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Ann Thorac Surg 2004;78:1556-1562
© 2004 The Society of Thoracic Surgeons

Original article: cardiovascular

Aortic Atheroma Burden and Cognitive Dysfunction After Coronary Artery Bypass Graft Surgery

Shahar Bar-Yosef, MDa,*, Marc Anders, MDa, G. Burkhard Mackensen, MDa, Lian K. Ti, MDa, Joseph P. Mathew, MDa, Barbara Phillips-Bute, PhDa, Robert H. Messier, MD, PhDb, Hilary P. Grocott, MDa the Neurological Outcome Research Group and CARE Investigators of the Duke Heart Center

a Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina, USA
b Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA

Accepted for publication May 3, 2004.

* Address reprint requests to Dr Bar-Yosef, Division of VA Anesthesia, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC, USA 27710
baryo001{at}mc.duke.edu


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
BACKGROUND: Neurocognitive dysfunction (NCD) after coronary artery bypass graft (CABG) surgery is a common problem. Atherosclerotic disease of the aorta is a known risk factor for stroke after cardiac surgery, but its relationship to NCD is unclear. This study investigates the relationship between aortic atherosclerotic disease and NCD after CABG.

PATIENTS AND METHODS: Patients undergoing primary elective CABG were enrolled in an ongoing investigation of NCD after CABG. Intraoperative transesophageal echocardiography (TEE) of the thoracic aorta was performed and analyzed off-line to quantify atheroma burden. Neurocognitive evaluation was performed, both preoperatively and at 6 weeks after surgery. Multivariable linear regression (controlling for age, years of education, and base line cognitive index) was used to determine the relationship between NCD and atheroma burden in the ascending, arch, and descending aorta.

RESULTS: One hundred sixty-two patients who had a complete neurocognitive evaluation and adequate TEE images were studied. No significant relationship was found between NCD and atheroma burden in the ascending (p = 0.22), arch (p = 0.89) or descending aorta (p = 0.64).

CONCLUSIONS: Although the etiology of NCD is likely multifactorial, our results suggest that aortic atherosclerosis may not be the primary factor in the pathogenesis of post-CABG cognitive changes.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Although patients undergoing cardiac surgery today are older and manifest increasingly more complex cardiac and systemic diseases, overall perioperative mortality and morbidity appear to be decreasing [1, 2]. However, neurocognitive dysfunction (NCD) continues to contribute substantially to perioperative morbidity [3, 4], emphasizing the need for a better understanding of its pathophysiology.

The incidence of NCD after cardiac surgery varies between 20% and 80%, depending upon the definition used, population studied, tests used to evaluate NCD, and the timing of the evaluation after surgery [5–7]. In a recent longitudinal study, the incidence of NCD after coronary artery bypass graft surgery (CABG) was found to be 53% at discharge, 36% at 6 weeks after operation, and 24% at 6 months [4]. Neurocognitive decline significantly reduced quality of life after surgery [8], again highlighting the importance of preventing this complication.

Some known risk factors for NCD after cardiac surgery include advanced age, lower level of education [4], apolipoprotein E4 genotype [9], rate of rewarming after hypothermic cardiopulmonary bypass (CPB) [10], and postoperative hyperthermia [11]. As one of the major mechanisms implicated in NCD after cardiac surgery is multiple brain microemboli [12–14], and a correlation has been described between atherosclerotic aortic disease and the number of cerebral emboli detected by transcranial Doppler (TCD) [15], it is reasonable to hypothesize a relationship between aortic atherosclerosis and postoperative NCD.

Aortic atheroma is a well-known risk factor for stroke after cardiac surgery, but the handful of studies that have indirectly looked at its relationship with NCD had conflicting results [16–19]. Therefore, the purpose of this study was to assess the relationship between the extent of aortic atherosclerotic disease and NCD after CABG by using a large population that had undergone rigorous neurocognitive evaluations and detailed quantitative assessment of aortic atherosclerosis.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
Patient Identification
Following Institutional Review Board approval, we identified patients who had been enrolled in previous prospective studies investigating NCD after primary elective CABG between March 1999 and June 2001 and who had an intraoperative transesophageal echocardiography (TEE) study suitable for analysis of atheroma burden. Exclusion criteria included a past cerebrovascular event with residual neurologic deficits, psychiatric disease, creatinine greater than 2 mg/dL, and less than 7 years of education.

