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Eur J Cardiothorac Surg 2004;25:791-800
© 2004 Elsevier Science NL
a Department of Thoracic and Cardiovascular Surgery, University Hospital, Essen, Germany
b Department of Neurology, University Hospital, Essen, Germany
c Institute of Diagnostic and Interventional Radiology, University Hospital, Essen, Germany
Received 27 October 2003; received in revised form 2 February 2004; accepted 4 February 2004.
* Corresponding author. Department of Thoracic and Cardiovascular Surgery, West German Heart Center, University of Essen, Hufelandstrasse 55, 45122 Essen, Germany. Tel.: +49-201-723-4901; fax: +49-201-723-5451
e-mail: stephan.knipp{at}uni-essen.de
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Abstract |
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 Top Abstract 1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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Key Words: Cardiopulmonary bypass • Cognitive function • Coronary artery bypass grafting • Magnetic resonance imaging • Neuropsychology
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1. Introduction |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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The pathogenesis of cognitive dysfunction after cardiac surgery is still uncertain. Variables that have been postulated to explain the development of postoperative neurocognitive decline include advanced age, concomitant cerebrovascular disease and severity of cardiovascular disease, and intraoperative factors such as embolization, cerebral hypoperfusion or hypoxia, activation of inflammatory processes, aortic cross-clamp (ACC) or cardiopulmonary bypass (CPB) time, and possibly low mean arterial pressure in patients with impaired cerebrovascular autoregulation [4]. There is increasing evidence that multiple microemboli arising from the ascending aorta, the heart chambers or the bypass circuit are the primary pathophysiological mechanisms producing diffuse ischemic cerebral injury [5–8]. Several methods have been used as potential indicators of cerebral injury associated with cardiac operations including comprehensive neurological and neuropsychological examinations, transcranial Doppler ultrasonography, quantitative electroencephalography, P 300 auditory evoked potentials, near infrared spectroscopy, serum studies of S100 protein and neuron-specific enolase, and magnetic resonance techniques. Using conventional magnetic resonance imaging (MRI), some investigators have observed new focal brain lesions after CABG in up to one-third of patients without overt neurological complications [9–11]. Advanced magnetic resonance techniques such as diffusion-weighted imaging (DWI) even allow for sensitive and early detection of ischemic damage within minutes after onset [12] and are therefore superior to conventional imaging. Diffusion-weighted MRI in conjunction with neuropsychological assessment has been scarcely employed in the study of patients after coronary re-vascularization. Also, most studies using diffusion-weighted sequences of MRI lack in a follow-up for more than 10 days or were performed on smaller groups. Finally, the clinical significance of new focal brain lesions for the development of neurocognitive deficits after heart surgery is still uncertain [10,13–15]. The purpose of the present prospective study was to determine the incidence of brain damage in patients undergoing elective CABG using conventional and diffusion-weighted MRI and neuropsychological testing before surgery, at the time of hospital discharge and 3 months after surgery. The relation between radiological data and clinical and surgical variables and neuropsychological test performance was analyzed.
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2. Materials and methods |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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2.2. Neuropsychological assessment
Cognitive brain function was assessed using a well-validated battery of 13 standardized psychometric tests including two questionnaires. All tests were performed by the same investigator who was an experienced neuropsychologist. To minimize learning effects the tests existed in parallel forms and were randomly assigned to the respective examination. The testing comprised the assessment of performance in five major cognitive domains known to be vulnerable to organic injury: attention, rate of information processing, memory and verbal learning, ability of logical thinking, and visual-spatial perception. The affective status of the patients was assessed with the use of standardized questionnaires on depression and mood. To measure the patient's attention and psychomotor speed Reitan's Trail making test version B (TMB) and Zimmermann's divided attention test were administered. Reitan's Trail making test version A was used to measure the speed of information processing. The digit span subtest of the Wechsler Memory Scale—Revised was further used to test short-term (digit span forward) and working memory for verbal material (digit span backward). The verbal learning test was used to test the ability of learning verbal material and to recall it immediately (word list immediate) and after a 30-min delay (word list delayed). The Corsi block tapping test investigates the memory of spatial structures and exists in two forms (Corsi block tapping forward and backward). The Horn's performance test 55+ subtest 9 tests for visual-spatial abilities and the subtest 3 tests for recognition of categories and regularities of geometrical objects. Except for the TMA, TMB and the divided attention test, a higher score indicates a better function. In addition to the psychometric tests, the patients were asked to fill in questionnaires on mood (von Zerssen's Bf-S', 28 items) and depression (general depression scale—short version, 15 items, modified from hospital anxiety and depression scale-short version). In both questionnaires a lower score indicates a lower level of depression and discontent.
