Limits...
Effects of fibrosis morphology on reentrant ventricular tachycardia inducibility and simulation fidelity in patient-derived models.

Ringenberg J, Deo M, Filgueiras-Rama D, Pizarro G, Ibañez B, Peinado R, Merino JL, Berenfeld O, Devabhaktuni V - Clin Med Insights Cardiol (2014)

Bottom Line: We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction.The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient.Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.

View Article: PubMed Central - PubMed

Affiliation: EECS Department, College of Engineering, University of Toledo, Toledo, OH, USA.

ABSTRACT
Myocardial fibrosis detected via delayed-enhanced magnetic resonance imaging (MRI) has been shown to be a strong indicator for ventricular tachycardia (VT) inducibility. However, little is known regarding how inducibility is affected by the details of the fibrosis extent, morphology, and border zone configuration. The objective of this article is to systematically study the arrhythmogenic effects of fibrosis geometry and extent, specifically on VT inducibility and maintenance. We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction. Additional synthesized models with morphologically varied extents of fibrosis and gray zone (GZ) distribution were derived to study the alterations in the arrhythmia induction and reentry patterns. Detailed electrophysiological simulations demonstrated that (1) VT morphology was highly dependent on the extent of fibrosis, which acts as a structural substrate, (2) reentry tended to be anchored to the fibrosis edges and showed transmural conduction of activations through narrow channels formed within fibrosis, and (3) increasing the extent of GZ within fibrosis tended to destabilize the structural reentry sites and aggravate the VT as compared to fibrotic regions of the same size and shape but with lower or no GZ. The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient. Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.

No MeSH data available.


Related in: MedlinePlus

Sample of VT reentry patterns on Patient 1 and Patient 2 on models with eroded fibrosis. (A) In Patient 1 with 1.35 mm of fibrosis eroded, reentry behavior is similar to that of the baseline model. Anatomical figure-eight-reentry is anchored to fibrosis contained within inferior and lateral walls. The black circles indicate fibrotic tissue; and (B) In Patient 2 with 1.35 mm of fibrosis eroded, anatomical figure-of-eight reentry is focused on lateral wall due to erosion of inferior fibrosis. The first image in each panel is shown translucently to expose fibrosis within walls.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC4210189&req=5

f6-cmc-2014-001: Sample of VT reentry patterns on Patient 1 and Patient 2 on models with eroded fibrosis. (A) In Patient 1 with 1.35 mm of fibrosis eroded, reentry behavior is similar to that of the baseline model. Anatomical figure-eight-reentry is anchored to fibrosis contained within inferior and lateral walls. The black circles indicate fibrotic tissue; and (B) In Patient 2 with 1.35 mm of fibrosis eroded, anatomical figure-of-eight reentry is focused on lateral wall due to erosion of inferior fibrosis. The first image in each panel is shown translucently to expose fibrosis within walls.

Mentions: Figure 6 shows the reentry patterns for a 1.35-mm eroded fibrosis model for each patient as an example. It was observed that in Patient 1, all models with decreased fibrosis (eroded) from baseline had similar reentry patterns to the baseline model, which included figure-of-eight reentry on the inferior and lateral epicardial regions and focal activations in the endocardium. In Patient 2, it was observed that eroding up to 450 μm from baseline did not produce significant changes in the reentry patterns. However, further erosion resulted in increasing differences in reentry patterns, primarily characterized by figure-of-eight reentry located on the lateral wall (Fig. 6, panel B). In all models, however, it was observed that reentry filaments tended to anchor to viable myocardium on the edges of the fibrotic regions.


Effects of fibrosis morphology on reentrant ventricular tachycardia inducibility and simulation fidelity in patient-derived models.

Ringenberg J, Deo M, Filgueiras-Rama D, Pizarro G, Ibañez B, Peinado R, Merino JL, Berenfeld O, Devabhaktuni V - Clin Med Insights Cardiol (2014)

Sample of VT reentry patterns on Patient 1 and Patient 2 on models with eroded fibrosis. (A) In Patient 1 with 1.35 mm of fibrosis eroded, reentry behavior is similar to that of the baseline model. Anatomical figure-eight-reentry is anchored to fibrosis contained within inferior and lateral walls. The black circles indicate fibrotic tissue; and (B) In Patient 2 with 1.35 mm of fibrosis eroded, anatomical figure-of-eight reentry is focused on lateral wall due to erosion of inferior fibrosis. The first image in each panel is shown translucently to expose fibrosis within walls.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4210189&req=5

f6-cmc-2014-001: Sample of VT reentry patterns on Patient 1 and Patient 2 on models with eroded fibrosis. (A) In Patient 1 with 1.35 mm of fibrosis eroded, reentry behavior is similar to that of the baseline model. Anatomical figure-eight-reentry is anchored to fibrosis contained within inferior and lateral walls. The black circles indicate fibrotic tissue; and (B) In Patient 2 with 1.35 mm of fibrosis eroded, anatomical figure-of-eight reentry is focused on lateral wall due to erosion of inferior fibrosis. The first image in each panel is shown translucently to expose fibrosis within walls.
Mentions: Figure 6 shows the reentry patterns for a 1.35-mm eroded fibrosis model for each patient as an example. It was observed that in Patient 1, all models with decreased fibrosis (eroded) from baseline had similar reentry patterns to the baseline model, which included figure-of-eight reentry on the inferior and lateral epicardial regions and focal activations in the endocardium. In Patient 2, it was observed that eroding up to 450 μm from baseline did not produce significant changes in the reentry patterns. However, further erosion resulted in increasing differences in reentry patterns, primarily characterized by figure-of-eight reentry located on the lateral wall (Fig. 6, panel B). In all models, however, it was observed that reentry filaments tended to anchor to viable myocardium on the edges of the fibrotic regions.

Bottom Line: We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction.The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient.Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.

View Article: PubMed Central - PubMed

Affiliation: EECS Department, College of Engineering, University of Toledo, Toledo, OH, USA.

ABSTRACT
Myocardial fibrosis detected via delayed-enhanced magnetic resonance imaging (MRI) has been shown to be a strong indicator for ventricular tachycardia (VT) inducibility. However, little is known regarding how inducibility is affected by the details of the fibrosis extent, morphology, and border zone configuration. The objective of this article is to systematically study the arrhythmogenic effects of fibrosis geometry and extent, specifically on VT inducibility and maintenance. We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction. Additional synthesized models with morphologically varied extents of fibrosis and gray zone (GZ) distribution were derived to study the alterations in the arrhythmia induction and reentry patterns. Detailed electrophysiological simulations demonstrated that (1) VT morphology was highly dependent on the extent of fibrosis, which acts as a structural substrate, (2) reentry tended to be anchored to the fibrosis edges and showed transmural conduction of activations through narrow channels formed within fibrosis, and (3) increasing the extent of GZ within fibrosis tended to destabilize the structural reentry sites and aggravate the VT as compared to fibrotic regions of the same size and shape but with lower or no GZ. The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient. Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.

No MeSH data available.


Related in: MedlinePlus