Anesthetic and Surgical Management
After induction of general anesthesia, a TEE probe was inserted and a comprehensive echocardiographic examination was performed, conforming to the American Society of Echocardiography/Society of Cardiovascular Anesthesia guidelines [20]. After systemic heparinization, cannulation for bypass was achieved through the ascending aorta. Hypothermic CPB (28° to 32°C) ensued with a nonpulsatile system with a membrane oxygenator and a 40-µm arterial line filter. Shed mediastinal blood was returned to the venous reservoir by the cardiotomy suction. Crystalloid prime was generally used, but blood was added to maintain a hematocrit of 18% or greater. Cold blood cardioplegia was used for myocardial protection. During CPB, pump flows were kept at 2 to 2.4 liters · min–1 · m–2 body surface area. Blood pressure was maintained at between 50 and 90 mm Hg by using phenylephrine, isoflurane, or sodium nitroprusside as needed (blood pressure >70 mm Hg was targeted in older patients or patients with known carotid disease). Arterial partial oxygen pressure was kept between 150 to 250 mm Hg and an {alpha}-stat pH management was used.

Neurocognitive Assessment
Neurocognitive testing protocol and data analysis have been described in detail previously [4] and conformed to the consensus recommendations for neurobehavioral assessment [21]. Tests used included the short story module of the Randt Memory Test, the Digit Span and Digit Symbol subtests of the Wechsler Adult Intelligence Scale-Revised, and the Trail Making Test, Part B. All tests were administered by experienced psychometricians (blinded to the atheroma assessments), both preoperatively and at 6 weeks after surgery.

Echocardiographic Analysis
The intraoperative TEE study was recorded on either videotape or optical disk, and was later analyzed off-line by an investigator blinded to the neurocognitive test results. The aorta was divided into three segments: ascending, arch, and descending. The most diseased part seen in each segment was captured and digitized as a single-frame image. Image analysis software (NIH Image 1.62, National Institutes of Health, Rockville, MD) was used to calculate the atheroma burden, defined as the percentage of the viewed aortic lumen area that is occupied by atherosclerotic plaque (Fig 1) [22]. The calculation was done separately for each of the three aortic segments. This method allows for a quantitative bidimensional evaluation of the atherosclerotic disease. We also recorded the maximal height of the atherosclerotic plaque in each of the three aortic segments, a unidimensional index traditionally used for grading atheroma [23].



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  		Fig 1. Calculation of the aortic atheroma burden from the intraoperative two-dimensional transesophageal echocardiographic cross-section of the aorta (A = atherosclerotic plaque; B = aortic lumen area). (Modified from J Thorac Cardiovasc Surg, 125, Ti LK et al, Apolipoprotein e4 increases aortic atheroma burden in cardiac surgical patients, 211–3, Copyright 2003, with permission from the American Association for Thoracic Surgery [22].)

 
Statistical Analysis
For the neurocognitive data, principal component analysis on the nine individual subscale raw scores identified four distinct factors (representing the cognitive domains of verbal memory, figure memory, attention and concentration, abstraction, and psychomotor processing speed) that together contributed to 86% of test score variability. Scores from these four factors were added to calculate a unified cognitive score for each patient at each time point [4]. A continuous outcome variable, a cognitive change score (CCS), was then defined as the difference between the 6-week and the baseline cognitive scores and was used as the primary endpoint in linear regression analysis. This score was usually positive, reflecting learning effect; therefore, lower values of this score reflected more severe NCD. As a secondary endpoint, a dichotomous outcome variable was defined based on a decline of at least one standard deviation (calculated from the baseline scores) in at least one of the four cognitive domains. This was analyzed using logistic regression analysis.

In a previous investigation, the main predictors for neurocognitive decline after CABG included age, number of years of education, and the baseline cognitive score [4]. Therefore, in the present study we used multiple regression analysis to control for these variables as well as for CPB length, aortic cross-clamp time, and the presence of diabetes mellitus. The analysis was repeated separately for each of the three aortic segments to determine the relationship between the CCS and the atheroma burden.

