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Ann Thorac Surg 2004;78:513-518
© 2004 The Society of Thoracic Surgeons

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Original article: cardiovascular

Neurocognitive deficit following coronary artery bypass grafting: a prospective study of surgical patients and nonsurgical controls

^a Department of Cardiothoracic Surgery, University of Vienna, Vienna, Austria
^b Department of Internal Medicine, University of Vienna, Vienna, Austria
^c Department of Cardiac Surgery, University of Innsbruck, Innsbruck, Austria

Accepted for publication December 29, 2003.

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

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
BACKGROUND: To objectively measure long-term neurocognitive deficit in patients undergoing coronary artery bypass grafting and compare the findings with nonsurgical controls.

METHODS: We prospectively measured neurocognitive function in patients undergoing coronary artery bypass grafting (CABG) with cardiopulmonary bypass (n = 104; mean age 64.1 years old; EuroSCORE 2.7 [means]). A cohort of age- and sex-matched patients (n = 80; mean age 63.4 years old) served as nonsurgical controls. After CABG, neurocognitive function was serially reevaluated at 7-day (n = 104), 4-month (n = 100), and 3-year follow-up (n = 88). Neurocognitive function was objectively measured by means of cognitive P300 evoked potentials. Additionally, standard psychometric tests were performed (Trailmaking Test A, Mini Mental State Examination).

RESULTS: As compared to preoperative measures (364 ± 36 ms), cognitive P300 evoked potentials were prolonged (=impaired) at 7-day (381 ± 36 ms; p = 0.001), 4-month (378 ± 31 ms; p = 0.08), and 3-year follow-up (379 ± 35 ms; p = 0.002), respectively. Trailmaking Test A was abnormal, as compared to preoperative, at 3-year follow-up (p < 0.001). Before the operation, surgical patients were fully comparable in P300 measures to nonsurgical controls (363 ± 32 ms; p = 0.362). Most importantly, throughout the entire postoperative follow-up cognitive measures in surgical patients were prolonged (=impaired) as compared with controls (7-day p = 0.001; 4-month p = 0.002 and 3-year p = 0.003, respectively). In stepwise multivariate regression analysis, neurocognitive deficit at 4-month follow-up (p < 0.001), age (p = 0.012), and persistent atrial fibrillation (p = 0.024) were predictive for long-term neurocognitive deficit at 3-year follow-up.

CONCLUSIONS: As shown by means of objective measures, and in comparison to nonsurgical controls, coronary artery bypass grafting with cardiopulmonary bypass grafting causes long-term neurocognitive deficit.

	Introduction

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Due to the continuous improvement of surgical techniques, extracorporal circulation as well as an aesthesia and intensive care, mortality and morbidity following coronary artery bypass grafting (CABG) have been significantly reduced. Therefore, adverse effects of coronary artery bypass with cardiopulmonary bypass such as neurocognitive deficit are increasingly being recognized.

Neurocognitive deficit has been reported to affect up to 80% of patients at hospital discharge and up to 42% of patients 5 years after surgery [1–4]. Neurocognitive deficit has been associated with an up to 10% increase in perioperative mortality and increase in length of in hospital stay, a prolonged process of rehabilitation and a later return to normal life [3]. This is associated with a tremendous increased use of health care resources.

The aim of the present study was to objectively measure long-term neurocognitive deficit following isolated coronary artery bypass grafting, to compare the findings with nonsurgical controls and to elucidate factors associated with long-term neurocognitive deficit. Defining patients with increased risk for long-term neurocognitive deficit will enable us to identify these patients in the future and develop treatment strategies especially devoted to them.

	Material and methods

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Patients
After approval was obtained by the Ethics Committee of the University of Vienna, 105 patients who underwent elective coronary artery bypass grafting at our department between January and December 1999, gave their written informed consent and were enrolled in this prospective study. Exclusion criteria were a history of one of the following medical conditions [1]: prior stroke with residual deficit [2], uncontrolled hypertension [4], carotid artery stenosis 75% [4], psychiatric illness requiring treatment [5], alcoholism [6], renal disease (defined as a creatinine more than 2.0 mg/dL [177 µmol per liter]) and [7] active liver disease.