2.3. Clinical evaluation
Clinical examination was carried out by an experienced neurologist before surgery, early before discharge, on the day of 3-month follow-up evaluation and in between, when necessary. The examination consisted of a medical history, physical examination and detailed neurological examination. By 3-month evaluation, neurological examination, neuropsychological testing and brain MRI were obtained on the same day of visit.
2.4. Magnetic resonance imaging of the brain
MRI scans of the brain were obtained by means of a standard 1,5 Tesla whole body system (Magnetom, Siemens AG, Erlangen, Germany). The MR-protocol included the following sequences: (a) transaxial T2-weighted (time to repeat [TR], 5120 ms, echo time [TE], 104 ms, average 1, matrix 256x256); (b) coronal T2-weighted (TR 4810 ms, TE 113 ms, averages 2, matrix 512x512); (c) transaxial fluid-attenuated inversion recovery [FLAIR]-weighted (TR 9000 ms, TE 115 ms, average 1, matrix 256x256); (d) conventional transaxial T1-weighted (TR 500 ms, TE 14 ms, averages 2, matrix 256x256); and (e) transaxial diffusion-weighted sequence (TR 4600 ms, TE 137 ms, averages 2, matrix 128x128, b-values 0, 500 and 1000). Field of view was 230 mm for all sequences. Slice thickness was 6 mm for turbo–spin–echo sequences and 5 mm for diffusion-weighted sequence. Images were evaluated by consensus of two experienced neuroradiologists using standardized evaluation forms. The presence of previous brain abnormalities, localization and volume of new lesions were recorded. On looking for the presence of any new brain lesion on postoperative MRI scans, the investigators were blind to the patient's individual postoperative course and the baseline status. For volumetry, the images were magnified fourfold, the area of lesion was delineated manually in each image slice and the volume was calculated using standard scanner software.
2.5. Anesthesia and surgery
CABG was performed with standard anesthesia techniques and surgical procedures. Ethmidate, sufentanyl and rocuronium were administered intravenously as needed to induce general anesthesia and isofluran to maintain it. All patients underwent a median sternotomy and CPB in mild hypothermia (32 °C). CPB was established by aortic and single venous cannulation. Aortic side clamping was performed for fashioning proximal anastomoses. Cardiac arrest was achieved by applying cold Bretschneider cardioplegia solution through a cardioplegia cannula. Arterial partial pressure of carbon dioxide (paCO2) was maintained at 35–40 mmHg and the arterial tension of oxygen was maintained at 200–250 mmHg during CPB. Non-pulsatile blood flow during CPB was maintained at 2.4 l/min m2 body surface area at normothermia and adjusted at hypothermia. Mean arterial pressure was kept higher than 50 mmHg throughout the operation with vasoactive agents when necessary. Packed red cells were administered when necessary to keep the hematocrit above 21% during CPB. The bypass circuit consisted of a roller pump (Stöckert SIII, Stöckert GmbH, Munich, Germany) and a 40-µm arterial blood filter. Heparin was added to the heart-lung machine to achieve an activated clotting time above 400 s during CPB. The acid–base status was managed using the 
-stat protocol.
