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1 London, Ontario
2 Halifax, Nova Scotia
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Article appraised |
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 TOP Article appraised Commentary by J. MurkinReferencesCommentary by R. HallReferences |
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Structured abstract
Question: In patients undergoing elective coronary artery bypass grafting (CABG) with cardiopulmonary bypass, what is the effect of perioperative neurocognitive decline on long-term neurocognitive function?
Design: Prospective cohort followed for five years.
Setting: Single academic centre.
Patients: Two hundred and sixty-one adult patients undergoing elective CABG were enrolled. Patients with symptomatic cerebrovascular disease, psychiatric illness, renal disease, active liver disease, less than seventh grade education, or inability to read were excluded.
Assessment of prognostic factors: Predictors of long-term cognitive decline were determined by multivariate logistic and linear regression methods.
Main outcomes: Overall neurocognitive function and frequency of cognitive decline were the main outcomes. Overall cognitive function was assessed using a composite cognitive index (CCI) score representing the sum of scores of four neurocognitive domains (verbal memory and language comprehension; abstraction and visuospatial orientation; attention, psychomotor speed, and concentration; visual memory). Cognitive decline was defined as a decrease, compared to baseline, of one standard deviation in performance in any of the domains. Domains were derived by factor analysis of test results from nine neurocognitive tests. All tests were administered before surgery (baseline), one day before discharge, and six weeks, six months, and five years post-CABG. The study took place from March 1989 to November 1998.
Main results: By the end of the study, 172 patients had completed five years of follow-up, 23 had died, 14 could not continue due to health problems, and 52 were lost to follow-up. Frequency of cognitive decline was 53% at discharge, 36% at six weeks, 24% at six months, and 42% at five years. CCI scores (means ± SD; positive value = improvement, negative value = decline) were -0.36 ± 2.05 at discharge, 0.99 ± 2.03 at six weeks, 1.37 ± 2.11 at six months, and -1.45 ± 4.09 at five years. Older age, lower level of education, and cognitive decline at time of discharge predicted long-term cognitive decline at five years.
Conclusion: There is a high prevalence of cognitive decline after CABG. Cognitive decline at time of discharge predicts later cognitive decline at five years.
Funding: National Institutes of Health and the American Heart Association.
Correspondence: Dr. Mark F. Newman, Division of Cardiothoracic Anesthesia, Box 3094, Duke University Medical Centre, Durham, NC 27710, USA. E-mail: newma005{at}mc.duke.edu
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Commentary by J. Murkin |
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TOPArticle appraisedCommentary by J. MurkinReferencesCommentary by R. HallReferences |
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There are several potential explanations for these observations: 1) the bimodal appearance of symptoms reflects areas of cortical damage with initial compensation by the remaining brain and subsequent brain aging unmasking the original lesions; or 2) there are patients with an innate susceptibility (ApoE 4 allele), in whom exposure to cardiopulmonary bypass (CPB) unmasks as being unable to withstand the aging process as well as other patients. Both are under intense investigation. Irrespective, the fact remains that significant numbers of CABG patients are experiencing measurable CNS abnormalities, especially cognitive decline, which is often associated with abnormal neurological signs and may be a predictor of magnetic resonance imaging defined loss of brain mass.
Newman et al. suggest that CABG surgery is associated with a decline in cognitive function that is two to three times higher than the baseline incidence; however, their study did not include a suitable control group. At least one large prospective study, an investigation of 8,000 Japanese-Hawaiian patients suffering myocardial infarction (MI), CABG surgery, or stroke, was unable to confirm either MI or CABG surgery as predictors of late cognitive impairment.3 Forty-five percent of patients with previous stroke, compared to 16% with prior MI and 10% of men with previous CABG, were cognitively impaired.3 However, patients in the CABG cohort had relatively low surgical risk, came from higher socioeconomic classes, and had high education. Other sociogenetic factors may have also altered the risk profile of this group. Thus, confounders in the CABG cohort may have obscured any adverse impact of CABG on cognitive function.