Nonsurgical controls
For nonsurgical controls, we screened patients admitted to the Department of Internal Medicine. The same exclusion criteria used in patients undergoing CABG were applied on control patients. Patients were contacted by the study coordinator. Patients were informed by the study coordinator about the planned tests as well as the frequency of reexamination. All patients serving as controls had to give their written and informed consent. Tests were not performed as part of another study. Of the patients contacted, 80 gave their written and informed consent and were enrolled.

Preoperative risk stratification
Preoperative risk stratification was performed using the European System for Cardiac Operative Risk Evaluation (EuroSCORE). The EuroSCORE is a risk stratification system to help in the assessment of quality of cardiac surgical care. The score consists of patient-, cardiac- and operation-related factors [5].

Neurocognitive testing
Neurocognitive testing and physical examinations were completed preoperatively, 7 days, 4 months, and 3 years after surgery, respectively. All examinations were performed individually by the same experienced investigator. Neurocognitive testing consisted of cognitive P300 evoked potentials, Mini Mental State Examination, and Trailmaking Test A. To avoid any influences due to biorhythm, all investigations were performed in the afternoon under comparable conditions. Special care was taken to ensure that patients were free from narcotics and sedatives for at least two days before testing.

Cognitive P300 evoked potentials
Cognitive P300 evoked potentials have previously been used to measure neurocognitive function in various metabolic disorders, patients undergoing heart transplantation and patients undergoing open heart surgery [6–10]. Cognitive P300 evoked potential are the result of an activation of a widespread network of cortical structures, including association areas in the parietal, temporal and prefrontal cortex, as well as the hippocampus [11]. As a result of the involvement of these brain regions in the P300 generation, P300 can be used as a general indicator for neurocognitive function [12–14]. Cognitive P300 evoked potentials were recorded with Ag/AgCl electrodes on a "Nicolet 2000" (Nicolet, Madison, WI). P300 evoked potentials were generated following a binaurally presented tone discrimination paradigm (odd-ball paradigm) with frequent (80%) tones of 1000 Hz and rare (20%) target-tones of 2000 Hz at 75 dB HL. Filter bandpass was 0.01 to 30 Hz. Active electrodes were placed at Cz (vertex) and Fz (frontal), respectively, and referenced to linked earlobe A1/2 electrodes (10/20 international system) [15]. During the paradigm, the patients were instructed to keep a running mental count of the rare 2000 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 patients were rejected and repeated. P300 evoked potential recording resulted in a stable sequence of positive and negative peaks. Latencies (milliseconds) of the cognitive P300 peak were assessed. To confirm reproducibility, two sets of P300 measurements were recorded in all patients. P300 evoked potential findings were compared with those of 80 age- and sex-matched control patients (mean age 63.3 ± 9 years, age range 40–87 years old).

Psychometric tests
Immediately after P300 recording, Trailmaking Test A (TTA) and Mini Mental State Examination (MMSE) were performed [16, 17]. Mini Mental state examination was used to ensure that all patients entering the present study were free from overt neurologic impairment or dementia. To minimize learning effects, five different Trailmaking Tables were randomly used.

Follow-up
In addition to neurocognitive testing, patients were studied by means of echocardiography, electrocardiogram (ECG), blood tests, and clinical investigations at all points of follow-up. Persistent atrial fibrillation was defined as presence of atrial fibrillation at 7-day, 4-month, and 3-year follow-up.

Anesthesia and surgical procedure
General anesthesia was administered using midazolam, ethmidate, fentanyl and pancuronium. Surgical access was gained through a median sternotomy in all patients. A transesophageal echocardiography probe (TEE) was placed in all patients. In the study group standard cardiopulmonary bypass (CPB) technique with membrane oxygenators (Bard HF 5701; C.R. Bard Inc, Havorhill, MA), roller pumps, mild hypothermia (35°C) was used. Mean arterial pressure during and after CPB was kept above 50 mm Hg. Intensive care treatment was performed according to institutional standards.

Statistical analysis
Data are reported as mean ± SD. Comparison of P300 evoked potentials and standard psychometric test were performed using analysis of variance (ANOVA) after testing for normality of distribution. Age and base line test scores served as covariates and group classification (CABG vs controls) as the independent variable. The time course of neurocognitive function was analyzed by means of paired t-test. As multiple testing was performed a Bonferroni-Holm correction was performed. Categorical variables were compared using ² test or Fischer's exact test as appropriate. To test the simultaneous influence of variables on changes of P300 peak latencies, stepwise multivariable regression analysis was performed. Neurocognitive deficit was defined as a decline of more than 1 standard deviation as compared to preoperative measures. In order to test if there is a correlation between individual changes in cognitive P300 auditory evoked potentials and Trail Making Test A, a regression analysis was performed. The entrance level into multivariable regression analysis was set to p value less than or equal to 0.15 based on univariate analysis; p values less than 0.05 were considered as significant, two sided. The study was analyzed using SAS, version 8 (Cary, NC).

