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Department of Anesthesiology, University Medical Center Utrecht, Heidelberlaan 100, Utrech, 3584 CX the Netherlands
(Email: d.vandijk{at}umcutrecht.nl).
Something remarkable has happened to our perception of postoperative cognitive decline (POCD). Until a few years ago, few doubted that POCD was a serious and frequently occurring complication of cardiac operations. Uncontrolled patient studies, some of which were published in prestigious journals, reported incidences of POCD of more than 40%. POCD was described not only in the first months after cardiac operations but also after long-term follow-up. Cardiopulmonary bypass was held responsible for the problem, either through hypoperfusion of the brain, through emboli, or through an inflammatory response. Even rats appeared to be suffering from POCD after a rodent minipump run.
Surprisingly, when on-pump coronary artery bypass grafting (CABG) patients were compared with off-pump CABG patients, there was very little difference in cognitive performance between them. Could be something wrong with the neuropsychologic test procedures we have been using to measure cognitive decline?
Selnes and colleagues [1], from Johns Hopkins, were amongst the first to recognize how difficult it is to discriminate true cognitive decline from random variation in neuropsychologic test performance. They therefore not only studied on-pump CABG patients but also recruited several control groups: off-pump CABG patients, nonsurgical patients with coronary artery disease, and healthy individuals. As in other studies that have incorporated control groups, there was no clear difference in long-term cognitive outcome between on-pump CABG patients, off-pump CABG patients, and even nonsurgical patients.
Does this mean that long-term POCD does not exist? Or has it ceased to exist as a result of improved cardiopulmonary bypass techniques? The answer is probably no. Studies using nonsurgical control groups are not randomized, and despite correction with multivariate modelling, the presence of residual confounding is inevitable. Moreover, every cardiac surgeon knows patients who were "just not the same" after their operation: no focal signs of a stroke, but unable to return to work or even their home due to memory and concentration problems. And how can we ignore the hundreds of emboli that can readily be demonstrated with transcranial Doppler imaging during cardiopulmonary bypass or close our eyes to the footprints of emboli that can be found in postmortem brains of cardiac surgical patients?
What we learn from this study from Johns Hopkins [1] and other controlled studies on POCD is that the effect of CABG on the brain is uncertain. Long-term POCD probably exists, but evidence is accumulating that advanced age and atherosclerosis may be more important determinants of long-term cognitive decline than a history of cardiac operations.
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