Post-CABG Cognitive Deficits

abstract & commentary

Synopsis: Undoubtedly, additional genetic factors will be found that increase stroke or intrinsic brain deterioration in life’s later years. These challenging threats deserve serious consideration and thoughtfully developed prevention.

Source: Selnes OA, et al. Lancet 1999;353:1601-1606.

This informative review states that coronary artery bypass grafting (CABG) as now performed has been remarkably successful in relieving the angina of 94% of survivors for five years. In the United States at least, increasing numbers of inpatients with hypertension, diabetes, and age older than 70 years now safely undergo CABG. Nevertheless, many high-risk candidates suffer from postoperative delirium, memory loss, depression, or stroke.

Although expected perioperative death amounts to only 2-4% following CABG surgery, prospective surveillance indicates that 1.5-5.2% of patients suffer postoperative strokes with a case fatality record of 20%. Cognitive impairment has been reported as high as 10% three months after surgery, with 30% of post-CABG patients complaining of memory defects as late as six months or more. This response may not be specific, however, inasmuch as patients who underwent total knee or hip replacements showed similar postoperative memory defects. Be that as it may, the Hopkins investigation found that some of the post-CABG patients retained space-related deficiencies for five years. Psychological depression following CABG has been emphasized in past investigations, but both Selnes and colleagues and others claim that this occurs only in persons who were preoperatively depressed. Depression, however, fairly frequently follows myocardial infarction and is associated with worse outcomes and increased deaths.

Selnes et al refer to several studies that link preoperative factors to new post-CABG cognitive defects. One report lists the following: increasing age, poor education, and increased cerebral emboli released during cardiac surgery. More chronic factors include diabetes and/or severe arterial sclerosis. Some authors have measured the S100 protein in the spinal fluid as an indicator of post-CABG brain damage, but its specificity remains unsure. Neuron-specific enolase has also been tested in spinal fluid but, again, appears to lack specificity.

Comment by Fred Plum, MD

Other factors cited as possible causes of post-CABG encephalopathy include the presence of intraoperative hypotension and the amount of intraoperative aortic emboli that become released into the brain. In another study of ancillary risk, Tardiff and colleagues suggest that persons carrying the apolipoprotein E-4 allele may accentuate the risk of precipitating post-CABG dementia.1 Undoubtedly, additional genetic factors will be found that increase stroke or intrinsic brain deterioration in life’s later years. These challenging threats deserve serious consideration and thoughtfully developed prevention. (Dr. Plum is University Professor, Weill Medical College; Attending Neurologist, New York Presbyterian Hospital.)

Reference

1. Tardiff, et al. Ann Thorac Surg 1997;90:715-720.

Preoperative factors linked to post-CABG cognitive defects include:

a. increasing age.

b. diabetes.

c. severe arterial sclerosis.

d. poor education.

e. All of the above