ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Georg M. Wieselthaler
Ernst Wolner
Michael Grimm
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zimpfer, D.
Right arrow Articles by Grimm, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zimpfer, D.
Right arrow Articles by Grimm, M.
Related Collections
Right arrow Cerebral protection

Ann Thorac Surg 2002;74:407-412
© 2002 The Society of Thoracic Surgeons

Original article: cardiovascular

Cognitive deficit after aortic valve replacement

Daniel Zimpfer, MSa, Martin Czerny, MDa, Juliane Kilo, MDa, Marie-Theres Kasimir, MDa, Christian Madl, MDb, Ludwig Kramer, MDb, Georg M. Wieselthaler, MDa, Ernst Wolner, MDa, Michael Grimm, MD*a

a Department of Cardio-Thoracic Surgery, Vienna General Hospital, University of Vienna, Vienna, Austria
b Department of Internal Medicine, Vienna General Hospital, University of Vienna, Vienna, Austria

Accepted for publication March 28, 2002.

* Address reprint requests to Dr Grimm, Department of Cardio-Thoracic Surgery, University of Vienna, Waehriger 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. Impairment of cognitive brain function after coronary artery bypass grafting (CABG) is well known. In contrast the potential neurocognitive damage related to aortic valve replacement (AVR) is uncertain.

Methods. In this contemporary case-matched control study we followed 30 patients (mean age 70 years) receiving isolated AVR with a biological prosthesis. A cohort of sex-and age-matched patients (n = 30, mean age 70 years) receiving CABG with cardiopulmonary bypass served as controls. Cognitive brain function was measured by means of auditory evoked P300 potentials (peak latencies, ms) before the operation and 7 days and 4 months after the operation. Additionally, two standard psychometric tests (Mini-Mental State Examination and the Trailmaking Test A) were performed.

Results. In preoperative measures there was no difference between patients undergoing AVR and patients undergoing CABG (AVR 378 ± 37 ms, CABG 374 ± 32 ms, p = 0.629). One week after surgery P300 peak latencies were prolonged (impaired) in both groups compared with preoperative values (AVR 405 ± 43 ms, p = 0.001; CABG 398 ± 44 ms, p = 0.004). At this point of follow-up there was no difference between the groups (p = 0.607). Finally, 4 months after surgery P300 auditory evoked potentials returned to normal in the CABG group (380 ± 24 ms, p = 0.940) while in contrast in the valve group they continued to become prolonged (worsened) compared with preoperative values (410 ± 47 ms, p = 0.005). At this time of follow-up P300 peak latencies were prolonged in AVR patients as compared with CABG patients (p = 0.032). The Trailmaking Test A and Mini-Mental State Examination failed to discriminate any difference.

Conclusions. Four-month impairment of cognitive brain function is more pronounced in patients undergoing biological AVR as compared with age-matched control patients undergoing CABG. Further studies are needed to clarify the potential pathologic mechanisms causing an ongoing cognitive impairment in patients with biological aortic valve prostheses.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Cognitive brain dysfunction after open heart surgery with cardiopulmonary bypass (CPB) has tremendous social and economical impact. It affects quality of life and has profound implications because neurocognitive impairment prolongs in hospital stay and increases use of resources [1, 2]. Despite technical improvement of CPB circuits resulting in less systemic activation and consecutively less systemic inflammatory response cognitive dysfunction appears in 30% to 70% of patients undergoing open heart surgery with CPB [3, 4].

Evoked potential measurements detected by cortical leads, representing stable sequences of negative and positive electroencephalogram peaks within a period of several hundred milliseconds, are a highly sensitive and reproducible tool for evaluation of cognitive and neuronal brain dysfunction caused by various disorders [5–9]. Cognitive P300 auditory evoked potentials elicited by a tone discrimination paradigm are objective measures related to information and cognitive processing which therefore allow a quantification of cognitive brain dysfunction [9, 10]. Furthermore the low coefficient of intraindividual test-retest variation of below 2% in cognitive P300 auditory evoked potential measurement, which is of particular importance in follow-up assessments, demonstrates its usefulness in patients after cardiac surgery [7, 17, 29]

The aim of this study was to compare postoperative cognitive deficit by objective P300 auditory evoked potentials and standard psychometric tests in patients undergoing aortic valve replacement (AVR) with an biological prosthesis and coronary artery bypass grafting (CABG).


