Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

Caroline Mendonca Costa; Aurel Neic; Eric Kerfoot; Bradley Porter; Benjamin Sieniewicz; Justin Gould; Baldeep Sidhu; Zhong Chen; Gernot Plank; Christopher A. Rinaldi; Martin J. Bishop; Steven A. Niederer

doi:10.1016/j.hrthm.2019.03.027

Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

Caroline Mendonca Costa, Aurel Neic, Eric Kerfoot, Bradley Porter, Benjamin Sieniewicz, Justin Gould, Baldeep Sidhu, Zhong Chen, Gernot Plank, Christopher A. Rinaldi, Martin J. Bishop, Steven A. Niederer

Medical University of Graz

Research output: Contribution to journal › Article › peer-review

44 Citations (Scopus)

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Abstract

Background

Cardiac resynchronization therapy (CRT) increases the risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when the left ventricular (LV) epicardial lead is implanted in proximity to scar.

Objective

The purpose of this study was to determine the mechanisms underpinning this risk by investigating the effects of pacing on local electrophysiology (EP) in relation to scar that provides a substrate for VT in ICM patients undergoing CRT.

Methods

Imaging data from ICM patients (n = 24) undergoing CRT were used to create patient-specific LV anatomic computational models including scar morphology. Simulations of LV epicardial pacing at 0.2–4.5 cm from the scar were performed using EP models of chronic infarct and heart failure (HF). Dispersion of repolarization and the vulnerable window were computed as surrogates for VT risk.

Results

Simulations predict that pacing in proximity to scar (0.2 cm) compared to more distant pacing to a scar (4.5 cm) significantly (P <.01) increased dispersion of repolarization in the vicinity of the scar and widened (P <.01) the vulnerable window, increasing the likelihood of unidirectional block. Moreover, slow conduction during HF further increased dispersion (∼194%). Analysis of variance and post hoc tests show significantly (P <.01) reduced repolarization dispersion when pacing ≥3.5 cm from the scar compared to pacing at 0.2 cm.

Conclusion

Increased dispersion of repolarization in the vicinity of the scar and widening of the vulnerable window when pacing in proximity to scar provides a mechanistic explanation for VT induction in ICM-CRT with lead placement proximal to scar. Pacing 3.5 cm or more from scar may avoid increasing VT risk in ICM-CRT patients.

Original language	English
Pages (from-to)	1475-1483
Number of pages	9
Journal	Heart Rhythm
Volume	16
Issue number	10
Early online date	29 Mar 2019
DOIs	https://doi.org/10.1016/j.hrthm.2019.03.027
Publication status	Published - Oct 2019

Keywords

Cardiac resynchronization therapy
Infarct scar
Patient-specific modeling
Ventricular tachycardia

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Pacing in proximity_COSTA_Publishedonline29March2019_GOLD VoR (CC BY)Final published version, 1.84 MBLicence: CC BY

Cite this

Mendonca Costa, C., Neic, A., Kerfoot, E., Porter, B., Sieniewicz, B., Gould, J., Sidhu, B., Chen, Z., Plank, G., Rinaldi, C. A., Bishop, M. J., & Niederer, S. A. (2019). Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis. Heart Rhythm, 16(10), 1475-1483. https://doi.org/10.1016/j.hrthm.2019.03.027

@article{7539bc5c743b45659d14c718d894e45c,

title = "Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.",

abstract = "BackgroundCardiac resynchronization therapy (CRT) increases the risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when the left ventricular (LV) epicardial lead is implanted in proximity to scar.ObjectiveThe purpose of this study was to determine the mechanisms underpinning this risk by investigating the effects of pacing on local electrophysiology (EP) in relation to scar that provides a substrate for VT in ICM patients undergoing CRT.MethodsImaging data from ICM patients (n = 24) undergoing CRT were used to create patient-specific LV anatomic computational models including scar morphology. Simulations of LV epicardial pacing at 0.2–4.5 cm from the scar were performed using EP models of chronic infarct and heart failure (HF). Dispersion of repolarization and the vulnerable window were computed as surrogates for VT risk.ResultsSimulations predict that pacing in proximity to scar (0.2 cm) compared to more distant pacing to a scar (4.5 cm) significantly (P <.01) increased dispersion of repolarization in the vicinity of the scar and widened (P <.01) the vulnerable window, increasing the likelihood of unidirectional block. Moreover, slow conduction during HF further increased dispersion (∼194%). Analysis of variance and post hoc tests show significantly (P <.01) reduced repolarization dispersion when pacing ≥3.5 cm from the scar compared to pacing at 0.2 cm.ConclusionIncreased dispersion of repolarization in the vicinity of the scar and widening of the vulnerable window when pacing in proximity to scar provides a mechanistic explanation for VT induction in ICM-CRT with lead placement proximal to scar. Pacing 3.5 cm or more from scar may avoid increasing VT risk in ICM-CRT patients.",

keywords = "Cardiac resynchronization therapy, Infarct scar, Patient-specific modeling, Ventricular tachycardia",

author = "{Mendonca Costa}, Caroline and Aurel Neic and Eric Kerfoot and Bradley Porter and Benjamin Sieniewicz and Justin Gould and Baldeep Sidhu and Zhong Chen and Gernot Plank and Rinaldi, {Christopher A.} and Bishop, {Martin J.} and Niederer, {Steven A.}",

