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Sources: Newman MF, et al. Longitudinal assessment of neurocongitive function after coronary artery bypass surgery. N Engl J Med. 2001;344:395-402. Selnes OA, McKhann GM. Editorial: Coronary artery bypass surgery and the brain. N Engl J Med. 2001;344:451-452.
More than 500,000 coronary artery bypass grafting (CABG) operations are performed in the United States each year. Although effective for revascularizing the heart, CABG can have neurological complications. After CABG, postoperative delirium occurs in up to one-third of patients, stroke occurs in up to 5%, and short-term cognitive abnormalities in 30-80% depending upon the population tested and the tests used to evaluate cognition. Long-term cognitive changes following CABG are commonly reported by patients and their families but may be subtle or mainly affect mood and personality (Curr Probl Cardiol. 1997;22:449-480.)
Newman and associates from Duke Medical Center determined the course of long-term cognitive change during the 5 years after CABG. In 261 patients they performed neurocognitive tests before surgery, before discharge, and then 6 weeks, 6 months, and in 172, 5 years after CABG. Cognitive decline was defined as a reduction of 1 standard deviation (approximately 20% from the patient’s preoperative baseline test score in 1 or more of 4 domains (verbal memory and language comprehension; abstraction and visuo-spatial orientation; attention, processing speed, and concentration; and visual memory). Factors predicting long-term cognitive decline were determined by multivariable logistic and linear regression.
Among study patients the incidence of cognitive decline was 53% at discharge, 36% at 6 weeks, 24% at 6 months, and 42% at 5 years. Cognitive function at discharge was a significant predictor of long-term function (P > .001) as were older age and lower level of education.
Newman et al found that a large proportion of CABG patients had cognitive decline when tested at the time of discharge. As pointed out by Selnes and McKhann in their accompanying editorial, the decline may reflect the fact that patients underwent neurocognitive assessment just days after major surgery. If the early cognitive decline is a valid finding, however, then cognitive change after CABG has a biphasic course of decline, improvement, and later decline. Since it is predicted by the presence of early postCABG decline, the later cognitive deterioration may be caused by perioperative events.
The mechanism of cognitive changes after CABG is probably multifactorial, including genetic and environmental factors, but intraoperative hypotension and microemboli are likely causes of cerebral injury. During CABG, ultrasonographic studies have demonstrated that showers of emboli enter the cerebral vessels especially when an atherosclerotic aorta is clamped and then unclamped (Curr Probl Cardiol. 1997;22:449-480.)
These findings underscore the importance of preventing or reducing perioperative brain damage in all patients, especially the elderly undergoing CABG. Patients in whom early postoperative decline is identified may be candidates for aggressive interventions to prevent later cognitive deterioration.—John J. Caronna