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 Acknowledgments
 References
 
Patients
After approval was obtained by the Ethics Committee of the University of Vienna 30 consecutive survivors (mean age 70 ± 12 years) undergoing aortic valve replacement with a biological prosthesis were enrolled in this prospective study. Thirty patients undergoing standard CABG with CPB (mean age 70 ± 7 years) served as age- and sex-matched controls. Exclusion criteria included a hemodynamically relevant carotid artery stenosis (of more than 75%) and a history of one of the following medical conditions: prior stroke with residual deficit, uncontrolled hypertension, psychiatric illness requiring treatment, alcoholism, renal disease (defined as a creatinine more than 2.0 mg/dL), active liver disease or presence of significant aortic sclerosis in routinely performed intraoperative transesophageal echocardiography (TEE). Narcotics for pain relieve were restricted to the time of chest tube drainage. Chest tubes were removed on postoperative day 2. All investigations were performed by the same investigator who was blinded to the group classification (single blind, prospective design).

Preoperative risk stratification
Preoperative risk stratification was performed using the EuroSCORE (European System for Cardiac Operative Risk Evaluation). 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 [11].

Neuropsychological testing
Neuropsychological testing and physical examinations were completed preoperatively and 7 days and 4 months after surgery. The investigator performing the preoperative and postoperative assessments was blinded to the group classification of each patient. Neuropsychological testing consisted of auditory P300 evoked potentials, Mini-Mental State Examination (MMSE), and Trailmaking Test A.

Auditory p300 evoked potentials
Cognitive P300 auditory evoked potentials were recorded with Ag/AgCl electrodes on a Nicolet 2000 (Nicolet, Madison, WI). P300 evoked potentials were generated after 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) and referenced to linked earlobe A12 electrodes (10/20 international system). During the paradigm the subjects 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 subjects were rejected and repeated. P300 evoked potential recording resulted in a stable sequence of positive and negative peaks. Latencies (ms) of the cognitive P300 peak were assessed. To confirm reproducibility two sets of P300 measurements were recorded in all patients. To avoid any influence of biorhythm alteration all study measurements were performed in the afternoon under comparable conditions by the same physician. Special care was taken that studied patients were free from narcotics or sedatives for at least 48 hours.

Psychometric tests
Immediately after P300 recording, the standard psychometric tests Trailmaking Test A and MMSE were performed to test cognitive impairment and psychometric performance. To minimize learning effects, five different Trailmaking Tables were randomly used. The Trail Making Test (Trails; part A) requires subjects to connect, by drawing a line, a series of numbers and letters in sequence (ie, 1-2–3) as quickly as possible [12]. The MMSE is a widely used method for assessing cognitive mental status. It assesses orientation, attention, immediate and short-term recall, language, and the ability to follow simple verbal and written commands. Furthermore it provides a total score that places the subject on a scale of cognitive function [13].

Anticoagulation regimen
Avr patients
Perioperative 2 x 7500 IE/d Dalteparin-Natrium (Fragmin; Pharmacia and Upjohn GmbH; Vienna, Austria) was started on day 5 with Phenoprocoumon (Marcumar; Roche Austria GmbH, Vienna, Austria) for 2 months (targeted international normalized ratio [INR] range: 2 to 3; targeted INR: 2.5). In case of persistent atrial fibrillation (AF) Phenoprocoumon was continued (targeted INR range: 2 to 3; targeted INR: 2.5). In case of sinus rhythm patients were switched to low-dose aspirin (Thrombo Ass; Lannacher Heilmittel GmbH, Lannach, Austria).