Because results of the atheroma assessment were often available intraoperatively to the surgeons and thus could potentially alter surgical technique, we collected data regarding one possible alteration (the use of a single aortic cross-clamp technique vs the use of a separate side-clamp for proximal vein graft anastomoses) and tested its significance in the multivariable model.

In addition, owing to concerns about the nonnormality of the aortic atheroma burden data, and in particular the large percentage of patients with no atheroma at all in the ascending aorta, we undertook a secondary analysis in which patients were dichotomized into "high" and "low" atheroma burden groups, with 25% of the patients belonging to the "high" burden group. This binary categorical variable was then tested in the multiple regression models in place of the continuous variable of atheroma burden.

Data are expressed as mean ± standard deviation, unless otherwise stated. For all tests, a p value of less than 0.05 was considered significant. Statistical analysis was performed by using SAS version 8.02 (SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
The study enrolled 201 patients, and their demographic data are presented in Table 1. The extent of atherosclerotic disease, as measured both by atheroma burden and atherosclerotic plaque height, was largest in the descending aorta and smallest in the ascending aorta. A strong correlation was found between these two methods of evaluating the extent of atherosclerotic disease (Table 2).


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  		Table 1. Patient Demographics

 

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  		Table 2. Correlation Between Atheroma Burden and Atherosclerotic Plaque Height in the Three Aortic Segments

 
Of the 201 patients, 162 (81%) completed the follow-up neurocognitive evaluation at 6 weeks after surgery. The other 39 patients were lost to neurocognitive follow-up; the reasons for their attrition are detailed in Table 3. These patients had a higher atheroma burden in the descending aorta and a lower baseline cognitive score (Table 4). The remainder of the analysis was based on the 162 patients with a complete neurocognitive evaluation and adequate TEE images.


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  		Table 3. Reasons for Attrition From the Study Before Completing 6-Week Neurocognitive Evaluation

 

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  		Table 4. Characteristics of Patients Who Were Lost to Follow-Up Versus Patients Who Completed Neurocognitive Evaluation

 
Only one patient suffered a perioperative stroke. Sixty-one out of 162 patients (38%) demonstrated a significant decline in at least one cognitive domain. A simple linear regression analysis found no relationship between the CCS and the atheroma burden in any of the three aortic segments (Fig 2 and Table 5). Multivariable models were constructed to relate the CCS to the atheroma burden, patient age, baseline cognitive score, years of education, CPB time, cross-clamp time, and the presence of diabetes mellitus. The last three factors were found nonsignificant (p = 0.77 to 0.82) and were therefore omitted from the final model (Table 6). The atheroma burden in the ascending aorta was not a significant predictor of NCD (p = 0.22). Similar results were seen for the aortic arch (p = 0.89) and descending aorta segments (p = 0.64) as well as when atherosclerotic plaque height was used instead of atheroma burden (data not shown).



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  		Fig 2. Scatter plots, fitted regression line (solid line), and 95% confidence limits for the regression line (dashed lines) of the relationship between the cognitive change score and the aortic atheroma burden in the (A) ascending aorta, (B) aortic arch, and (C) descending aorta.

 

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  		Table 5. Atherosclerotic Burden as a Predictor of Cognitive Change Score: Simple Linear Regression Analysis

 

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  		Table 6. Atherosclerotic Burden in the Ascending Aorta as a Predictor for Cognitive Change Score: Multiple Regression Model

 
The dichotomous neurocognitive outcome variable was also tested for its relationship with the atheroma burden in a logistic regression analysis, but none of the models (one for each aortic segment) was statistically significant. As many patients had no detectable atheroma, especially in the ascending aorta (Fig 2), a secondary analysis was conducted with atheroma burden as a binary categorical variable, and again no significant relationship with CCS was observed.

Information about the aortic clamp technique was available for 146 of the 162 patients (90%): in 98 patients a single aortic cross-clamp was used, and in 48 patients the proximal anastomoses were performed with a side-biting partial-occluding clamp after the aortic cross-clamp was removed. This choice was found to be highly surgeon-specific, and the inclusion of this factor in the multiple regression models did not affect the results.

