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Ann Thorac Surg 2001;72:1926-1932
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Cardiopulmonary bypass affects cognitive brain function after coronary artery bypass grafting

^a Department of Cardiothoracic Surgery, Vienna General Hospital, Vienna, Austria

Accepted for publication August 2, 2001.

* Address reprint requests to Dr Grimm, Department of Cardiothoracic Surgery, Vienna General Hospital, Waehringer Guertel 18-20, A-1090 Vienna, Austria
e-mail: michael.grimm{at}akh-wien.ac.at

	Abstract

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Background. The causes for cognitive impairment after coronary artery bypass grafting (CABG) have long been a topic for debate.

Methods. We prospectively followed 308 consecutive, unselected survivors of CABG at our institution. In addition to determination of clinical measurements, cognitive brain function was measured objectively by P300 auditory-evoked potentials before CABG, at 7-day and at 4-month follow-up. Standard psychometric tests (Trail Making Test A, Mini Mental State Examination) were also performed.

Results. At 7-day follow-up cognitive P300 auditory-evoked potentials were significantly impaired compared with preoperative levels (peak latencies: 376 ± 40 ms versus 366 ± 37 ms, p = 0.0001). P300 measurements were almost normalized at 4-month follow-up (peak latencies: 369 ± 33 ms, p = NS versus preoperative). Standard psychometric tests failed to detect this subclinical cognitive impairment. Multiple regression analysis revealed that use of cardiopulmonary bypass was the only independent predictor of impaired cognitive brain function at 7-day (p < 0.0001) and 4-month follow-up (p = 0.0008). The presence of diabetes mellitus (p = 0.0135) or concomitant repair of significant carotid artery stenosis (p = 0.0049) was predictive of late improvement of cognitive brain function at 4-month follow-up.

Conclusions. Objective cognitive P300 auditory-evoked potential measurements demonstrate that the use of cardiopulmonary bypass is the only predictor of short- and long-term cognitive brain dysfunction after CABG. Interestingly, the presence of diabetes mellitus and concomitant repair of a significant carotid artery stenosis were predictive for long-term cognitive benefit.

	Introduction

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Impairment of cognitive brain function is frequently associated with coronary artery bypass grafting (CABG). The perioperative level of cognitive brain dysfunction after CABG has been shown to be predictive of long-term cognitive brain function up to 5 years after operation, markedly affecting the rehabilitation process, work performance, and quality of life [1, 2]. By means of standard psychometric testing numerous studies have shown that the incidence of cognitive brain dysfunction after CABG may range from 20% through 80% [1–4]. This wide variability may be related to different sensitivities of the test batteries used to assess cognitive brain function. Because standard psychometric tests are adversely affected by various biases, these findings need to be confirmed by objective measures.

P300 cognitive auditory-evoked potentials are a highly sensitive and reproducible tool for evaluation of cognitive function in various neurologic, metabolic, or hemodynamic disorders [5–10]. Evoked potentials are stable sequences of negative and positive electroencephalography (EEG) peaks after a stimulus within a period of several hundred milliseconds. P300 event-related potentials are late positive cortical deflections occurring after certain cognitive tasks [11]. They objectively reflect important aspects of neurocognitive function. P300 latency increases with age and is a neuropsychological correlate of information processing, such as stimulus evaluation, alertness, and memory updating [11]. Cognitive P300 auditory-evoked potential measurement is an objective tool related to information and cognitive processing that allows quantification of impaired cognitive function [5, 6, 12]. The use of the P300 technique has proved to be even more sensitive than EEG and standard psychometric tests for detecting subclinical impairment of cognitive brain function [5, 9, 13].

The aim of this prospective study was to determine predictors of individual changes of cognitive brain function after CABG by means of objective cognitive P300 auditory-evoked potential measurements.

	Patients and methods

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Patients
A total of 308 consecutive, unselected survivors of either elective or urgent CABG at our institution entered the study. Preoperative patient characteristics are displayed in Table 1. If a hemodynamically relevant carotid artery stenosis (of more than 75%) was present, the carotid endarterectomy was performed as a combined procedure. Patency of the internal carotid artery was controlled by ultrasound at 4-month follow-up. Postoperative outcome was monitored. Perioperative myocardial infarction was defined as any new Q-wave or loss of R in the electrocardiogram, significant creatine kinase (CK)/CK-MB elevation (CK-MB higher than 40 U/L). Prolonged inotropic support was defined as inotropic therapy for low-output syndrome for more than 1 day or prolonged intubation as ventilatory support for more than 5 days. Narcotics for pain relief were restricted to the time of chest tube drainage. Chest tubes were removed on postoperative day 2. Neurologic disorder was defined as history of previous transient ischemic attacks or stroke, not severely impairing the patient’s daily life.