CABG patients
Perioperative 2 x 5000 IE/d low-molecular-weight heparin Dalteparin-Natrium (Fragmin), and in case of AF 2 x 7500 IE Dalteparin-Natrium, and aspirin (Thrombo Ass) was started on postoperative day 1 life long. In case of persistent AF Phenoprocoumon was continued (targeted INR range: 2 to 3; targeted INR: 2.5).

Follow-up
In addition to the neuropsychological testing patients were studied by means of echocardiography, electrocardiography, blood tests, and clinical investigation at all points of follow-up.

Anesthesia and surgical procedure
Patients were premedicated with midazolam. Additionally midazolam in 1 mg increments was administered intravenously as needed for general anesthesia with midazolam, ethmidate, fentanyl, and pancuronium. Patients were ventilated with oxygen in air; ventilation was set to a tidal volume of 8 mL/kg and a respiratory rate of 12/min, PEEP 5. The TEE probe was placed after anesthetic induction in all patients. The TEE views used to assess regional wall motion abnormalities included the transesophageal four- and two-chamber views and the transgastric short- and long-axis views.

Surgical access in both groups was gained through a median sternotomy. All patients underwent normothermic CPB with intermittent cold blood cardioplegia with a hot shot before opening the cross clamp. The CPB circuit consisted of a hollow-fiber oxygenator (Bard HF 5701; C.R. Bard, Havorhill, MA) and a lining system primed with ringer lactate, mannitol, heparine, and apoproteine. Flow during CPV was maintained at 2.5 l · min-1 · m-2. Blood cardioplegia was maintained at 4:1 ratio. Hematocrit was kept above 20% with packed red blood cells if necessary. Perfusion pressure during CPB was kept above 50 mm Hg with phenylephrine if necessary. Before opening of cross-clamp as well as weaning from cardiopulmonary bypass careful deairing was performed through the apex of the heart and the ascending aorta under continuous inflation of the lungs. This was vigorously controlled by TEE monitoring. Heparin was antagonized with protamine sulfate until preoperative activated clotting time was achieved. Mean arterial pressure after CPB was kept above 60 mm Hg with volume and vasoactive drugs as appropriate. Intensive care unit treatment was performed according to institutional standards.

Statistical analysis
Data are reported as mean ± SD. Comparison of P300 auditory evoked potentials and standard psychometric tests were performed using two-way analysis of variance (ANOVA) after testing for normality of distribution. Categoric variables were compared using the {chi}2 test or Fisher’s exact test as appropriate. Values of p less than 0.05 were considered as significant, two sided. The study was analyzed using SAS software, version 8 (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 Acknowledgments
 References
 
Thirty elective patients receiving aortic valve replacement at our institution were prospectively observed. These patients were age and sex matched with a cohort of patients receiving elective CABG with CPB. Preoperative risk measured with EuroSCORE (AVR 5.9 ± 2.5 versus CABG 4.9 ± 1.5, p = 0.0425) as was higher in the valve group. Patient characteristics are given in Table 1.


View this table:
[in this window]
[in a new window]
  		Table 1. Patient Characteristics

 
Clinical outcome
As only survivors entered this prospective study, operative mortality was 0%. In the period of follow-up there was no death in either group. Although operation time was higher in the CABG group (AVR 193 minutes versus CABG 227 minutes, p = 0.043) CPB times were comparable (AVR 92 minutes versus CABG 88 minutes, p = 0.677). One patients in the CABG group had a postoperative myocardial infarction (defined as any new Q wave or loss of R in the electrocardiogram, significant creatinine kinase-MB elevation [>40 U/L]). There was no postoperative stroke. A total of 27 patients developed postoperative atrial fibrillation (AVR n = 10 versus CABG n = 7, p = 0.344). Reexploration for bleeding was performed in 1 patient in the AVR group. On the first postoperative day, 2 patients in the CABG group had "transitory psychotic syndrome" (defined as preserved wakefulness with affective liability and disorientation, which completely resolved with 24 hours) [37]. Clinical outcome is shown in Table 2.