	Results

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One hundred four patients undergoing isolated coronary artery bypass grafting at our institution were prospectively followed. The baseline characteristics of patients as well as controls are given in Table 1.

View larger version (18K): [in this window] [in a new window]   Fig 1. (A) P300 peak latencies of patients undergoing coronary artery bypass grafting (n = 104) before operation; individual measurements are indicated by . Solid line represents latency-age regression of age- and sex-matched controls; dotted lines represent upper and lower 95% confidence limits. (B) P300 peak latencies of patients undergoing coronary artery bypass grafting (n = 88) at 3-year follow-up. Individual measurements are indicated by . Solid line represents latency age regression of age- and sex-matched controls (after a 3-year follow-up); dotted lines represent upper and lower 95% confidence limits.

View larger version (10K): [in this window] [in a new window]   Fig 2. Graph illustrates serial assessments of cognitive brain function by cognitive P300 evoked potentials. The black line represents patients undergoing coronary artery bypass grafting, the gray line represents age- and sex-matched controls. *p < 0.05 compared with preoperative values; p < 0.05 within the two groups. (FUP = follow-up; pre-OP = pre-operative.)

To elucidate which demographic and perioperative factors were associated with neurocognitive deficit at 3-year follow-up, suspected univariate predictors of cognitive decline were assessed by means of linear regression analysis (Table 3). Significant univariate predictors were neurocognitive deficit at 4-month follow-up (p < 0.001), age (p = 0.002) and persistent atrial fibrillation (p = 0.003). The entrance level into multivariable regression analysis was set to p values less than or equal to 0.15 based on univariate analysis. Multivariate analysis revealed neurocognitive deficit at 4-month follow-up (p < 0.001), age (p = 0.012) and persistent atrial fibrillation (p = 0.024) as independent predictors of neurocognitive deficit at 3-year follow-up. The inclusion of data for the patients lost for follow-up, patients with perioperative stroke or patients who died during the period of follow-up did not appreciable change the predictors or their significance.

	Comment

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When compared with nonsurgical controls, coronary artery bypass grafting truly causes long-term neurocognitive deficit. Predictive variables for long-term neurocognitive deficit are neurocognitive deficit at 4-month follow-up, age, and persistent atrial fibrillation.

Neurocognitive deficit, defined as a combination of deficits in memory, learning, concentration and visual motor response, is an adverse event of coronary artery bypass grafting with an incidence of up to 80% perhaps the most common adverse event [1–4, 8, 18]. Roach and colleagues [3] reported on a multi-institutional prospective study that that neurocognitive deficit is associated with increased mortality (10%), a twofold increase in hospital length of stay and a sixfold likelihood of discharge to a nursing home. This is associated with a tremendously increased use of health care resources. From the patients view, the impact of neurocognitive deficit is devastating as it has been shown to reduce subjective working capacity, decrease quality of life, job related abilities, productive working status and to impair car driving abilities [19, 20]. Summarizing, neurocognitive deficit is a drawback of coronary artery bypass grafting as it may reduce the merits of surgical intervention.