Cognitive brain function
Cognitive brain function was evaluated before CABG and at 7-day and 4-month follow-up. Only patients who completed follow-up were included in the study. Cognitive P300 auditory-evoked potentials were recorded with Ag-AgCl electrodes on a Nicolet Spirit (Audiometrics, Oceanside, CA). P300 evoked potentials were generated after a binaurally presented tone discrimination paradigm with frequent (85%) tones of 1,000 Hz and rare (15%) target tones of 2,000 Hz at 65dB hearing level. Filter band-pass was 0.01 to 30 Hz. Active electrodes were placed at Cz (vertex) and Fz (frontal), respectively, and referenced to a linked earlobe A-12 electrode (10-20 International System). During the paradigm, the subjects were instructed to keep a running mental count of the rare 2,000-Hz target tones. To verify attention, P300 recordings with a discrepancy of more than 10% between the actual number of stimuli and the number counted by the subjects were rejected and repeated. P300 auditory-evoked potential recording resulted in a stable sequence of positive and negative peaks. Latencies (in milliseconds) of the cognitive P300 peak were assessed. To confirm reproducibility, two sets of P300 measurements were recorded in all patients [9]. P300 auditory-evoked potentials were measured with the informed consent of the patient and after approval of the local ethics commission.

Two standard psychometric tests (Mini Mental State Examination, Trail Making Test A) were performed immediately after P300 measurement to detect any overt cognitive impairment and psychomotor performance. To minimize learning effects, three different Trail Making tables were used. To avoid any influence of biorhythm alterations, the same physician performed the P300 recordings and the psychometric tests in the morning under comparable conditions. Patients had to be in stable condition, free from narcotics for more than 48 hours, and ready for discharge from hospital at 7-day follow-up.

Statistical analysis
Data are reported as mean ± standard deviation. The influence of different measurements on individual changes in cognitive brain function throughout follow-up was analyzed by linear correlation analysis of differences in P300 peak latencies in each patient. To test the simultaneous influence of variables on changes of P300 peak latencies, multiple regression analysis was performed. The entrance level into multiple regression analysis was set to p less than or equal to 0.15 based on univariate analysis. Variables with significant influence on cognitive brain function were compared. Student’s t test was applied after testing for normality of distribution to analyze group differences at the three time points. The time course of cognitive brain function was analyzed by means of paired t test for the different groups.

	Results

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Operation-related variables and postoperative outcome are shown in Table 2. Because only survivors were entered into the study, mortality was 0%. CPB was used in 72.7% of all study patients. Mean operation time was 228 minutes, mean intubation time 21.4 hours, and mean intensive care unit stay was 2.2 days. Nonfatal myocardial infarction occurred in 2.1%, and 13.1% needed prolonged inotropic support. Reexploration for bleeding was required in 2.1% of the patients, and 21.4% developed atrial fibrillation postoperatively (Table 2).

View larger version (13K): [in this window] [in a new window]   Fig 1. Representative tracing of P300 measurement.

View larger version (10K): [in this window] [in a new window]   Fig 2. Serial recordings of P300 peak latencies before coronary artery bypass grafting (CABG), at 7-day and at 4-month follow-up. (Solid line = P300 peak latencies recorded at CZ. Dotted line = P300 peak latencies recorded at FZ + Impairment of P300 peak latencies, p < 0.05 versus preoperative.)

Predictors of individual changes of cognitive P300 peak latencies
Univariate linear correlation analysis
From preoperatively through 7-day follow-up, the use of CPB (p = 0.0001), number of grafts (p = 0.0006), and number of diseased vessels (p = 0.0039) were associated with an impairment of cognitive P300 peak latencies (Table 3). From preoperatively through 4-month follow-up, the use of CPB (p = 0.0006) and number of diseased vessels (p = 0.0066) were associated with impaired cognitive P300 peak latencies. In contrast, concomitant repair of significant carotid artery stenosis was associated with improvement of P300 peak latencies from preoperatively through 4-month follow-up (p = 0.0195, Table 3).