View this table:
[in this window]
[in a new window]
  		Table 2. Clinical Outcome

 
Objective p300 auditory evoked potentials
In preoperative measures there was no difference between patients undergoing aortic valve replacement (AVR) and patients undergoing CABG (AVR 378 ± 37 ms versus CABG 374 ± 32 ms, p = 0.629). One week after surgery P300 peak latencies were prolonged (impaired) in both groups compared with preoperative values (AVR 405 ± 43 ms versus 378 ± 37 ms preoperative, p = 0.001; CABG 398 ± 44 ms versus 374 ± 32 ms preoperative, p = 0.004). At this point of follow-up there was no difference between the groups (p = 0.607). Finally, 4 months after surgery P300 auditory evoked potentials returned to normal in the CABG group (380 ± 24 ms versus 374 ± 32 ms preoperative, p = 0.940) whereas in contrast in the AVR group they continued to become prolonged (worsened) compared with preoperative values (410 ± 47 ms versus 378 ± 37 ms preoperative, p = 0.005). At 4 months of follow-up P300 measures were worse in AVR patients as compared with CABG patients (p = 0.032; Fig 1).



View larger version (12K):
[in this window]
[in a new window]
  		Fig 1. P300 auditory evoked potentials: graph shows serial assessments of cognitive brain function by P300 auditory evoked potentials. The solid line represents coronary artery bypass graft surgery patients, the dotted line aortic valve replacement patients. *p < 0.05 compared with preoperative values. {dagger}p < 0.05 within the two groups.

 
Standard psychometric tests
To detect clinically overt changes of cognitive brain function we used the MMSE and Trailmaking Test A. Both tests showed no statistically significant changes throughout the study period. This finding only suggests that all patients were without clinical neurologic problems. Results of Trailmaking Test A and MMSE are given in Table 3.


View this table:
[in this window]
[in a new window]
  		Table 3. Scores on Tests of Neurocognitive Function

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
Acknowledgments
 References
 
In this prospective series we found by objective P300 auditory evoked potentials that patients undergoing AVR with a biological prosthesis and CABG have markedly decreased cognitive brain function in postoperative measures (7 days). Most important, in 4-month follow-up cognitive brain dysfunction returns to normal in patients undergoing CABG, whereas it persists or even worsens in patients after AVR.

Postoperative cognitive dysfunction has been reported to occur in 30% to 70% of patients undergoing open heart surgery with CPB [2–4, 15]. The most frequently reported deficits related to surgery with CPB are those of concentration, memory, and learning, and speed of visual-motor response [16]. We have to keep in mind that neurologic and neuropsychological impairments related to CPB are not only disconcerting and demoralizing and therefore affect the daily life of patients but also have tremendous social and economic implications [4].

In 7-day postoperative investigations we found that both patient groups exhibited a similar extent of impaired cognitive processing. It is generally suspected that postoperative cognitive decline may be caused by impaired cerebral perfusion during CPB and postoperative systemic inflammatory response as well as microembolism and macroembolism [2, 15]. Comparing two different types of operative procedures—AVR versus CABG—we speculate now that perioperative cognitive decline seems to reflect primarily extensive operative trauma (eg, tissue trauma, use of CPB, and potential systemic inflammation) mimicking the potential impact of factors particularly related to the type of operative procedure (eg, air embolism, particulate matter, blood-valve prosthesis interaction in AVR versus, for example, partial cross-clamping in CABG).