2.6. Statistical analysis
All analyses were performed using SPSS software for windows (SPSS 11.0, SPSS Inc., Chicago, IL, USA). A P-value below 0.05 was considered to be statistically significant. All variables were tested for normal distribution with the Kolmogorov Smirnov-1 sample test. Differences of neuropsychological variables between the three times of testing were analyzed with repeated measures univariate analysis of variance and the Friedman test, respectively. For comparison of two group means, Student's t-test and Wilcoxon test were used, respectively. The relation between demographic and clinical variables (e.g. preoperative stroke risk factors, operative parameters and postoperative adverse events) and cognitive function (as determined by the difference between the postoperative and preoperative neuropsychological test score) or MRI findings was analyzed using repeated measures multiple linear regression analysis. In order to analyze whether cognitive dysfunction at the 3-month follow-up examination was related to new ischemic MRI lesions, a two-step analysis was performed: (1) the unpaired Student's t-test was calculated between patients with and without new MRI lesions for the respective neuropsychological variable, (2) in case of a significant difference between the two subgroups, a regression analysis was administered.
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3. Results |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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The preoperative neuropsychological testing was performed 3.0±2.0 days (1–7 days) before CABG with MRI scanning obtained within 24 h. The first postoperative neuropsychological testing was performed 5.0±2.0 days (2–20 days) after CABG and the 3-month follow-up study was done 96.8±9.9 days (86–122 days) after operation. Twenty-two of the 29 patients (76%) had at least three risk factors for atherosclerosis. The most common risk factors were hypertension (76%), hyperlipidemia (76%) and diabetes (35%). Duration of extracorporeal circulation was 96.1±27.9 min (38–160 min) to achieve on average 3.1±0.8 grafts (1–5 grafts). Lacunes were seen on preoperative brain MRI in 11 of 29 patients (38%). Table 1 shows the most relevant demographic, clinical and perioperative data of the study group. There was no statistical difference between the two subgroups of patients with and without new lesions on postoperative MRI.
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Diffusion-weighted MRI of the brain detected new lesions on postoperative scans in 13 of the 29 patients (45%). Five patients had 1 new lesion, 7 patients had 2–4 lesions, and 1 patient had 7 lesions. There were 32 new focal lesions, 18 in the left hemisphere and 14 in the right. The lesions were rounded and their volume was small ranging from 32.5 to 745.5 mm3. Most of the lesions were supratentorial with 10 lesions in the frontal lobe, 9 in the parietal, 7 in the occipital and 1 lesion in the temporal lobe. Three of the four infratentorial lesions were in the cerebellum. The greatest single new lesion was found in a 78-year-old patient without overt neurological abnormalities on serial postoperative examinations (Fig. 1) . Preoperative Doppler sonography showed plaques in the carotid arteries on both sides but no stenosis, and preoperative brain MRI was normal. The patient was discharged from hospital on postoperative day 4 after an uneventful course. In all five patients with more than three lesions, the abnormalities were dispersed in different cerebral artery territories.
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4. Discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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Advances in modern cardiac surgery over the past 2 decades have resulted in a relatively low mortality and cardiac morbidity. Nevertheless, cardiac surgery may be associated with adverse neurological and neuropsychological outcome. Clinically recognized cerebral infarction occurs in 0.8–6% of patients [16]. Moderate complications such as obvious deterioration in intellectual function and seizures have been detected in an additional 3% of cases. Postoperative encephalopathy or delirium occurs in 10–28% of patients and is often transient [1,2]. More subtle postoperative changes in cognitive function as detected by a decline in neuropsychological testing scores from baseline are considerably more common. The incidence of severe cognitive decline and behavioral change related to open heart surgery is highest at the time of discharge ranging from 50 to 80% [3]. In the following weeks, many symptoms restore, but even 6 months after operation neurocognitive decline is found in approximately 10–30% of patients [3]. In some patients, longer-term cognitive dysfunction is reported to be present 1–5 years after operation [1,3]. The relatively high prevalence and persistence of postoperative cognitive decline is of particular importance since it may result in decrease in quality of life and work performance [2]. The frequency of postoperative neuropsychological impairment and the pattern of early decline and late recovery in this study is in line with numerous studies [1,3,17]. Significant cognitive decline had occurred early postoperatively in three cognitive domains. By 3 months, most of these deficits had recovered to baseline in most patients, but verbal learning ability was still severely deteriorated. Longitudinal assessment of cognitive function needs to be awaited to determine the significance of this impairment on long-term outcome of patients. The cause of postoperative cognitive dysfunction is yet unknown, and particularly cognitive decline years after operation is subject to much debate. It may represent the effect of age in patients with underlying neurological disease, or it may be the result of subtle brain injury at the time of coronary surgery [15]. Further long-term studies with patients undergoing CABG compared to patients with coronary disease without CABG as a control group (treated either medically or by percutaneous coronary intervention) are required to provide answers to these questions.
