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Ann Thorac Surg 1997;63:322-323
© 1997 The Society of Thoracic Surgeons
Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina
Cardiac surgery has made enormous progress over the past quarter century. Great progress has been made in protection of the heart, and the new frontier is protecting other organs at risk during cardiac operations. Acute alterations in cerebral function after coronary artery bypass grafting is arguably the most important and an increasingly challenging problem primarily because of the older age of patients and their concurrent diseases. Patients undergoing myocardial vascularization procedures, now exceeding 800,000 annually throughout the world, are particularly prone to stroke, encephalopathy, and cognitive dysfunction. Cerebral dysfunction is often attributed to significant atherosclerotic disease subject to hemodynamic fluctuations, cerebral embolization, or a combination of the two. The increasing proportion of perioperative morbidity and mortality that brain injury represents [1–3] has been only partially addressed. Two reports in this issue of The Annals from McKhann and colleagues [4, 5] represent an attempt to more accurately stratify the incidence and persistence of cognitive dysfunction after bypass, as well as determine predictors of stroke in patients undergoing coronary artery bypass grafting. This systematic approach is welcome because the first step in solving a clinical problem is defining it and identifying those patients likely to suffer from it. The second step is identifying the mechanisms that cause the problem, and the final step is perfecting methods to prevent the problem, in this case brain injury.
The first study in this issue, by McKhann and colleagues [4] of cognitive outcome after coronary bypass demonstrates intriguing changes in cognitive dysfunction occurring 1 month and 1 year after cardiac operations. McKhann and colleagues characterize patterns of cognitive decline including persistent impairment, improvement, and late decline. The study helps to better identify the changes that occur and confirms the persistence of cognitive dysfunction in patients undergoing cardiac operations. The study also delineates a group that appears to show little change in cognitive function in the first month after coronary artery bypass grafting but demonstrates a significant "late decline." McKhann and colleagues offer potential mechanisms including delayed effects of injury as the explanation of this unexpected trend; however, multiple other mechanisms including progression of concurrent disease (eg, Alzheimer's), secondary loss of damaged tissue due to ischemic programmed cell death (apoptosis), or the lack of neuronal repair mechanisms associated with apolipoprotein genotype [6] may also play a role in these patients' late or persistent declines. The root cause of cerebral injury during operation is thought to be ischemia and the cascade of biochemical events that result [7]. Many different laboratory studies have suggested multiple pharmacologic interventions that may be used in the future to protect the brain from ischemia [8].
The determination of which patients are at the greatest risk is important not only because it helps us clinically in making decisions, but because it is a fundamental step in testing neuroprotective regimens. The second report by McKhann and colleagues [5] describing predictors of stroke risk in coronary bypass patients is similar to our recent findings [9] and assists in the identification of perioperative and intraoperative predictors and uses these data for stratification of patients into low-risk, medium-risk, and high-risk groups for perioperative stroke. Many preoperative predictors of stroke described by McKhann and colleagues are similar to those previously identified: previous stroke, diabetes mellitus, and increasing age [10]. Carotid bruit remains a controversial predictor [9, 10]. The major notable differences in predictive variables defined in this versus other recent studies is the absence of peripheral vascular disease and severity of coronary artery disease or anginal symptoms. These factors are associated with aortic atherosclerosis, the strongest perioperative predictor of stroke in a soon to be published multicenter epidemiologic study [10].
McKhann and colleagues' study population of 456 patients from which the risk factors were identified included 26 patients with strokes, an incidence of 5.7%. The final multivariable model that McKhann and colleagues use includes five variables as significant predictors. However, with such a small number of patients and outcomes (26), only two to three predictor variables would be supported in maintaining a stable predictive model [11]. Although the sample size is adequate for determining factors associated with stroke in their sample, the large number of predictors with a small number of outcomes may "overfit" the model, explaining some of the difficulty they noted in the prospective validation.
As we contemplate progress in cardiac surgery in the new century, a time likely to bring increasing numbers of "high-risk" patients primarily because of age [9, 10], the systematic search for neuroprotective strategies, both pharmacologic and physiologic, is proceeding rapidly on many fronts. New clinical approaches to cerebral protection are imminent, just as investigation in the 1970s and 1980s led to perfected myocardial protection. We predict laboratory and clinical studies over the next quarter century will bring successful methods to protect the brain during cardiac operations.
Footnotes
Address reprint requests to Dr Reves, Division of Cardiac Anesthesia, Department of Anesthesiology, Heart Center of Duke University Hospital, Box 3094, Durham, NC 27710.
References
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  R. J. Petrucci Finding our way from the heart to the head J. Thorac. Cardiovasc. Surg., October 1, 2003; 126(4): 944 - 946. [Full Text] [PDF]
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D. P. Taggart, S. M. Browne, P. W. Halligan, and D. T. Wade IS CARDIOPULMONARY BYPASS STILL THE CAUSE OF COGNITIVE DYSFUNCTION AFTER CARDIAC OPERATIONS? J. Thorac. Cardiovasc. Surg., September 1, 1999; 118(3): 414 - 420. [Abstract] [Full Text] [PDF]
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