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Ann Thorac Surg 2001;72:S1838-S1844
© 2001 The Society of Thoracic Surgeons
a Department of Anesthesiology and Perioperative Medicine, University Hospital Campus—London Health Sciences Center, University of Western Ontario, London, Ontario, Canada
* Address reprint requests to Dr Murkin, Department of Anesthesiology and Perioperative Medicine, University Hospital Campus—London Health Sciences Center, University of Western Ontario, 339 Windermere Rd, London, Ontario, Canada N6A 5A5
e-mail: jmurkin{at}uwo.ca
Presented at Mechanisms and Attenuation of Abnormalities in Hemostasis/Inflammation and Neurologic Injury: Implications for Patient Outcomes, Vancouver, BC, Canada, May 6, 2001.
Neurologic injury after cardiac surgery can be divided into type I, including clinically apparent stroke, seizures stupor, or coma, and much more occurring type II injury, including intellectual deterioration, memory deficit, or seizures. Cerebral embolization is demonstrably etiologic in many such cases, and several new aortic cannulas are being introduced that are aimed at capturing or diverting potential cerebral emboli. No outcome data are yet available. Several potentially cerebroprotective pharmacologic therapies including thiopental, propofol, and nimodipine, have been assessed clinically but, generally, the results have been poor. Meta-analysis of the large North American aprotinin database of prospective, randomized, placebo-controlled clinical trials is suggestive of a cerebroprotective potential associated with high-dose aprotinin administration.
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