Most interestingly, from 7-day through 4-month follow-up cognitive processing takes different courses. In CABG patients cognitive brain function normalizes again whereas in AVR patients (with biological valve prostheses) cognitive impairment continues. The reasons for this remain unclear and may only be—for the moment—subject to speculation. It seems likely that more extensive injury occurs during operation in the "open heart" AVR patients owing to potential particulate matter and air emboli. One might speculate now that in AVR patients this intraoperative damage may result in neurocognitive changes that persist or even worsen over time. This speculation is supported by data from Braekken and associates [17] who report that AVR leads to a higher number of intraoperative microemboli as compared with CABG. Another potential explanation may be the fact that the biological valve itself serves as a possible source of microemboli. Whereas cavitation phenomena do not seem likely in biological prostheses, disturbances at the blood valve-surface interface may be speculated (eg, subclinical insufficiency of anticoagulation regimen). Recently postoperative AF has been found to affect cognitive brain function [31]. We have found no difference in the occurrence of AF between CABG and AVR patients at 7-day and 4-month follow-up. Therefore the impact of AF on the diverging development of cognitive brain function in this study seems to be limited.

To compare cognitive function between patients we used P300 auditory evoked potentials and standard psychometric tests. P300 peak latencies of auditory evoked potentials have widely been used to evaluate cognitive brain function in different diseases and have been proven in their usefulness for measuring cognitive brain function in patients undergoing open heart surgery [5–8, 18, 19]. In our series psychometric tests failed to reveal any subtle cognitive decline. This only suggests that all patients were without any overt neurologic disorders throughout the study period. It is generally accepted that psychometric tests are not without bias, eg, in part because of long performance times (stressing attention), visual impairment, influence of psychomotor function, level of education, or learning effects [19–21]. The latter are of particular interest for follow-up studies [22]. Cognitive P300 evoked potentials elicited by a tone discrimination paradigm represent an objective and valid measure of cognitive brain function. P300 peak latencies, which increase with age in healthy subjects, are related to cognitive impairment rating, rapid evaluation of cognitive function test, orientation, stimulus evaluation, selective attention, visual pattern recognition, and digit span and were shown to be much more sensitive in detecting metabolically induced cognitive brain dysfunction than psychometric tests or electroencephalograms [6, 8, 18, 23–29]. Moreover the P300 technique has a very low intraindividual test-retest variability with a coefficient of variation of 2%, which further stresses its usefulness for cognitive follow-up studies [5].

Limitations
It has to be taken into account that cognitive brain function can be influenced by various biases in 4-month follow-up and that there might be confounding factors we did not list in this study. In the present study selected CABG-patients served as age-matched controls to patients after aortic valve surgery. Therefore the presented measures of P300 potentials are only valid for CABG patients in the mean age range of 70 years undergoing normothermic cardiopulmonary bypass. These data can not be extrapolated to other age ranges, different comorbidities (eg, diabetes mellitus, significant carotid artery stenosis), and perfusion protocols. From the present data we are also unable to totally exclude that 4-month cognitive impairment in AVR patients is only a result of extremely delayed return to normal values. Still, the major limitation of the present paper is that we are only able to show that a patient carrying a biological aortic valve prosthesis has a more pronounced cognitive deficit as compared with an age-matched CABG patient. As to potential pathologic mechanisms, we can only speculate and proceed with further studies.

Taking these limitations into account we conclude that after a 4-month follow-up impairment of cognitive brain function is more pronounced in patients undergoing biological AVR as compared with sex- and age-matched CABG patients who served as controls. The underlying mechanisms of this particular ongoing cognitive damage need to be elucidated by further studies.14,30