View larger version (11K): [in this window] [in a new window]   Fig 3. (A) Serial recordings of P300 peak latencies before coronary artery bypass grafting (CABG), at 7-day and at 4-month follow-up. Solid line = P300 peak latencies of patients undergoing CABG with cardiopulmonary bypass (CPB). Dotted line = P300 peak latencies of patients undergoing CABG without CPB. +Impairment of P300 peak latencies, p < 0.05 versus before CABG. ++Improvement of P300 peak latencies, p < 0.05 versus before CABG. *P300 peak latencies with versus without CPB, p < 0.053. (B) Serial recordings of P300 peak latencies before CABG, at 7-day and at 4-month follow-up. Solid line = P300 peak latencies of patients with diabetes mellitus. Dotted line = P300 peak latencies of patients without diabetes mellitus. +Impairment of P300 peak latencies, p < 0.05 versus before CABG. ++Improvement of P300 peak latencies, p < 0.05 versus 7 days. *P300 peak latencies with versus without diabetes mellitus, p < 0.053. (C) Serial recordings of P300 peak latencies preoperative, 7 days and 4 months postoperatively. Solid line = P300 peak latencies of patients with internal carotid artery stenosis. Dotted line = P300 peak latencies of patients without internal carotid artery stenosis. +Impairment of P300 peak latencies, p < 0.05 versus before CABG. ++Improvement of P300 peak latencies, p < 0.05 versus before CABG. *P300 peak latencies with versus without internal carotid artery stenosis, p < 0.05.

The presence of significant carotid artery stenosis resulted in impairment of cognitive brain function preoperatively (carotid artery stenosis: 388 ± 32 ms; no carotid artery stenosis: 364 ± 38 ms, p = 0.0112, Fig 3C). At 7-day follow-up patients without carotid artery stenosis performed worse (371 ± 41 ms, p = 0.0101 versus before CABG). In contrast, concomitant repair of carotid artery stenosis did not affect P300 peak latencies (389 ± 30 ms, p = 0.8763; carotid artery stenosis versus no carotid artery stenosis, p = 0.0765). At 4-month follow-up cognitive brain function of patients with concomitant repair of carotid artery stenosis improved (367 ± 28 ms, p = 0.0180 versus before CABG and concomitant carotid artery operation). Patients without carotid artery stenosis remained unchanged (368 ± 33 ms, p = 0.1372 versus before CABG; carotid artery stenosis versus no carotid artery stenosis, p = 0.6851, Fig 3C). In control ultrasound investigation, the carotid artery was patent in all patients.

	Comment

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
Objective P300 auditory-evoked potential measurement revealed that cognitive brain function is impaired after CABG. The use of CPB turns out to be the only independent predictor of impaired cognitive brain function. Interestingly, the presence of diabetes mellitus and concomitant repair of significant carotid artery stenosis were predictive of long-term cognitive benefit.

Our results confirm what numerous studies have already shown: Cognitive brain dysfunction is a significant adverse event related to CABG (reported from 20% to 80%), which may affect length of hospital stay, quality of life, the rehabilitation process, and work performance [1–4]. Cognitive brain dysfunction after CABG has been demonstrated only by psychometric testing [1–4]. However, it is generally accepted that psychometric tests are not unbiased, for example, because of the occasionally long performance times, influence of psychomotor function, level of education, or learning effects [14]. Learning effects are of particular interest for follow-up studies [7]. Cognitive P300 evoked potentials, elicited by a tone discrimination paradigm, represent an objective and valid measure of cognitive brain function, registering brain activity required in the maintenance of working memory [6, 11]. P300 peak latencies—increasing with age in healthy subjects [5]—were shown to be related to cognitive impairment rating [6], rapid evaluation of cognitive function testing, orienting, stimulus evaluation, selective attention, and digit span [15]. Additionally, P300 peak latencies were shown to be much more sensitive in the detection of metabolically induced cognitive brain dysfunction than psychometric tests or EEGs [5, 7, 9]. Furthermore, the low coefficient of intraindividual test–retest variation of 2% in cognitive P300 auditory-evoked potential measurement, which is of particular importance in follow-up assessments, demonstrates its usefulness in our study [5]. Based on P300 measurements we were able to show that cognitive brain function was markedly impaired after CABG.

