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Ann Thorac Surg 2006;82:1166
© 2006 The Society of Thoracic Surgeons
Department of Anesthesia, University Health Network, University of Toronto, 200 Elizabeth St, Toronto, Ontario, Canada M5G 2C4
(Email: george.djaiani{at}uhn.on.ca).
We would like to thank Drs Harrison and colleagues [1] for their interest in our study [2], and we appreciate this opportunity to comment on their interesting results. In their exploratory analysis of 111 patients enrolled in a previous study, Harrison and colleagues [1] did not find an association between nadir hematocrit during cardiopulmonary bypass (CPB) and neurocognitive dysfunction after coronary artery bypass surgery (CABS). We agree that the absence of an association may be due to the higher average nadir hematocrit concentrations in their sample relative to ours (27% vs 23%, respectively).
However, there are at least two other possible reasons why the findings of the studies differ. First, owing to their inclusion of only 111 patients, their analysis may have been underpowered to detect an association. Second, their outcome was cognitive dysfunction measured by neuropsychological testing, with all its attendant weaknesses, whereas ours was stroke based on objective clinical and radiologic criteria. Although some believe stroke to be the tip of the iceberg with a much larger body of cognitive dysfunction underneath the surface, others divide the two into separate entities. It is likely that cognitive dysfunction has multiple causes, whereas intraoperative stroke is mainly attributable to macroembolic phenomenon.
Ultimately we are in full agreement with Harrison and colleagues [1] that further research is needed to determine the ideal hematocrit before, during, and after cardiac surgery. Just as importantly, research is required to determine how to best achieve that ideal hematocrit.
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