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J Thorac Cardiovasc Surg 2001;122:622-623
© 2001 The American Association for Thoracic Surgery

Brief Communications

Apolipoprotein E genotype differentially influences the proinflammatory and anti-inflammatory response to cardiopulmonary bypass

From the Departments of Anesthesiology^a and Medicine (Neurology),^b Duke University Medical Center, Durham, NC.

Dr Grocott was supported by a Pepper Center Junior Faculty Award (NIA-AG11268); Dr Laskowitz was supported by the Paul Beeson Physician Faculty Award and National Institutes of Health (NIH) grant 1R01NS368087-01A2; Dr Newman was supported by NIH grant 1R01HL54316 and American Heart Association Grants-In-Aid 95010970 and M01-RR-30; Drs Grocott and Laskowitz serve as consultants to Biosite Inc, which performed the cytokine assays.

Received for publication Dec 20, 2000. Accepted for publication Feb 13, 2001. Address for reprints: Hilary P. Grocott, MD, Department of Anesthesiology, Duke University Medical Center, Box 3094, Durham, NC 27710 (E-mail: h.grocott@duke.edu).

Neurocognitive deficits are common sequelae of cardiac operations, affecting both long-term functional outcome and quality of life. The cause of perioperative cerebral injury remains incompletely understood, but it is multifactorial and likely represents a complex interaction among cerebral microembolization, global hypoperfusion, temperature modulation, and inflammatory processes. In addition, genetic factors have been shown to influence neurocognitive outcome after cardiac operations. Specifically, the presence of the APOE4 allele, one of the common human polymorphisms of the gene encoding apolipoprotein E (apoE), has been associated with a worsened cognitive outcome after coronary artery bypass grafting. ¹ This is consistent with prior clinical and experimental observations implicating the APOE4 allele in poor outcome after a variety of acute brain insults, including stroke, intracranial hemorrhage, and traumatic brain injury. ²

In addition to its role in cholesterol transport, recent reports have suggested that apoE plays a biologically relevant role in downregulating the systemic and central nervous system immune responses. ^3,4 Thus, one potential mechanism by which apoE influences outcome after acute . . . [Full Text of this Article]

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