Many different methods have been used as potential sensitive indicators of cerebral injury associated with heart surgery. Because of its superiority to other imaging methods, MRI has been increasingly employed in the study protocols before and after open heart surgery. Using T2 MRI sequences, Toner et al. (1994) found new cerebral lesions in 30% (6/20) of patients undergoing CABG, mainly deep white matter lesions. In a larger series of Vanninen et al. (1998), postoperative T2 MRI brain scans revealed new focal lesions in 21% (8/38) of patients. No patient experienced major neurological complications and there was no significant deterioration in mean cognitive performance 3 months after surgery. For the detection of ischemia, new MRI technology with diffusion-weighted sequences is more sensitive than T2-weighted images [18], but studies using DWI are yet scanty. Bendszus et al. (2002) prospectively evaluated brain damage before and after CABG using diffusion-weighted MRI. They found 17 new ischemic DWI lesions in 26% of patients. Similarly, Restrepo et al. (2002) demonstrated that focal brain diffusion abnormalities can occur after CABG, even in patients without clinically identified neurological deficit. The correlation of the presence of new MRI lesions with postoperative neurocognitive decline is variable in the few studies that have assessed cognition. Some investigations report that the new MRI lesions were associated with neurocognitive decline [10,14,15]. In the series of Restrepo et al. (2002), from 13 patients studied, all four patients with postoperative DWI defects had a larger neurocognitive decline than their counterparts with stable MRI. Other clinical characteristics were similar between patients with and without new DWI lesions, including stroke risk factors [15]. In contrast, other studies, including our own, failed to find an association between the presence of new postoperative lesions and neuropsychological decline [11,13]. In the present study, this was even true when cognitive decline was persistently impaired 3 months after operation. The occurrence of new focal brain lesions in our series is more frequent than in others [11,13], but less than in a valve replacement surgery study where it was 58% [19]. Despite a good interobserver agreement for the detection of new diffusion lesions on postoperative scans, we cannot preclude an overestimation of subtle areas of hyperintensity particularly in patients with preexisting cerebral vasculopathy. Since the new lesions are also visible on T2-weighted images, there is evidence of structural brain damage. The discrepancy between the presence of new MRI lesions and the absence of clinically overt neurological deficits prompts the proposal that the severity of brain damage is limited. It may be hypothesized, however, that new postoperative lesions result in subtle brain injury that will leave patients more susceptible to cognitive decline from degenerative or atherosclerotic disease years later. Larger series are required to determine the significance of postoperative brain abnormalities with regard to neurological and neuropsychological long-term outcome of patients.
