Postoperative Cognitive Dysfunction and Aortic Atheroma
Evered LA, Silbert BS, Scott DA. Ann Thorac Surg 2010;89:1091-7.
Reviewer: Nanhi Mitter, MD
Johns Hopkins Hospital, Baltimore, MD
Evered et al present data from the Australian Trial Evaluating Postoperative Cognitive Dysfunction, Early Extubation and Survival (ANTIPODES), a prospective randomized trial that helps to clarify the relationship between aortic atheroma and postoperative cognitive dysfunction (POCD). The study assessed 311 patients undergoing elective coronary artery bypass grafting (CABG) Intraoperative transesophageal echocardiography and epiaortic echocardiography imaging were used to ascertain the atheroma burden. Each of the four quadrants of the ascending and the proximal descending aorta were assessed and the atheroma was graded on a scale of 0 to 3, with 0 signifying normal or minimal plaque and 3 signifying mobile or rough plaque. Neuropsychological evaluation, a series of 8 tests, was performed the week prior to surgery and then 1 week, 3 months and 12 months postoperatively. POCD was defined as a decrease by one standard deviation from baseline in two or more tests. At each testing time, the atheroma burden was higher in patients with POCD than those without POCD. Furthermore, at one week, it was statistically significant (10.4 +/- 14.7 versus 4.4 +/- 9.0, p = 0.0002) but this difference dissipated progressively at both 3 months (8.9 +/- 14.1 versus 5.4 +/- 10.1, p= 0.06) and 12 months (6.6 +/- 12.0 versus 5.0 +/- 10.2, p= 0.56). In addition, the authors determined that age, which has been shown in the past to be a predictor of POCD, did not remain as a statistically significant predictor based on these results.
This is an interesting article that highlights the most common complication of CABG surgery – POCD. One of the best aspects of the study design was the fact that the anesthetic regimen was standardized avoiding labeling of the anesthetic technique as a potential confounding variable. However there were some limitations to the study that bear mentioning. First, the study patients were those that had only CABG surgery as opposed to those having valvular surgery – this latter group represents a population in which the incidence of stroke and POCD is higher. Secondly, patients with a PFO were not identified. Furthermore, only those patients in whom at least 8 images were obtained were included in the analyses. Although this may be a confounding variable, it certainly adds to the ability for the aortic atheroma burden score to reliably predict POCD. Finally, only 25% of the patients enrolled were female, which does not necessarily represent the surgical population presenting for CABG.
Although the incidence varies depending on the time of testing, the incidence of POCD at the time of hospital discharge is 53% with reports of 24% at 6 months and 42% at 5 years. The mechanism is multifactorial and largely unclear. One plausible explanation is that it occurs from those emboli originating in the aorta which by themselves are not large enough to cause stroke and therefore manifest as POCD. Aortic atheroma has been associated with perioperative stroke in patients undergoing CABG surgery and the incidence of stroke has been reported to be approximately 1% and can be as high as 15.3% in patients with severe aortic arch plaque. POCD is multifactorial and although the results of this study cannot definitively state that the POCD is a result of the aortic atheroma, it does suggest that this may be a predictor at one week.
In conclusion, Evered and colleagues present an elegant study that demonstrates that atheroma burdens can be a predictor of POCD one week after CABG surgery but may not be as reliable an indicator as time progresses.