 hours, 24 hours, and 48 hours, respectively, after surgery in the cell-saving device patients compared with 0.076 ± 0.04 before surgery (p = 0.32) and 1.48 ± 0.66 (p < 0.0001 compared with cell-saving device group), 0.35 ± 0.21 (p = 0.149), 0.19 ± 0.08 (p = 0.896), and 0.14 ± 0.06 µg/L (p = 0.712) in the control group (Fig 1). The difference between preoperative baseline values and all postoperative values was statistically significant in the two groups (p = 0.001). The difference between the two groups was significant 30 minutes after surgery (p < 0.0001).

View larger version (14K): [in this window] [in a new window]   Fig 1. Levels of protein S100 before and after surgery. All postoperative levels are higher when compared with preoperative baseline values (p < 0.05), and protein S100B level was significantly higher in the control group of patients 30 minutes after coronary artery bypass graft surgery (p < 0.0001). (h = hours; min = minutes; Pre-op = preoperative.)

	Comment

Top Abstract Introduction Patients and Methods Results Comment References

 
The present study shows that protein S100B, a nonspecific marker of brain damage, increases significantly after CABG and remains higher than preoperative values throughout the first 48 hours after surgery. However, this increase in the level of protein S100B was not associated with any difference in brain oxygen saturation, nor with evidence of neurologic complications. Patients of the cell-saving device group had a significantly lower levels of protein S100B 30 minutes after CABG compared with patients of the control group, but no difference remains between the two groups at 4, 24, and 48 hours after surgery. Moreover, 3 patients of the cell-saving device group had a previous history of stroke before surgery with no recurrence after CABG compared with 1 stroke complication in the control group without past history of stroke. The former suggesting that a reduction in lipid microemboli could be protective against focal neurologic ischemia.

Although the measure of protein S100B was suggested to reflect neuronal damage after surgery [15, 16], several authors have shown that extracerebral sources of protein S100B could explain in part the increase of serum levels after CABG [17]. Anderson and associates [18] and Jonsson and associates [19] have shown that the use of a cell-saving device to process pericardial blood decreases the serum levels of protein S100B after CABG. The present study showed higher serum levels of protein S100B after surgery compared with preoperative baseline values in patients of both groups and higher serum levels of protein S 100B 30 minutes after surgery in patients in whom pericardial shed blood was directly reinjected through the aortic canula, a confirmation of previous findings.

Advanced age is an important risk factor for neurologic and cognitive deficits after heart surgery [2]. With increased life expectancy, the prevalence of these complications will probably rise further. Intraoperative cerebral desaturation has been associated with higher protein S100B [20] and early postoperative neuropsychological dysfunction [9], and active correction of abnormal brain saturation values may improve morbidity and mortality [21].

Rasmussen and associates [22], Westaby and coworkers [23], Lloyd and associates [6], and Robson and colleagues [20] were unable to show a clear relationship between serum levels of protein S100B and neuropsychologic dysfunction after CABG. Aldea and associates [24] showed that the use of cell-saving devices to process red blood cells from pericardial shed blood decreased the overall inflammatory reaction including the serum levels of protein S100B. Contrary to overt brain damage, serum levels of protein S100B can also reflect disruption of the blood-brain barrier and inflammation during CPB, as suggested by a small but significant increase in serum levels after surgery in patients in whom cell-saving devices were used. In the Robson experience, there was no correlation between the 3-month neurocognitive assessment, the level of protein S100B, and intermittent jugular venous brain saturation [20] in 98 patients after CABG. The main determinant of neurologic outcome at 3 months was preoperative neurologic score in the latter study. However, brain saturation was monitored using intermittent jugular venous blood samples and not continuous NIRS. Anderson and associates [25] measured protein S100B in 27 patients after CABG, in17 of whom a cell-saving device was used. They also observed higher levels of S100B protein in patients without cell saving of the pericardial shed blood during surgery. Our study, however, correlates continuous NIRS monitoring and formal neurologic examination with protein S100B measurements.

There are several limitations to the present study. First, it represents a pilot study and the number of patients was small; a larger population would have been required to detect clinical differences in neurologic complication. The extent to which brain desaturation measured with NIRS can predict neurocognitive dysfunction complications is controversial [11]. Subtle neurologic signs are much more common and can occur in as many as 17% to 23% [20, 26]. These abnormalities can be detected using the NIH stroke scale, which has been validated as a prognostic instrument in predicting functional outcome [14]. Both brain saturation values and stroke scale values were similar in the two groups of the present study. Some authors have also suggested that protein S100B measured 6 to 8 hours after surgery bears the most significant prognostic value [22] in terms of neurologic complications. We measured serum levels for as long as 48 hours after surgery and only observed a significant difference 30 minutes after surgery in the control group, suggesting an extracerebral source of protein S100B or an increased inflammatory reaction with transient disruption of the blood brain barrier as the cause of the increase value in S100B protein [22, 25].

In summary, the release of protein S100B is increased after CABG compared with preoperative baseline values in all patients, and it is reduced in patients with the use of a cell-saving device to process pericardial shed blood. No correlation was observed with brain oximetry level and postoperative neurologic complications in elderly patients undergoing CABG. Although elevated S100B protein levels may be due to the presence of noncerebral sources or to transient disruption of the blood-brain barrier with inflammation, the cell-saving device was effective in decreasing serum levels of this nonspecific marker of brain injury in elderly patients. Further studies including neuropsychological testing should assess the exact role of a cell-saving device in processing pericardial shed blood during CABG, especially in elderly patients.

	References

Top Abstract Introduction Patients and Methods Results Comment References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michel Carrier Louis P. Perrault Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Carrier, M. Articles by Perrault, L. P. Search for Related Content PubMed PubMed Citation Articles by Carrier, M. Articles by Perrault, L. P. Related Collections Cerebral protection