Because of the potentially important clinical implications of reporting a "no relationship" finding and the limitations imposed by our sample size, we did a sensitivity analysis to determine the largest effect size that our analysis might have missed owing to power. Given our sample size of 162 and {alpha} of 0.05, we had a 90% power to detect a correlation coefficient of 0.25 between the ascending aorta atheroma burden and the CCS. A correlation of this magnitude corresponds to an r2 = 0.0625. Therefore, it is possible that atheroma burden could account for as much as 6.25% of the variability in the CCS, without being detected by our study.


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
We were unable to show a relationship between the extent of atherosclerotic disease in any segment of the thoracic aorta and the degree of neurocognitive dysfunction after CABG. Although we were technically underpowered to rule out this correlation altogether, the fact that we were at least powered to detect a 6.25% contribution of atheroma to the variability of NCD, along with the widely scattered data seen in Figure 2, make it unlikely that we missed any clinically meaningful relationship. This suggests that aortic atherosclerosis, unlike its proven relationship to stroke after cardiac surgery [24–26], may not be a primary factor in the pathogenesis of NCD that develops after cardiac surgery. This unexpected finding deserves some further elaboration.

Although focal macroemboli are considered a major etiologic factor for stroke after cardiac surgery, NCD probably reflects a more diffuse cerebral injury with different pathophysiologic mechanisms and risk factors [27]. Possible mechanisms include cerebral microemboli, global cerebral hypoperfusion, cerebral and systemic inflammatory responses, hyperthermia-related cerebral damage, cerebral edema formation, and genetically determined vulnerabilities [11, 28–30]. Several studies have shown a correlation between post-CABG NCD and the number of microemboli detected by TCD [13, 14]. However, Doppler techniques cannot determine the composition of the microemboli, be they particulate (derived from atheromatous plaque, thrombus, lipid, or materials from the CPB circuit) or gaseous. In fact, conflicting results exist regarding the relationship between atheromatous disease and TCD-detected microemboli [15, 31]. As a result, although TCD-detected emboli correlate with NCD, and atheroma may also have a correlation (albeit weak) with TCD results, other sources of emboli may be equally or even more important.

The significance of gaseous airborne emboli is suggested by an increased rate of NCD after open heart surgery compared with CABG [32] and by a positive correlation between NCD and the number of perfusionist interventions that introduce minute air bubbles into the bloodstream, such as injection of medications or blood withdrawal through the CPB machine [33]. An increased number of brain emboli related to use of the cardiotomy suction suggests the importance of lipid-containing emboli originating from tissues in the mediastinum, pericardial sac, and sternal bone marrow [34]. In addition, both aluminum and silicon that originated from the CPB apparatus were found in histologic sections of brain emboli after cardiac surgery [35].

The evidence supporting a relationship between aortic atherosclerosis and postoperative NCD is weak. Goto and colleagues found a correlation between "total atherosclerosis load" and 7-day postoperative NCD [18]. However, their definition of total atherosclerotic score included carotid atherosclerosis as well as preexisting ischemic brain damage (as seen on magnetic resonance imaging), both factors that may increase the risk for NCD independent of aortic atherosclerosis.

Two studies have indirectly examined the relationship between atherosclerosis and NCD by assessing the effect of modification of the surgical technique on the incidence of postoperative NCD:

In contrast to these studies, our study tested directly the isolated effect of atheroma burden, and neurocognitive testing was rigorously performed at relevant time points.

Several potential limitations of the current study, however, merit consideration. TEE is typically limited in its ability to detect distal ascending aortic disease owing to acoustic shadowing from the major airways [36]. The use of epiaortic echocardiographic imaging can be very useful in imaging this area and in guiding the surgeon to avoid manipulating the aorta in the presence of atherosclerotic plaques [16]. Nevertheless, one study that compared TEE with epiaortic scan showed 100% sensitivity of TEE to diagnose ascending aorta atheroma [37]. The incidence of atherosclerosis in the ascending aorta, as diagnosed by epiaortic scan, ranges between 26.2% (for plaque height > 0.5 mm) [26] and 17% (plaque height > 3 mm or protruding) [37]. In our series, 22.4% of the patients had an ascending aorta plaque greater than 1 mm, so it is unlikely that a significant number of patients with ascending aorta disease were missed.