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
References
 
We thank Daniela Dunkler, MS (Stat), for the statistical analysis of the work.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Weintraub W.S., Jones E.L., Craver J., Guyton R., Cohen C. Determinants of prolonged length of hospital stay after coronary bypass surgery. Circulation 1989;80:276-284.[Abstract/Free Full Text]
  2. Roach G.W., Kanchuger M., Mangano C.M., et al. Adverse cerebral outcomes after coronary bypass surgery. Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators. N Engl J Med 1996;335:1857-1863.[Abstract/Free Full Text]
  3. Sotaniemi K.A. Long-term neurologic outcome after cardiac operations. Ann Thorac Surg 1995;59:1336-1339.[Abstract/Free Full Text]
  4. Newmann M.F., Kircher L.J., Phillips-Buke B., et al. Longitudinal assessment of neurocognitive function after coronary artery bypass grafting. N Engl J Med 2001;6:369-402.
  5. Grimm G., Oder W., Prayer L., Ferenci P., Madl C. Evoked potentials in assessment and follow-up of patients with Wilson’s disease. Lancet 1990;336:963-964.[Medline]
  6. Madl C., Grimm G., Kramner L., et al. Cognitive brain function in non-demented patients with low grade and high-grade aortic stenosis. Eur J Clin Invest 1994;24:559-564.[Medline]
  7. Engelhardt W., Dierks T., Pause M., Sold M., Hartung E., Silber R. P300-mapping—a neurophysiological tool to quantify cerebral dysfunction after coronary artery bypass grafting. Eur J Cardiothorac Surg 1995;9:12-17.[Abstract]
  8. Polich J., Ehlers C.L., Otis S., Mandell A.J., Bloom F.E. P300 latency reflects the degree of cognitive decline in dementing illness. Electroencephalogr Clin Neurophysiol 1986;63:138-144.[Medline]
  9. Pozzessere G., Valle E., De Crignis S., et al. Abnormalities of cognitive functions in IDDM revealed by P300 event-related potential analysis. Comparison with short-latency evoked potentials and psychometric tests. Diabetes 1991;40:952-958.[Abstract]
  10. Caracco R.Q., Bodis-Wolner I. . Frontiers of clinical neuroscience. New York: Alan R Liss, 1986.
  11. Nashef S., Roques F., Michel P., et al. Coronary surgery in Europe: comparison of the national subsets of the European system for cardiac operative risk evaluation database. Eur J Cardiothorac Surg 2000;17:396-399.[Abstract/Free Full Text]
  12. Reitan R.M. Validity of the Trail Making Test as an indicator of organic brain damage. Percept Mot Skills 1958;8:271-276.
  13. Folstein MF, Folstein, SE, McHugh PR. Mini-Mental State. A practical method for grading the state of patients for the clinician. J Psych Res 12:189–98.
  14. Spittler J.F. Disorders of consciousness: the basis for ethical assessment. Fortschr Neurol Psychiatr 1999;67:37-47.[Medline]
  15. Taylor K.M. Brain damage during cardiopulmonary bypass. Ann Thorac Surg 1998;65:20-26.
  16. Shawn P.J., Bates D., Cartlidge N.E., et al. Neurologic and neuropsychologic morbidity following major surgery: comparison of coronary artery bypass and peripheral vascular disease. Stroke 1987;14:700-707.
  17. Braekken S.K., Reinvang I., Russel D., Brucher R., Svenneving J.L. Association between intraoperative cerebral microembolic signals and postoperative neuropsychological deficit: comparison between patients with cardiac valve replacement and patients with coronary artery bypass grafting. J Neurol Neurosurg Psychiatry 1998;65:573-576.[Abstract/Free Full Text]
  18. Grimm M., Czerny M., Baumer H., et al. Normothermic cardiopulmonary bypass is beneficial for cognitive brain function after coronary artery bypass grafting—a prospective randomized trial. Eur J Cardiothoracic Surg 2000;18:270-275.[Abstract/Free Full Text]
  19. Rossini E.D., Karl M.A. The Trail Making Test A and B: a technical note on structural nonequivalence. Percept Mot Skills 1994;78:625-626.[Medline]
  20. Kempen J.H., Krichevsky M., Feldman S.T. Effect of visual impairment on neuropsychological test performance. J Clin Exp Neuropsych 1994;16:223-231.[Medline]
  21. Rossini E.D., Karl M.A. The Trail Making Test A and B: a technical note on structural nonequivalence. Percept Mot Skills 1994;78:625-626.
