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Original Articles: Adult Cardiac

Invited Commentary

Department of Anesthesiology & Critical Care Medicine, The Johns Hopkins Hospital, 600 N Wolfe St, Tower 711, Baltimore, MD 21287

(Email: chogue2{at}jhmi.edu).

Assessing neuropsychological testing performance has been widely used as a means for detecting subtle brain injury from cardiac surgery. As the demographics of patients change to include more elderly patients and those with hypertension, diabetes, and other conditions, controlling for the effects of cerebral vascular disease on perioperative cognitive test results becomes important. In a seminal report, Selnes and colleagues [1], for example, followed a cohort of patients undergoing coronary artery bypass surgery (CABG) surgery with cardiopulmonary bypass and a group of patients with documented coronary artery disease undergoing medical management for 6 years. These investigators found that late cognitive decline after CABG surgery was common, but that the degree of decline was no different than that observed in the nonsurgical control group. These provocative results suggest that late cognitive decline after CABG surgery is not necessarily related to delayed effects of anesthesia, cardiopulmonary bypass, or other surgical perturbations, but it is more likely the result of intercurrent medical events or the natural progression of cerebral vascular disease. Within this context, Evered and colleagues [2] report results of a study in 332 patients undergoing first time CABG surgery linking preoperative levels of amyloid proteins β42 and β40 with postoperative cognitive dysfunction at 3 months after surgery, but not 12 months after surgery. Amyloid beta (Aβ) peptides accumulate in the brain of patients with mild cognitive impairment and Alzheimer disease. Low plasma levels of Aβ42, unchanged levels of Aβ40, and a low Aβ42/Aβ40 ratio have been found in community dwelling individuals with these conditions [3]. It is suggested that low plasma Aβ42/Aβ40 ratio indicates prodromal neurodegenerative disease as Aβ are deposited selectively in the brain. The study by Evered and colleagues [2] provide evidence linking postoperative cognitive dysfunction with blood Aβ protein levels, but more work is needed before definitive conclusions can be drawn, preferably from larger studies and those that include diverse patient populations. These studies will need to address why this relationship was present in patients with cognitive dysfunction at 3 months but not at 12 months after surgery. If postoperative cognitive dysfunction is the result of the same neurodegenerative changes as mild cognitive impairment and Alzheimer disease, one might expect cognitive decline at both 3 and 12 months to show a relationship with Aβ levels. Alternatively, these findings might indicate that cognitive dysfunction 3 months after CABG surgery is a distinct pathologic process from that occurring 12 months after surgery. It is notable that the Aβ "signature" in this study of CABG surgery patients was not the same as that noted in community dwelling adults with mild cognitive impairment or Alzheimer disease, whereas the Aβ42/Aβ40 ratio is reduced. Finally, one must not conclude that the degree of cognitive change observed in this study is similar in severity to mild cognitive impairment or early Alzheimer disease. The approach to diagnosing postoperative cognitive dysfunction has not been rigorously evaluated for its ability to detect these severe forms of cognitive impairment [4]. Regardless, the results by Evered and colleagues [2] add to a growing body of literature that underscores the importance of patient-related factors, such as the natural progression of cerebral disease in cognitive decline after cardiac surgery.

	References

Top References

 

1. Selnes O, Grega M, Bailey M, et al. Cognition 6 years after surgical or medical therapy for coronary artery disease Ann Neurol 2008;63:581-590.[Medline]
2. Evered LA, Silbert BS, Scott DA, et al. Plasma amyloid β₄₂ and amyloid β₄₀ levels are associated with early cognitive dysfunction after cardiac surgery Ann Thorac Surg 2009;88:1426-1432.[Abstract/Free Full Text]
3. Graff-Radford N, Crook J, Lucas J, et al. Association of low plasma Abeta42/Abeta40 ratios with increased imminent risk for mild cognitive impairment and Alzheimer disease Arch Neurol 2007;64:354-362.[Abstract/Free Full Text]
4. Kanne S, Balota D, Storandt M, McKeel D, Morris J. Relating anatomy to function in Alzheimer's disease neuropsychological profiles predict regional neuropathology 5 years later Neurology 1998;50:979-985.[Abstract/Free Full Text]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted 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 Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hogue, C. W. Search for Related Content PubMed PubMed Citation Articles by Hogue, C. W. Related Collections Coronary disease Related Article