Despite these uncertainties, CABG surgery with CPB is associated with a degree of increased CNS risk that is amenable to changes in intraoperative management: arterial line filtration and membrane oxygenation,3 alpha-stat pH management,4 and CABG without CPB.5 As CPB is a very important modality for circulatory support in a variety of clinical and therapeutic settings, the challenge is to enhance the circulatory support characteristics, with their attendant potential for powerful therapeutic extracorporeal blood and organ treatments, while minimizing CNS morbidity. The important work of Newman and colleagues underscores the need for further research in this area.
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TOPArticle appraisedCommentary by J. MurkinReferencesCommentary by R. HallReferences |
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2 Murkin JM, Baird DL, Martzke JS, Adams SJ, Lok P. Long-term neurological and neuropsychological outcome 3 years after coronary artery operations. Anesth Analg 1996; 82(Suppl.): S328.
3 Petrovitch H, White L, Masaki KH, et al. Influence of myocardial infarction, coronary artery bypass surgery, and stroke on cognitive impairment in late life. Am J Cardiol 1998; 81: 1017–21.[Medline]
4 Pugsley W, Klinger L, Paschalis C, Treasure T, Harrison M, Newman S. The impact of microemboli during cardiopulmonary bypass on neuropsychological functioning. Stroke 1994; 25: 1393–9.[Abstract]
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Murkin JM, Boyd WD, Ganapathy S, Adams SJ, Peterson RC. Beating heart surgery: why expect less central nervous system morbidity? Ann Thorac Surg 1999; 68: 1498–1501.
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Commentary by R. Hall |
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TOPArticle appraisedCommentary by J. MurkinReferencesCommentary by R. HallReferences |
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This study is important as it describes the magnitude of ongoing neurocognitive dysfunction following CABG surgery. The major criticism of the study design is the failure to follow a group of patients, who did not undergo CABG surgery, of similar age and disease burden over time to determine the degree to which non-surgical variables, such as age, influence the results. Does a change of one standard deviation in cognitive scores represent an important clinical difference? Evidence from a previous study suggests that, in the short-term, it does2 and anecdotal reports of patient outcomes suggest the same is true in the long-term ("Dad was never the same after his heart surgery").
What is the mechanism and what can be done to prevent the problem? Current wisdom suggests that cognitive decline is a combination of cerebral embolization, hypoperfusion, and the systemic inflammatory response.3 The independent role of cardiopulmonary bypass (CPB) should be evident from comparative studies of "off-pump" vs "on-pump" surgery. Preliminary results4 suggest that the role of CPB may not be as large as previously thought.
Efforts to reduce atheroemboli (use of epiaortic scanning to detect plaques, blood flow diversion using different types of arterial cannulation, or avoidance of aortic manipulation altogether), to monitor and maintain cerebral perfusion with avoidance of hyperthermia, and to avoid unprocessed blood from cardiotomy suction may all be useful manoeuvers.3 Preliminary observations suggest that pharmacological manipulation of the systemic inflammatory response using aprotinin may also prove useful.5
Arguably, improvement in neurological outcomes is the next major challenge facing cardiac surgery. By demonstrating that the neurocognitive component of central nervous system dysfunction is present in a significant number of patients at five years postsurgery, Newman et al. have helped to define the problem and establish a research agenda that must examine strategies to improve neurological outcomes.
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TOPArticle appraisedCommentary by J. MurkinReferencesCommentary by R. HallReferences |
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2
Roach GW, Kanchuger M, Mangano CM, et al., for the Multicenter Study of Perioperative Ischemia Research Group and the Ischemia Research and Education Foundation Investigators. Adverse cerebral outcomes after coronary bypass surgery. N Engl J Med 1996; 335: 1857–63.
3
Murkin JM. Attenuation of neurologic injury during cardiac surgery. Ann Thorac Surg 2001; 72: S1838–44.
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Lloyd CT, Ascione R, Underwood MJ, Gardner F, Black A, Angelini GD. Serum S-100 protein release and neuropsychologic outcome during coronary revascularization on the beating heart: a prospective randomized study. J Thorac Cardiovasc Surg 2000; 119: 148–54.
5
Levy JH, Pifarre R, Schaff HV, et al. A multicenter, double-blind, placebo-controlled trial of aprotinin for reducing blood loss and the requirement for donor-blood transfusion in patients undergoing repeat coronary artery bypass grafting. Circulation 1995; 92: 2236–44.
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