Fibrosis Microstructure Modulates Reentry in Non-Ischemic Dilated Cardiomyopathy: Insights from Imaged Guided 2D Computational Modelling

Gabriel Balaban, Brian P. Halliday, Caroline Mendonca Costa, Wenjia Bai, Bradley Porter, Christopher A. Rinaldi, Gernot Plank, Daniel Rueckert, Sanjay K. Prasad, Martin Bishop

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)
151 Downloads (Pure)


Aims: Patients who present with non-ischemic dilated cardiomyopathy (NIDCM) and enhancement on late gadolinium magnetic resonance imaging (LGE-CMR), are at high risk of sudden cardiac death (SCD). Further risk stratification of these patients based on LGE-CMR may be improved through better understanding of fibrosis microstructure. Our aim is to examine
variations in fibrosis microstructure based on LGE imaging, and quantify the effect on reentry inducibility and mechanism. Furthermore, we examine the relationship between transmural activation time differences and reentry.

Methods and Results: 2D Computational models were created from a single short axis LGE-CMR image, with 401 variations in fibrosis type (interstitial, replacement) and density, as well as presence or absence of reduced conductivity (RC). Transmural activation times (TAT) were
measured, as well as reentry incidence and mechanism. Reentries were inducible above specific density thresholds (0.8, 0.6 for interstitial, replacement fibrosis). RC reduced these thresholds (0.3, 0.4 for interstitial, replacement fibrosis) and increased 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. Differences in TAT at coupling intervals 210 and 500ms predicted reentry in the models (sensitivity 89%, specificity 93%). A sensitivity analysis of TAT and reentry incidence showed that these quantities were robust to small changes in the pacing location.

Conclusion: Computational models of fibrosis micro-structure underlying areas of LGE in 21 NIDCM provide insight into the mechanisms and inducibility of reentry, and their dependence 22 upon the type and density of fibrosis. Transmural activation times, measured at the central extent 23 of the scar, can potentially differentiate microstructures which support reentry.
Original languageEnglish
JournalFrontiers in Physiology
Early online date19 Dec 2018
Publication statusPublished - 19 Dec 2018


  • arrhyhthmia
  • dilated cardiomyopathy
  • nonischemic cardiomyopathy
  • cardiac electrophyiology
  • computational modelling


Dive into the research topics of 'Fibrosis Microstructure Modulates Reentry in Non-Ischemic Dilated Cardiomyopathy: Insights from Imaged Guided 2D Computational Modelling'. Together they form a unique fingerprint.

Cite this