  22. Conn H.O., Lieberthal M. The hepatic coma syndromes and lactulose. Baltimore, MD: Williams and Wilkins, 1979:169-198.
  23. Gil R., Neau J.P., Toullat G., Rivasseau-Jonveaux T., Lefevre J.P. Maladie de Parkinson et potentiels évoqués cognitifs. Rev Neurol (Paris) 1989;145:201-207.[Medline]
  24. Courchnesne E., Hillyard S.A., Galambos R. Stimulus novelty, task relevance, and the visual potential in man. Electroencephalogr Clin Neurophysiol 1975;39:131-143.[Medline]
  25. McCarthy G., Douchin E. A metric for thought: a comparison of P300 latency and reaction time. Science 1981;211:77-80.[Abstract/Free Full Text]
  26. Hansen J.C., Hillyard S.A. Endogenous brain potentials associated with selective auditory attention. Electroencephalogr Clin Neurophysiol 1980;49:277-290.[Medline]
  27. Ritter W., Simson R., Vaughan H.G., Jr, Macht M. Manipulation of event related potential manifestations of information processing stages. Science 1982;218:909-911.[Abstract/Free Full Text]
  28. De Feo P., Gallai V., Mazzota G., et al. Modest decrements in plasma glucose concentration cause early impairment in cognitive function and later activation of glucose counterregulation in the absence of hypoglycemic symptoms in normal men. J Clin Invest 1988;82:436-444.
  29. Ginn H.E. Neurobehavioral dysfunction in uremia. Kidney Int 1975;7(suppl 2):S217-S221.
  30. Kilo J., Czerny M., Gorlitzer M., et al. Cardiopulmonary bypass affects cognitive brain function after coronary artery bypass grafting. Ann Thorac Surg 2001;72:1926-1932.[Abstract/Free Full Text]
  31. Stanley T.O., Mackensen G.B., Grocott H.P., et al. The impact of postoperative atrial fibrillation on neurocognitive outcome after coronary artery bypass graft surgery. Anesth Analg 2002;94:290-295.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 CirculationHome page
T. Feldman and M. B. Leon
Prospects for Percutaneous Valve Therapies
Circulation, December 11, 2007; 116(24): 2866 - 2877.
[Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
D. Zimpfer, M. Czerny, P. Schuch, R. Fakin, C. Madl, E. Wolner, and M. Grimm
Long-Term Neurocognitive Function After Mechanical Aortic Valve Replacement
Ann. Thorac. Surg., January 1, 2006; 81(1): 29 - 33.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
S. C. Knipp, N. Matatko, M. Schlamann, H. Wilhelm, M. Thielmann, M. Forsting, H. C. Diener, and H. Jakob
Small ischemic brain lesions after cardiac valve replacement detected by diffusion-weighted magnetic resonance imaging: relation to neurocognitive function
Eur. J. Cardiothorac. Surg., July 1, 2005; 28(1): 88 - 96.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
D. Zimpfer, M. Czerny, F. Vogt, P. Schuch, L. Kramer, E. Wolner, and M. Grimm
Neurocognitive deficit following coronary artery bypass grafting: a prospective study of surgical patients and nonsurgical controls
Ann. Thorac. Surg., August 1, 2004; 78(2): 513 - 518.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
M. Grimm and D. Zimpfer
Reply to Jahangiri and Motallebzadeh
Eur. J. Cardiothorac. Surg., October 1, 2003; 24(4): 666 - 666.
[Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
D. Zimpfer, J. Kilo, M. Czerny, M.-T. Kasimir, C. Madl, E. Bauer, E. Wolner, and M. Grimm
Neurocognitive deficit following aortic valve replacement with biological/mechanical prosthesis
Eur. J. Cardiothorac. Surg., April 1, 2003; 23(4): 544 - 551.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
M. Grimm, D. Zimpfer, M. Czerny, J. Kilo, M.-T. Kasimir, L. Kramer, A. Krokovay, and E. Wolner
Neurocognitive deficit following mitral valve surgery
Eur. J. Cardiothorac. Surg., March 1, 2003; 23(3): 265 - 271.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Georg M. Wieselthaler
Ernst Wolner
Michael Grimm
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zimpfer, D.
Right arrow Articles by Grimm, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zimpfer, D.
Right arrow Articles by Grimm, M.
Related Collections
Right arrow Cerebral protection

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS