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Ann Thorac Surg 2009;87:820-825. doi:10.1016/j.athoracsur.2008.12.042
© 2009 The Society of Thoracic Surgeons

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Right arrow Cerebral protection


Original Articles: Adult Cardiac

Cerebral Protection by Lidocaine During Cardiac Operations: A Follow-Up Study

Simon J. Mitchell, FANZCA, PhDa,c,*, Alan F. Merry, FANZCAa,c, Christopher Frampton, PhDb, Elaine Daviesa, Diana Grieve, MAa, Brigid P. Mills, MHSc(Hons)a, Craig S. Webster, PhDa, F. Paget Milsom, FRACSd, Timothy W. Willcox, CCPe, Desmond F. Gorman, MD, PhDa

a Department of Anaesthesiology, University of Auckland, Auckland, New Zealand
b StatistEcol, Mount Eden, Auckland, New Zealand
c Department of Anaesthesia, Auckland City Hospital, Auckland, New Zealand
d Department of Surgery, Auckland City Hospital, Auckland, New Zealand
e Department of Clinical Perfusion, Auckland City Hospital, Auckland, New Zealand

Accepted for publication December 5, 2008.

* Address correspondence to Dr Mitchell, Department of Anaesthesiology, University of Auckland, Private Bag 92019, Auckland, 1142, New Zealand (Email: sj.mitchell{at}auckland.ac.nz).

Background: A previous study showed less postoperative neurocognitive impairment in open-chamber cardiac surgery patients given lidocaine for 48 hours after induction of anesthesia. In the present study, we aimed to test the benefit of a 12-hour infusion in a broader group of cardiac surgery patients, including those undergoing coronary artery bypass graft surgery.

Methods: This was a randomized, double-blind, intention-to-treat trial. Before cardiac surgery, 158 patients completed 7 neurocognitive tests and a self-rating scale for memory. They received a 12-hour infusion of either lidocaine in a standard antiarrhythmic dose or placebo, beginning at induction of anesthesia. The cognitive tests and memory scale were repeated at postoperative weeks 10 and 25. A deficit in any cognitive test was defined as a decline in score by more than or equal to the preoperative group standard deviation.

Results: All tests were completed by 118 and 107 patients at 10 and 25 weeks, respectively. The proportions of patients in the lidocaine and placebo groups exhibiting a deficit in one or more tests were as follows: 45.8% versus 40.7% at 10 weeks, and 35.2% versus 37.7% at 25 weeks (not significant). There were no significant differences between groups in self-ratings of memory function or length of intensive care unit or hospital stay.

Conclusions: Lidocaine was not neuroprotective. The result of the previous trial may represent a type 1 error. Alternatively, benefit may be more likely for open-chamber surgery patients exposed to larger numbers of emboli or with a longer lidocaine infusion.







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