Newly Published
Perioperative Medicine  |   January 2018
18F-florbetapir Positron Emission Tomography–determined Cerebral β-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery
Author Notes
  • From the Department of Anesthesiology (R.Y.K., T.B., M.B., N.T., M.F.N., J.P.M.), Department of Radiology (O.G.J., S.B.-N.), Department of Biostatistics and Bioinformatics (Y.-J.L., W.Q.), and the Department of Psychiatry and Behavioral Science (P.M.D.), Duke University, Durham, North Carolina.
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  • Mayo Clinic, Rochester
  • University of London
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  • Submitted for publication June 19, 2017. Accepted for publication December 27, 2017.
    Submitted for publication June 19, 2017. Accepted for publication December 27, 2017.×
  • Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).
    Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).×
  • *Members of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) Study Group are listed in appendix 1. Data used in preparation of this article were obtained from the ADNI database (https://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ANDI and/or provided data but did not participate in the analysis or writing of this report. A complete listing of ADNI investigators can be found at https://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf and in appendix 1.
    Members of the Alzheimer’s Disease Neuroimaging Initiative (ADNI) Study Group are listed in appendix 1. Data used in preparation of this article were obtained from the ADNI database (https://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ANDI and/or provided data but did not participate in the analysis or writing of this report. A complete listing of ADNI investigators can be found at https://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf and in appendix 1.×
  • Members of the Neurologic Outcomes Research Group (NORG) are listed in appendix 2.
    Members of the Neurologic Outcomes Research Group (NORG) are listed in appendix 2.×
  • Acknowledgments: The authors thank Abhinay Joshi, M.S., from Avid Radiopharmaceuticals for assistance with image analytics in a blinded fashion. The authors also thank Avid Radiopharmaceuticals (Philadelphia, Pennsylvania) for their support of this study through the provision of 18F-florbetapir.
    Acknowledgments: The authors thank Abhinay Joshi, M.S., from Avid Radiopharmaceuticals for assistance with image analytics in a blinded fashion. The authors also thank Avid Radiopharmaceuticals (Philadelphia, Pennsylvania) for their support of this study through the provision of 18F-florbetapir.×
    Regarding the ADNI data used in this study: data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI; National Institutes of Health [Bethesda, Maryland] grant No. U01 AG024904) and Department of Defense ADNI (grant No. W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai, Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd. and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC; Johnson & Johnson Pharmaceutical Research & Development LLC; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer, Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (http://www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. This study is supported in part by grant Nos. HL108280, HL096978, and HL109971 from the National Institutes of Health. 18F-florbetapir is provided courtesy of Avid Radiopharmaceuticals, but Avid had no input into the clinical study design or decision to publish this report.
    Regarding the ADNI data used in this study: data collection and sharing for this project was funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI; National Institutes of Health [Bethesda, Maryland] grant No. U01 AG024904) and Department of Defense ADNI (grant No. W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai, Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd. and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC; Johnson & Johnson Pharmaceutical Research & Development LLC; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer, Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (http://www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. This study is supported in part by grant Nos. HL108280, HL096978, and HL109971 from the National Institutes of Health. 18F-florbetapir is provided courtesy of Avid Radiopharmaceuticals, but Avid had no input into the clinical study design or decision to publish this report.×
  • Competing Interests: Dr. Doraiswamy has received research grants (through Duke University) from Avid (Philadelphia, Pennsylvania), Lilly (Indianapolis, Indiana), Neuronetrix (Louisville, Kentucky), Avanir (Aliso Viejo, California), Alzheimer’s Drug Discovery Foundation (New York, New York), Forum (Waltham, Massachusetts), and has received speaking or advisory fees from Anthrotronix (Silver Spring, Maryland), Cognoptix (Acton, Massachusetts), Takeda (Deerfield, Illinois), Genomind (King of Prussia, Pennsylvania), Sonexa (San Diego, California), Targacept (Winston-Salem, North Carolina), Neurocog Trials (Durham, North Carolina), Forum (Waltham, Massachusetts), T3D Therapeutics (Research Triangle Park, North Carolina), Alzheimer’s Association (Chicago, Illinois), Hintsa (Zurich, Switzerland), MindLink (London, England), Global Alzheimer’s Platform (Washington, D.C.), and University of Miami (Miami, Florida). Dr. Doraiswamy owns shares in Maxwell Health (Boston, Massachusetts), Muses Labs (Raleigh, North Carolina), Anthrotronix, Evidation Health (San Mateo, California), Turtle Shell Technologies (Karnataka, India), and Advera Health Analytics (Santa Rosa, California). Dr. Doraiswamy is a coinventor on patents relating to dementia biomarkers that are unlicensed. The other authors declare no competing interests.
    Competing Interests: Dr. Doraiswamy has received research grants (through Duke University) from Avid (Philadelphia, Pennsylvania), Lilly (Indianapolis, Indiana), Neuronetrix (Louisville, Kentucky), Avanir (Aliso Viejo, California), Alzheimer’s Drug Discovery Foundation (New York, New York), Forum (Waltham, Massachusetts), and has received speaking or advisory fees from Anthrotronix (Silver Spring, Maryland), Cognoptix (Acton, Massachusetts), Takeda (Deerfield, Illinois), Genomind (King of Prussia, Pennsylvania), Sonexa (San Diego, California), Targacept (Winston-Salem, North Carolina), Neurocog Trials (Durham, North Carolina), Forum (Waltham, Massachusetts), T3D Therapeutics (Research Triangle Park, North Carolina), Alzheimer’s Association (Chicago, Illinois), Hintsa (Zurich, Switzerland), MindLink (London, England), Global Alzheimer’s Platform (Washington, D.C.), and University of Miami (Miami, Florida). Dr. Doraiswamy owns shares in Maxwell Health (Boston, Massachusetts), Muses Labs (Raleigh, North Carolina), Anthrotronix, Evidation Health (San Mateo, California), Turtle Shell Technologies (Karnataka, India), and Advera Health Analytics (Santa Rosa, California). Dr. Doraiswamy is a coinventor on patents relating to dementia biomarkers that are unlicensed. The other authors declare no competing interests.×
  • Correspondence: Address correspondence to Dr. Klinger: Department of Anesthesiology, Duke University Box 3094, 2301 Erwin Road, Durham, North Carolina 27710. kling004@mc.duke.edu. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Perioperative Medicine / Cardiovascular Anesthesia / Central and Peripheral Nervous Systems / Radiological and Other Imaging / Technology / Equipment / Monitoring
Perioperative Medicine   |   January 2018
18F-florbetapir Positron Emission Tomography–determined Cerebral β-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery
Anesthesiology Newly Published on January 31, 2018. doi:10.1097/ALN.0000000000002103
Anesthesiology Newly Published on January 31, 2018. doi:10.1097/ALN.0000000000002103
Abstract