In previous studies [15, 22] and again in the current one, we have used the concept of "atheroma burden" as a two-dimensional measure of atherosclerotic plaque in order to better define the extent of the disease compared with the one-dimensional measure of plaque height. This does have an inherent limitation in that an even more accurate method to quantify disease extent would be to perform a three-dimensional assessment. However, this is not yet technically feasible with existing TEE hardware and software. Another limitation is that our definition of aortic burden ignores the factor of mobile atheromas. The macroembolization of a mobile part, however, would be expected to result in a more focal stroke-like injury rather then diffuse neurocognitive damage.

As our study is retrospective in nature and the TEE findings were known to the surgeon at the time of operation, the surgical technique could have been affected in a way that would reduce the risk for NCD. We specifically examined one important aspect of surgical technique, namely the use of a single versus a double aortic clamp. The use of a single cross-clamp is one of the surgical modifications advocated to reduce the incidence of post-CABG NCD, the rational being the detection by TCD of microemboli during cross-clamping and removal of the partial clamp [17, 38]. We did not find evidence that the TEE findings had a major impact on the surgical choice, and inclusion of this factor in the multivariable model did not affect the results of the study. It is still conceivable, however, that surgical decision-making was affected in some other way that our study did not control for, such as the location chosen for the aortic cross-clamp.

Age is a significant predictor for post-CABG NCD [4]. It is also significantly correlated with the extent of atherosclerotic disease [39]. Therefore, the inclusion of both age and atheroma burden in the multivariable model may lead to a statistical problem of collinearity. However, in our sample the correlation coefficient between atheroma burden and age is small (r < 0.33) and the confidence intervals around the coefficient estimates in our regression models are relatively narrow, arguing against a possible problem of collinearity.

The rate of attrition before we completed the 6-week neurocognitive testing was 19%, which is about average in studies of post-CABG NCD. The lost patients tended to have a higher atheroma burden, especially in the descending aorta, which may introduce a bias whereas patients with higher atheroma burden suffered more severe neurocognitive damage, decreasing their likelihood of returning at 6 weeks. However, only in 8 of the 39 patients who were lost to follow-up the reason is reported as "being too ill to return." In most patients, technical reasons accounted for their loss to follow-up; therefore, we do not think that our results are significantly biased by the attrition rate.

In summary, based on large cohort of patients, a sensitive quantitative two-dimensional evaluation of aortic atheroma burden, and rigorous neurocognitive evaluation at clinically relevant time points, this study shows that although atherosclerosis is a proven risk factor for post-CABG stroke, it is unlikely to be a major etiologic factor for post-CABG NCD. Additional studies are needed to further explore the pathogenesis of this important clinical problem.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
The authors wish to thank Jonathan B. Mark, MD, vice chairman in the Department of Anesthesiology, Duke University Medical Center and chief of Anesthesiology Service, VA Medical Center, Durham, NC, for his helpful comments in preparation of this manuscript.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

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G. Haljan, A. Maitland, A. Buchan, R. C. Arora, M. King, J. Haigh, B. Culleton, P. Faris, and D. Zygun
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W. S. Whitley and K. E. Glas
An Argument for Routine Ultrasound Screening of the Thoracic Aorta in the Cardiac Surgery Population
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C. W. Hogue, R. Fucetola, T. Hershey, K. Freedland, V. G. Davila-Roman, A. M. Goate, and R. E. Thompson
Risk Factors for Neurocognitive Dysfunction After Cardiac Surgery in Postmenopausal Women
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G. Djaiani, M. Ali, M. A. Borger, A. Woo, J. Carroll, C. Feindel, L. Fedorko, J. Karski, and H. Rakowski
Epiaortic Scanning Modifies Planned Intraoperative Surgical Management But Not Cerebral Embolic Load During Coronary Artery Bypass Surgery
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R. Lee, N. Matsutani, A. C. Polimenakos, L. C. Levers, M. Lee, and R. G. Johnson
Preoperative Noncontrast Chest Computed Tomography Identifies Potential Aortic Emboli
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F. D. Rubens, M. Boodhwani, and H. Nathan
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R. Lin, L. Svensson, R. Gupta, B. Lytle, and D. Krieger
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H. P. Grocott
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Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2006; 10(2): 143 - 157.
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