Key result
In computational models of NIDCM, the presence of reduced conductivity increased reentry incidence compared to no reduced conductivity (33.1% vs 11.9%).
Why the study?
Patients with NIDCM and LGE-CMR enhancement are at high risk of sudden cardiac death, and risk stratification based on LGE-CMR may be improved by better understanding how fibrosis microstructure affects reentry.
How do variations in fibrosis microstructure and density affect reentry inducibility and mechanism in computational models of non-ischemic dilated cardiomyopathy?
How do variations in fibrosis microstructure and density affect reentry inducibility and mechanism in computational models of non-ischemic dilated cardiomyopathy?
Absolute Event Rate: 33.1% vs 11.9%
Computational modeling demonstrates that fibrosis type, density, and reduced conductivity modulate reentry inducibility in NIDCM, which can be predicted by transmural activation time differences.
Reduced conductivity may heighten reentry risk in NIDCM models; hypothesis-generating for fibrosis-targeted strategies pending human validation.
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 402 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%). Conclusions: Computational models of fibrosis micro-structure underlying areas of LGE in NIDCM provide insight into the mechanisms and inducibility of reentry, and their dependence upon the type and density of fibrosis. Transmural activation times can differentiate microstructures which support reentry.
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Balaban et al. (2018) studied Non-ischemic dilated cardiomyopathy (NIDCM) (n=402). Reduced conductivity (RC) vs. No reduced conductivity was evaluated on Reentry incidence. In computational models of NIDCM, the presence of reduced conductivity increased reentry incidence compared to no reduced conductivity (33.1% vs 11.9%).
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