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J Thorac Cardiovasc Surg 2007;134:1443-1452
© 2007 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Effects of sustained mild hypothermia on neurocognitive function after coronary artery bypass surgery: A randomized, double-blind study

^a Division of Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, Canada
^b Division of Cardiovascular Anesthesia, University of Ottawa Heart Institute, Ottawa, Canada.

Read at the Eighty-seventh Annual Meeting of The American Association for Thoracic Surgery, Washington, DC, May 4-9, 2007.

Received for publication March 20, 2007; revisions received July 18, 2007; accepted for publication August 15, 2007.

^_* Address for reprints: Howard J. Nathan, MD, H341, 40 Ruskin Street, Ottawa, Ontario K1Y 4W7 Canada. (Email: hnathan{at}ottawaheart.ca).

Objective: Neurocognitive deficits occur frequently in patients undergoing cardiac surgery and may be caused, in part, by ischemic cerebral injury. Cerebral hypothermia has been proposed as a neuroprotective strategy to reduce ischemic injury in animal studies, in postcardiac arrest, and during cardiac surgery. We sought to evaluate the effects of sustained mild intraoperative hypothermia, without rewarming, on neurocognitive function after coronary artery bypass surgery.

Methods: Patients (aged 60 years) undergoing non-urgent coronary surgery were randomized to an intraoperative nasopharyngeal temperature of 34°C (hypothermic; n = 133) or 37°C (normothermic; n = 134), maintained using water-circulating thermal control pads. No active rewarming was used. Transcranial Doppler was used intraoperatively to monitor middle cerebral artery emboli. Neuropsychometric testing, consisting of a battery of 16 tests, was performed by blinded observers preoperatively, before discharge, and at 3 months, and tests were divided into 4 cognitive domains. A deficit was prospectively defined as a 1 standard deviation decrease in individual scores from baseline in 1 or more domains.

Results: The number of intraoperative cerebral emboli was similar between the control and the treated groups (188 [115–331] vs 182 [100–305], P = .71). At discharge, neurocognitive deficits were present in 45% of control patients and in 49% of treated patients (P = .49) and at 3 months decreased to 8% in control patients and 4% in treated patients (P = .28). There was no correlation between the total number of cerebral emboli and the occurrence of neurocognitive deficits (r = –0.01; P = .88). Hypothermic patients demonstrated trends toward reduced intensive care unit stay (1.4 ± 1.0 days vs 1.2 ± 0.7 days, P = .06) and increased chest tube output (655 ± 327 mL/24 h vs 584 ± 325 mL/24 h, P = .09).

Conclusions: Mild intraoperative hypothermia has no major adverse effects but does not decrease the incidence of neurocognitive deficits in patients undergoing coronary artery bypass surgery. In the absence of rewarming and cerebral hyperthermia, sustained mild hypothermia does not improve cognitive outcome.

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Discussion
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