The Negative Long-term Neurocognitive Effects of CABG Surgery
Abstract & commentary
Synopsis: Patients with post-CABG cognitive abnormalities subsequently demonstrated early improvement followed by a significant later decline.
Source: Newman MF, et al. N Engl J Med. 2001;344: 395-401.
For more than 40 years, coronary-artery bypass grafting (CABG) surgery has proven to be a superbly effective procedure for revascularizing the coronary arterial circulation. With improvement in both surgical and anesthetic techniques, the CABG mortality rate has diminished significantly over the years, and now more than 500,000 bypass procedures are being performed in the United States each year. In contrast to the numerous infrequent complications that can occur post-CABG, postoperative cognitive decline has been detected in a significant number of elderly patients with the incidence being highest at discharge (ie, 50-80%), dropping down to 20-50% at 6 weeks, and even further (10-30%) at 6 months.1-4
Newman and associates, representing the Neurological Outcome Research Group and the Cardiothoracic Anesthesiology Research Endeavors Investigators from Duke University, conducted a prospective investigation to accurately determine the long-term effects on cognitive function in those patients who suffered immediate perioperative cognitive deterioration by following them longitudinally for 5 years after cardiac surgery. Neurocognitive tests were performed preoperatively, before discharge, and at 6 weeks, 6 months, and 5 years after CABG surgery in 261 patients. The incidence of cognitive decline was 53% at discharge, 36% at 6 weeks, 24% at 6 months, and 42% at 5 years. These results suggested that patients with post-CABG cognitive abnormalities subsequently demonstrated early improvement followed by a significant later decline.
Comment by Harold L. Karpman, MD, FACC, FACP
Advances in medical care and invasive revascularization procedures (ie, PTCA, stenting, etc) have in many cases prevented but, in many other cases, simply delayed CABG procedures thereby resulting in an increasing number of patients coming to CABG surgery at more advanced ages. Besides the well-recognized post-CABG complications of stroke, delirium, and/or short-term cognitive changes, long-term cognitive changes have not been fully appreciated. Even though many patients have complained that "I am just not the same as I was before surgery," cognitive changes had often not been recognized because the associated personality changes were usually quite subtle, often involving neuromuscular activity deterioration, mood swings, and loss of ability to plan complex activities.
Newman et al carefully performed a multivariate factor analysis to minimize the redundancy of tests and potential errors. In order to include as much data as possible, they gave patients who were unable to complete the testing at 5 years because of events such as death or stroke a worst-case score for cognitive function and then analyzed the data with and without these patients included; the inclusion of these patients resulted in only minimal changes in the calculated incidence of dysfunction and made no difference in the predictors of long-term cognitive decline. They concluded that the observed consistency of the predictors of cognitive decline and the composite cognitive index validated the stability of their model in which a patient’s age, educational level, and the presence or absence of perioperative cognitive decline consistently predicted the level of long-term cognitive function.
The results of the study were most intriguing because of what appeared to be a biphasic course to the negative effects on cognitive function observed in many patients post-CABG, that is, an immediate postoperative decline was followed by improvement and then a subsequent late decline. There was a distinct association between early postoperative and late cognitive decline even after adjustment for many covariates—suggesting that the patient with perioperative decline is at distinctly increased risk for long-term cognitive decline. The study suffered because it did not include a control group, although it should be noted that studies of other normal control groups similar in nature to those undergoing CABG reported in the past have not found a similar incidence in decline of cognitive performance over a 5-year period.5
If, in fact, a late decline in cognitive performance occurs after CABG, what is the explanation for it? Some authors have speculated that showers of embolic material from an atherosclerotic aorta are released during manipulation of that vessel and enter the cerebral vasculature resulting in occlusion of both small and large arterial vessels. Hypoperfusion with secondary ischemic encephalopathy must also be considered as a possible etiological factor.6 Finally, it should be recognized that the effects of anesthesia may result in short-term cognitive changes but almost certainly have no effect upon long-term cognitive performance.
Columnist Lance Morrow authored an essay about Vice President Dick Cheney’s recent hospitalization, which was published in the March 19, 2001, issue of Time magazine. He wrote, "Some lore has it that bypass people are a little crazier than most, that the cabbage’ (coronary-artery bypass) activates a wild hair." I am beginning to think there’s truth in the theory that bypass surgery damages the memory. Mine was once photographic. Now I have to work harder sometimes to fetch a name. The other day, for some reason, I wanted to retrieve the name of you know, the gonzo journalist of fear-and-loathing fame—Rolling Stone—you know. But the once perfectly familiar words skittered off into the dark, and it was half a day before I caught sight of them as they dodged around another corner of the mind—Hunter Thompson! I have seen no evidence of Cheney’s being depressed or acting screwy or forgetting things. He seems the perfect Duke of Kent, who was King Lear’s bluff, loyal, sane liegeman, and exec.
It would appear from the data presented by Newman et al that we must make every effort to prevent or reduce perioperative cognitive decline in order to preserve long-term cognitive function and, thereby, maintain or improve the quality of life in the rapidly growing population of patients who are being subjected to CABG. Those patients who demonstrate early postoperative cognitive decline should be treated aggressively with diet, medications, psychological support, and changes in lifestyle aimed at reducing the incidence or even preventing long-term cognitive impairment. Equally important, results of this study should encourage physicians to narrow their indications for recommending CABG surgery to only those patients who have solid, unquestionable indications for having this surgery performed. In particular, even though most elderly patients even with multiple health problems are now able to safely undergo surgical procedures without serious concern about loss of life, the fact remains that the elderly patient is at the greatest risk for developing a significant long-term impairment in cognitive function and, therefore, the indications for CABG in the elderly should be especially carefully considered and any appropriate alternative methods of therapy of the ischemic myocardium should be considered before selecting CABG as the treatment of choice. CABG should be avoided in all patients whose clinical situation permits them to be treated by noninvasive atraumatic techniques such as diet control, weight reduction, increasing physical activity, reducing emotional stress or strain, eliminating cigarette smoking, reducing cholesterol, and using statin drugs and/or other agents that will enhance the health of the endothelial linings of the coronary arteries.
References
1. Selnes OA, et al. Lancet. 1999;353:1601-1606.
2. Blumenthal JA, et al. Ann Thorac Surg. 1995;59: 1345-1350.
3. Newman MF, et al. Ann Thorac Surg. 1995;59: 1326-1330.
4. Murkin JM, et al. Anesth Analg. 1996;82(suppl 328): abstract.
5. Hornick P, et al. Curr Opin Cardiol. 1994;9:670-679.
6. Wilson RS, et al. Arch Neurol. 1999;56:1274-1279.
7. Caplan LR, Hennerici M. Arch Neurol. 1998;55: 1475-1482.
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