By means of objective P300 measurements, we were able to show that the use of CPB is the only predictor of impaired cognitive brain function after CABG. The role of CPB as a cause of cognitive impairment remains unclear, however. Suspected mechanisms of cognitive impairment after CPB may be insufficient intraoperative cerebral perfusion [16, 17] or cerebral microembolism, caused by gas, biological aggregates, or particles of silicone or polyvinyl chloride [3, 18, 19]. It has therefore been hypothesized that CABG without CPB may preserve cognitive brain function after CABG [20–22]. By means of neuropsychological testing, Taggart and colleagues [23] recently stated that the similar early decline and late recovery of cognitive brain function in patients undergoing CABG with and without CPB excludes CPB as the major cause of cognitive impairment. In contrast we were able to demonstrate an association between postoperative cognitive brain dysfunction and the use of CPB. However, in agreement with Taggart and colleagues [23], we, too, failed to detect any postoperative cognitive changes using standard neuropsychological testing. Therefore, cognitive decline in patients investigated by Taggart and colleagues [23] may have been missed because of the lower sensitivity of the neuropsychological test battery. For the first time, our findings stress the use of CPB as the only independent predictor of cognitive brain dysfunction as revealed by multivariate analysis.

We showed that the presence of diabetes mellitus was predictive of late improvement in cognitive brain function after CABG. In noncardiac patients, various studies have shown that patients with a history of diabetes mellitus have cognitive impairment [12, 13, 24, 25]. A history of hypoglycemia does not correlate with cognitive dysfunction [24], whereas a history of hyperglycemia correlated with impaired cognitive function [25]. These findings suggest that cognitive dysfunction may be related to chronic hyperglycemia. Selnes and coworkers [26] identified diabetes mellitus as a predictor of cognitive decline after CABG. Their study, however, was based on neuropsychological testing and diabetes mellitus proved to be predictive in only one of 16 performed neuropsychological tests. By means of P300 measurement, however, we found that patients with diabetes mellitus showed an improvement in cognitive function at 4-month follow-up, thus suggesting potential cognitive benefit for patients with diabetes mellitus after successful CABG.

Objective P300 auditory-evoked potential measurement revealed that concomitant repair of significant carotid artery stenosis is predictive of improvement in brain function during follow-up. Our results agree with those of Madl and colleagues [9], who showed that cognitive brain function is impaired in patients with carotid artery stenosis. In a prospective study on patients either with or without concomitant carotid artery stenosis undergoing open-heart operations, Vingerhoets and colleagues [27] found no difference in cognitive function between the two patient groups. The variable results from different studies relating to the effect of carotid endarterectomy on cognitive brain function are discussed by Lunn and coworkers [28]. Irvine and colleagues [29] demonstrated that the controversy might be related to the methodologic bias of psychometric testing with less sensitivity. Based on objective P300 auditory-evoked potentials, we were able to demonstrate that patients with concomitant repair of carotid artery stenosis showed significant improvement in cognitive brain function after CABG, probably because of better cerebral perfusion after CABG and carotid endarterectomy.

The validity of our conclusions may be limited by several factors. First, the clinical relevance of cognitive dysfunction is still uncertain. Because investigation of cognitive brain function became a field of interest for the research community only a few years ago, data on this area are still rare. P300 measurement detects minute changes of cognitive function that have to be primarily interpreted as subclinical. The real clinical impact of cognitive dysfunction, especially regarding quality of life and rehabilitation, needs to be confirmed by further investigations. Second, we did not use an external control group but referred the cognitive changes to the preoperative base line cognitive state of the individual patient. This base line could perhaps have been influenced by, for example, preoperative anxiety. Therefore the preoperative values might not be true measurements of cognitive state. Another limitation to the study arises from the fact that we did not control myocardial performance at follow-up. It is therefore impossible to determine whether improvement of cognitive brain function may be related to improvement of myocardial function. Additionally, we cannot exclude the possibility that other unknown factors that did not enter our investigation may have influenced P300 measures. Furthermore, the follow-up time of 4 months is relatively short and changes in cognitive function after 4-month follow-up period may be lacking. Finally, the study was limited by the fact that we investigated nonrandomized patient groups, because the decision regarding the surgical strategy (with or without CPB) was left to the individual surgeon.

When the above-mentioned limitations are taken into consideration, this study shows that the use of CPB is the only independent predictor of cognitive decline after CABG at 7-day and 4-month follow-up. Patients with preoperatively impaired cognitive function because of carotid artery stenosis or diabetes mellitus are those most likely to benefit from CABG.

	Acknowledgments

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 
We thank Meinhard Ploner, MSc (Stat), for statistical analysis of the work.

	References

Top Abstract Introduction Patients and methods Results Comment Acknowledgments References

 

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