Background: Amyloid deposition is a potential contributor to postoperative cognitive dysfunction. The authors hypothesized that 6-week global cortical amyloid burden, determined by 18F-florbetapir positron emission tomography, would be greater in those patients manifesting cognitive dysfunction at 6 weeks postoperatively.

Methods: Amyloid deposition was evaluated in cardiac surgical patients at 6 weeks (n = 40) and 1 yr (n = 12); neurocognitive function was assessed at baseline (n = 40), 6 weeks (n = 37), 1 yr (n = 13), and 3 yr (n = 9). The association of 6-week amyloid deposition with cognitive dysfunction was assessed by multivariable regression, accounting for age, years of education, and baseline cognition. Differences between the surgical cohort with cognitive deficit and the Alzheimer’s Disease Neuroimaging Initiative cohorts (normal and early/late mild cognitive impairment) was assessed, adjusting for age, education, and apolipoprotein E4 genotype.

Results: The authors found that 6-week abnormal global cortical amyloid deposition was not associated with cognitive dysfunction (13 of 37, 35%) at 6 weeks postoperatively (median standard uptake value ratio [interquartile range]: cognitive dysfunction 0.92 [0.89 to 1.07] vs. 0.98 [0.93 to 1.05]; P = 0.455). In post hoc analyses, global cortical amyloid was also not associated with cognitive dysfunction at 1 or 3 yr postoperatively. Amyloid deposition at 6 weeks in the surgical cohort was not different from that in normal Alzheimer’s Disease Neuroimaging Initiative subjects, but increased over 1 yr in many areas at a rate greater than in controls.

Conclusions: In this study, postoperative cognitive dysfunction was not associated with 6-week cortical amyloid deposition. The relationship between cognitive dysfunction and regional amyloid burden and the rate of postoperative amyloid deposition merit further investigation.