On the basis of P300 measurements, we were able to show that neurocognitive function is impaired in patients undergoing coronary artery bypass grafting with cardiopulmonary bypass at 7-day, 4-month, and 3-year (long-term) follow-up, as compared with preoperative and age- and sex-matched controls. Our data support previous findings indicating that postoperative neurocognitive decline may persist up to 5 years after surgery [1, 2, 4]. To assess long-term neurocognitive function following CABG we used a previously described diagnostic tool consisting of cognitive P300 evoked potentials and standard psychometric tests [7, 8, 9]. Previous series used standard psychometric test batteries to assess long-term neurocognitive function [1, 2, 4, 18, 19, 21]. Although such batteries are well introduced, it is generally accepted that psychometric test batteries are not without biases, eg, in part because of long performance times (stressing attention), visual impairment, influence of psychomotor function, level of education and learning effects [22–28]. The latter are of particular interest for follow-up studies, especially in CABG patients representing eldery, in part multimorbid patients. P300 peak latencies increase with age in healthy patients. The clinical relevance of cognitive P300 evoked potentials is based on the fact that they were demonstrated to be related to cognitive impairment rating, rapid evaluation of cognitive function tests, orientation, stimulus evaluation, selective attention, visual pattern recognition, and digit span, and were revealed to be much more sensitive in detecting neurocognitive deficit than psychometric tests or electroencephalograms [6, 7, 13]. Moreover, P300 technique has a very low intraindiviual test-retest variability with a coefficient of variation of below 2%, which further stresses its usefulness for cognitive follow-up studies [7]. All P300 recordings were taken repeatedly (double tracing) to confirm reproducibility of measurements. The high standard deviations of mean P300 peak latencies in patients and age- and sex-matched control patients are the result of age dependency of cognitive P300 measurements. Psychometric tests in part confirm the findings of P300 measurements: Mini Mental State examination, a standard test of cognitive impairment, was normal in all patients (ranging from 27 to the maximum of 30). This indicates that only patients without overt neurologic impairment or dementia entered the study. More discriminating were the findings in Trailmaking Test A. Patients undergoing coronary artery bypass grafting scored significantly abnormal at 3-year follow-up. Furthermore we found a good correlation between individual development of cognitive P300 peak latencies and Trailmaking Test A.

Our results suggest that coronary artery bypass grafting with cardiopulmonary bypass may cause irreversible damage to cerebral tissue resulting in significantly impaired neurocognitive function. Suspected underlying mechanisms are impaired cerebral perfusion during CPB, postoperative systemic inflammatory response, and micro- and macroembolism [29]. The finding that neurocognitive deficit at 4-month follow-up and advanced age are independent predictors for long-term neurocognitive deficit suggests that the amount and nature of damage varies in different patients and that elderly patients are at higher risk to develop irreversible damage. Possible underlying mechanisms rendering elderly patients especially vulnerable might be advanced sclerosis of the ascending aorta (a possible source of micro and macroemboli during cross clamping and cannualtion) as well as partial loss of cerebral autoregulation resulting from occult cerebrovascular disease [30]. There might also be decreased ability to recover and to compensate in these patients. The pathophysiology of the impact of atrial fibrillation, although previously described, has not yet been clarified [31]. Suspected underlying mechanisms are an increased potential for thrombus formation and subsequent embolization into cerebral tissue and atrial fibrillation-related decrease in cardiac output [32]. Nevertheless, further investigations are warranted to clarify the underlying mechanisms. Specifically, it remains to be studied, whether in the future this atrial fibrillation-related neurocognitive impairment may be improved by additional surgical MAZE procedure.

Limitations
Our study is limited by a certain loss of follow-up that is inevitable in a study that follows patients for 3 years. However, the loss of follow-up is comparable to other studies dealing with the same topic [1, 2, 4]. Another limitation of the present study is that we provide normative data obtained in age- and sex-matched controls only for cognitive P300 evoked potentials. The present data are only valid for elective patients with a comparable age range undergoing coronary artery bypass grafting with mildly hypothermic cardiopulmonary bypass and cannot be extrapolated to patients undergoing other than elective isolated coronary artery bypass grafting. Patients undergoing coronary artery bypass grafting were matched with their nonsurgical control counterparts with regard to age and sex. No further matching with regard to risk factors for cardiovascular disease has been performed. Nevertheless, we found non difference between risk factors for cardiovascular disease except incidence of hypertension between patients undergoing coronary artery bypass grafting and nonsurgical controls.

By means of objective measures the present study proofs the evidence of long-term neurocognitive deficit following coronary bypass surgery and strongly supports its clinical significance by comparison to, nonsurgical controls. Predictors for long-term neurocognitive deficit are neurocognitive deficit at 4-month follow-up, age and persistent atrial fibrillation. These data will enable us to identify patients with increased risk for long-term neurocognitive deficit in the future and to develop treatment strategies especially devoted to them.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
We thank Daniela Dunkler, MS(Stat), for the statistical analysis of the work.

	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): Martin Czerny Ernst Wolner Michael Grimm Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zimpfer, D. Articles by Grimm, M. Search for Related Content PubMed PubMed Citation Articles by Zimpfer, D. Articles by Grimm, M. Related Collections Cerebral protection