The pathogenesis of new ischemic brain injury after CABG is unknown. Possible underlying mechanisms are embolization and hypoperfusion [5,8,20–22]. From the pattern of distribution, most of the MRI lesions in the present study are considered embolic even though hypoperfusion-induced border zone edema and small infarcts may not be precluded in a few cases. Emboli are made of gas, thrombi, fragments of atheromatous plaques from the ascending aorta, cell aggregates, fat or inorganic debris from the bypass circuit tubing [6]. The sensitivity of diffusion-weighted MRI is limited by the spatial resolution. Lesions smaller than the pixel size are hardly to detect. Microbubble emboli would produce diffuse cerebral hypoxemia with cytotoxic edema resulting in a reduced attenuated diffusion coefficient on magnetic resonance spectroscopy [13]. As elevated diffusion coefficient values were found on brains of patients after CABG [13] and with respect to the absence of apparent neurological events, we assume that the lesions are probably due to thromboemboli or macroscopic air emboli rather than microbubbles or big plaque fragments, the latter being probably more harmful.
There are some limitations to our study. One limitation is the restricted number of patients, even though only two studies comprised more patients [11,13]. There is also a possible selection bias, because only patients who seemed compliant were enrolled. The follow-up of patients was 3 months, therefore the significance of the new postoperative MRI lesions on the neuropsychological long-term outcome of patients remains uncertain.
In summary, the present study is, to our knowledge, the first to systematically employ conventional and diffusion-weighted MRI before and after CABG and to follow-up the patients for a mean of 3 months after operation. We found no association between the appearance of new small brain lesions on postoperative MRI and short-term and mid-term neurocognitive outcome. We conclude that the new focal ischemic brain damage detected by MRI does not seem to account for the deterioration of neurocognitive function three months after coronary surgery. Further studies on larger series including control groups are required to corroborate these initial findings. These studies might also help to evaluate the influence of non-surgery related factors on the long-term course of cognitive function in patients with coronary artery disease.
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Acknowledgments |
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Footnotes |
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Appendix A. Conference discussion |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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However, as almost always, there is a lack of controls, of what happens without surgery and what happens with the competing technology, the PCI. Are you planning to repeat the same very interesting investigation in patients who were treated without surgery, without the pump and with PCI?
Dr Knipp: We are actually planning to control these patients and to compare them with OPCAB patients without use of pump and even with patients who have major surgical procedures on the vascular system without the use of cardiopulmonary bypass and with no touch on the ascending aorta, which is certainly one of the main sources of embolization causing these MRI lesions.
Mr V. Zamvar (Edinburgh, UK): Did you find any difference in the MRI findings between immediate postoperative period and the three-month postoperative period? Did the lesions disappear?
Dr Knipp: Also early after surgery we didn't find any association between the appearance of new lesions and neurocognitive dysfunction.
Mr Zamvar: Sorry. My question is, what happened to the MRI lesions? Did the lesions disappear at the three-month scan?
Dr Knipp: I see. The lesions were seen on the diffusion-weighted sequences but also on T2-weighted images, indicating structural damage to the brain. Most of the lesions did persist.
Dr R. Frater (Bronxville, NY, USA): You mentioned that the cardiopulmonary bypass was standard, but there surely are a large number of possible variables in the way you conduct bypass which can influence at least cerebral flow and perhaps cerebral function. Can you be sure that the cognitive effects you are talking about are related to the way you conducted the bypass rather than to any embolic phenomena?
Dr Knipp: You mean that there was a difference in laboratory data between the two situations?
Dr Frater: No. What I mean is, if you do cardiopulmonary bypass by itself you are potentially affecting cerebral function through flow, through oxygenation, through carbon dioxide concentrations and so on. Now, you just say it is standard, but in fact you need to define that at the same time as you are looking for emboli, don't you think, in order to be able to separate embolic lesions versus other mechanisms for cerebral dysfunctions?
Dr Knipp: I didn't comment on the details of the cardiopulmonary bypass, but all of the patients had a median sternotomy, all of them were managed by alpha-stat protocol, all patients had a mean bypass flow of 2.4 liters per minute and square meter body surface area, and so on. So this is a standard protocol that we follow. That is why I said that the bypass itself was not changed in this prospective study.
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References |
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TopAbstract1. Introduction2. Materials and methods3. Results4. DiscussionAppendix A. Conference...References |
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