Imperial College London

ProfessorDanielRueckert

Faculty of EngineeringDepartment of Computing

Professor of Visual Information Processing
 
 
 
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Contact

 

+44 (0)20 7594 8333d.rueckert Website

 
 
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Location

 

568Huxley BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Balaban:2018:10.3389/fphys.2018.01832,
author = {Balaban, G and Halliday, BP and Costa, CM and Bai, W and Porter, B and Rinaldi, CA and Plank, G and Rueckert, D and Prasad, SK and Bishop, MJ},
doi = {10.3389/fphys.2018.01832},
journal = {Frontiers in Physiology},
title = {Fibrosis Microstructure Modulates Reentry in Non-ischemic Dilated Cardiomyopathy: Insights From Imaged Guided 2D Computational Modeling},
url = {http://dx.doi.org/10.3389/fphys.2018.01832},
volume = {9},
year = {2018}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Aims: Patients who present with non-ischemic dilated cardiomyopathy (NIDCM) andenhancement on late gadolinium magnetic resonance imaging (LGE-CMR), are at highrisk of sudden cardiac death (SCD). Further risk stratification of these patients basedon LGE-CMR may be improved through better understanding of fibrosis microstructure.Our aim is to examine variations in fibrosis microstructure based on LGE imaging, andquantify the effect on reentry inducibility and mechanism. Furthermore, we examine therelationship between transmural activation time differences and reentry.Methods and Results: 2D Computational models were created from a single short axisLGE-CMR image, with 401 variations in fibrosis type (interstitial, replacement) and density,as well as presence or absence of reduced conductivity (RC). Transmural activationtimes (TAT) were measured, as well as reentry incidence and mechanism. Reentrieswere inducible above specific density thresholds (0.8, 0.6 for interstitial, replacementfibrosis). RC reduced these thresholds (0.3, 0.4 for interstitial, replacement fibrosis) andincreased reentry incidence (48 no RC vs. 133 with RC). Reentries were classified as rotor,micro-reentry, or macro-reentry and depended on fibrosis micro-structure. Differencesin TAT at coupling intervals 210 and 500ms predicted reentry in the models (sensitivity89%, specificity 93%). A sensitivity analysis of TAT and reentry incidence showed thatthese quantities were robust to small changes in the pacing location.Conclusion: Computational models of fibrosis micro-structure underlying areas ofLGE in NIDCM provide insight into the mechanisms and inducibility of reentry, andtheir dependence upon the type and density of fibrosis. Transmural activation times,measured at the central extent of the scar, can potentially differentiate microstructureswhich support reentry.
AU - Balaban,G
AU - Halliday,BP
AU - Costa,CM
AU - Bai,W
AU - Porter,B
AU - Rinaldi,CA
AU - Plank,G
AU - Rueckert,D
AU - Prasad,SK
AU - Bishop,MJ
DO - 10.3389/fphys.2018.01832
PY - 2018///
SN - 1664-042X
TI - Fibrosis Microstructure Modulates Reentry in Non-ischemic Dilated Cardiomyopathy: Insights From Imaged Guided 2D Computational Modeling
T2 - Frontiers in Physiology
UR - http://dx.doi.org/10.3389/fphys.2018.01832
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000453893100001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - http://hdl.handle.net/10044/1/67119
VL - 9
ER -