ISSN: 2161-0460

Journal of Alzheimers Disease & Parkinsonism
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  • Research Article   
  • J Alzheimers Dis Parkinsonism 2017, Vol 7(6): 409
  • DOI: 10.4172/2161-0460.1000409

Brain Microstructural White and Gray Matter Alterations after Cardiopulmonary Bypass: Anatomical Distribution and Corresponding Neurocognitive Deficit

Dan Abrahamov1*, Oren Lev Ran1, Efrat Sasson2, Sharon Naparstek1, Mordechai Salti1, Mahmoud Abu Salah1, Reut Hizkiya1, Yaron Ishay1, Evgeny Brotfine1, Gideon Sahar1 and Yael Refaely1
1Department of Cardiothoracic Surgery, Soroka University, Medical Center, Beer-Sheva, Israel
2WiseImage - Medical Imaging Services, , Hod Hasharon, Israel
*Corresponding Author : Dan Abrahamov, Department of Cardiac Surgery, Soroka Medical Centre, Beer Sheva, Israel, Tel: +972-6400-962, Email: danab3@clalit.org.il

Received Date: Dec 06, 2017 / Accepted Date: Dec 14, 2017 / Published Date: Dec 21, 2017

Abstract

Background: We sought to detect microstructural brain injury after coronary artery bypass grafting (CABG) using cardiopulmonary bypass (CPB) and to define its anatomical distribution. Analyses were performed to determine possible correlation with postoperative neurocognitive deficit.
Methods: Seven patients undergoing CPB-CABG were assigned for serial cerebral designated diffusion tensor (DTI)-magnetic resonance imaging (MRI) examinations, preoperatively, on postoperative day (POD) 1 and 5. Levels of mean diffusivity (MD) and fractional anisotropy (FA) were analysed to assess gray and white matter injury. BBBdisruption and microembolic load were concomitantly evaluated by dynamic contrast enhancement (DCE)-MRI and diffusion-weighted imaging (DWI)-MRI methods, respectively. Neuropsychological tests were performed one day preoperatively and on POD 5.
Results: Increase in MD and decrease in FA were evident on POD 1 in gray matter structures including the hippocampus (MD, 0.000768 mm2/s ± 0.0000347 versus 0.000804 mm2/s ± 0.0000267, p<0.01; FA, 0.180 ± 0.03 mm2/s versus 0.163 mm2/s ± 0.032, p<0.01), middle frontal gyrus (MD, 0.000989 mm2/s ± 0.0000487 versus 0.001068 mm2/s ± 0.0000553, p<0.01), orbital gyrus (MD, 0.000867 mm2/s ± 0.0000374 versus 0.000908 mm2/s ± 0.0000356, p<0.01) and in the following white matter structures: Superior longitudinal fasciculus (MD, 0.000836 mm2/s ± 0.0000384 versus 0.000874 mm2/s ± 0.0000359, p<0.01; FA, 0.324 mm2/s ± 0.018 versus 0.305 mm2/s ± 0.022, p<0.01), frontal white matter (FA, 0.277 mm2/s ± 0.031 versus 0.26 mm2/s ± 0.033, p<0.01) internal capsule (MD, 0.000772 mm2/s ± 0.0000648 versus 0.000803 mm2/s ± 0.0000601, p<0.01; FA,0.364 mm2/s ± 0.032 versus 0.343 mm2/s ± 0.029, p<0.01) and corticospinal tract (MD, 0.000759 mm2/s ± 0.0000557 versus 0.00078 mm2/s ± 0.0000591, p<0.01; FA, 0.440 mm2/s ± 0.023 versus 0.411 mm2/s ± 0.023, p<0.01). Corticospinal tract fibre tracing showed significant decrease in postoperative fibre number. DTI findings persisted through POD 5 without spontaneous regression. BBB-disruption reflected by increased K^trans was detected in five patients (71%) on POD 1, mainly in frontal lobes and spontaneously restored by POD 5. Postoperative global cognitive score was reduced in all patients (98.2 ± 12 vs. 95.1 ± 11, p=0.032), predominantly in executive function and attention (91.8 ± 13 vs. 86.9±12, p=0.042). Postoperative FA decline significantly correlated with delta K^trans (R=0.6) and with postoperative decline in attention and Go-no-Go response inhibition tests (R=0.66 and 0.63, respectively).
Conclusion: CABG using CPB elicits gray and white matter microstructure injury in the above-mentioned anatomical distribution. These alterations are associated with transient BBB-disruption and may account for postoperative neurocognitive dysfunction.

Keywords: Magnetic resonance imaging; Diffusion tensor imaging; Cardiopulmonary bypass; Neuropsychological test; Cognition

Citation: Abrahamov D, Ran OL, Sasson E, Naparstek S, Salti M, et al. (2017) Brain Microstructural White and Gray Matter Alterations after Cardiopulmonary Bypass: Anatomical Distribution and Corresponding Neurocognitive Deficit. J Alzheimers Dis Parkinsonism 7: 409. Doi: 10.4172/2161-0460.1000409

Copyright: © 2017 Abrahamov D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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