note = "The data supporting this study is openly available at http://doi.org/10.18742/RDM01-570",

year = "2019",

month = oct,

doi = "10.1016/j.hrthm.2019.03.027",

language = "English",

volume = "16",

pages = "1475--1483",

journal = "Heart Rhythm",

issn = "1547-5271",

publisher = "Elsevier",

number = "10",

}

Mendonca Costa, C, Neic, A, Kerfoot, E , Porter, B , Sieniewicz, B , Gould, J , Sidhu, B , Chen, Z, Plank, G, Rinaldi, CA , Bishop, MJ & Niederer, SA 2019, 'Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.', Heart Rhythm, vol. 16, no. 10, pp. 1475-1483. https://doi.org/10.1016/j.hrthm.2019.03.027

TY - JOUR

T1 - Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

AU - Mendonca Costa, Caroline

AU - Neic, Aurel

AU - Kerfoot, Eric

AU - Porter, Bradley

AU - Sieniewicz, Benjamin

AU - Gould, Justin

AU - Sidhu, Baldeep

AU - Chen, Zhong

AU - Plank, Gernot

AU - Rinaldi, Christopher A.

AU - Bishop, Martin J.

AU - Niederer, Steven A.

N1 - The data supporting this study is openly available at http://doi.org/10.18742/RDM01-570

PY - 2019/10

Y1 - 2019/10

N2 - BackgroundCardiac resynchronization therapy (CRT) increases the risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when the left ventricular (LV) epicardial lead is implanted in proximity to scar.ObjectiveThe purpose of this study was to determine the mechanisms underpinning this risk by investigating the effects of pacing on local electrophysiology (EP) in relation to scar that provides a substrate for VT in ICM patients undergoing CRT.MethodsImaging data from ICM patients (n = 24) undergoing CRT were used to create patient-specific LV anatomic computational models including scar morphology. Simulations of LV epicardial pacing at 0.2–4.5 cm from the scar were performed using EP models of chronic infarct and heart failure (HF). Dispersion of repolarization and the vulnerable window were computed as surrogates for VT risk.ResultsSimulations predict that pacing in proximity to scar (0.2 cm) compared to more distant pacing to a scar (4.5 cm) significantly (P <.01) increased dispersion of repolarization in the vicinity of the scar and widened (P <.01) the vulnerable window, increasing the likelihood of unidirectional block. Moreover, slow conduction during HF further increased dispersion (∼194%). Analysis of variance and post hoc tests show significantly (P <.01) reduced repolarization dispersion when pacing ≥3.5 cm from the scar compared to pacing at 0.2 cm.ConclusionIncreased dispersion of repolarization in the vicinity of the scar and widening of the vulnerable window when pacing in proximity to scar provides a mechanistic explanation for VT induction in ICM-CRT with lead placement proximal to scar. Pacing 3.5 cm or more from scar may avoid increasing VT risk in ICM-CRT patients.

AB - BackgroundCardiac resynchronization therapy (CRT) increases the risk of ventricular tachycardia (VT) in patients with ischemic cardiomyopathy (ICM) when the left ventricular (LV) epicardial lead is implanted in proximity to scar.ObjectiveThe purpose of this study was to determine the mechanisms underpinning this risk by investigating the effects of pacing on local electrophysiology (EP) in relation to scar that provides a substrate for VT in ICM patients undergoing CRT.MethodsImaging data from ICM patients (n = 24) undergoing CRT were used to create patient-specific LV anatomic computational models including scar morphology. Simulations of LV epicardial pacing at 0.2–4.5 cm from the scar were performed using EP models of chronic infarct and heart failure (HF). Dispersion of repolarization and the vulnerable window were computed as surrogates for VT risk.ResultsSimulations predict that pacing in proximity to scar (0.2 cm) compared to more distant pacing to a scar (4.5 cm) significantly (P <.01) increased dispersion of repolarization in the vicinity of the scar and widened (P <.01) the vulnerable window, increasing the likelihood of unidirectional block. Moreover, slow conduction during HF further increased dispersion (∼194%). Analysis of variance and post hoc tests show significantly (P <.01) reduced repolarization dispersion when pacing ≥3.5 cm from the scar compared to pacing at 0.2 cm.ConclusionIncreased dispersion of repolarization in the vicinity of the scar and widening of the vulnerable window when pacing in proximity to scar provides a mechanistic explanation for VT induction in ICM-CRT with lead placement proximal to scar. Pacing 3.5 cm or more from scar may avoid increasing VT risk in ICM-CRT patients.

KW - Cardiac resynchronization therapy

KW - Infarct scar

KW - Patient-specific modeling

KW - Ventricular tachycardia

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U2 - 10.1016/j.hrthm.2019.03.027

DO - 10.1016/j.hrthm.2019.03.027

M3 - Article

SN - 1547-5271

VL - 16

SP - 1475

EP - 1483

JO - Heart Rhythm

JF - Heart Rhythm

IS - 10

ER -

Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

Abstract

Keywords

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A Virtual Cohort of Twenty-four Left-ventricular Models of Ischemic Cardiomyopathy Patients

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Pacing in proximity to scar during cardiac resynchronization therapy increases local dispersion of repolarization and susceptibility to ventricular arrhythmogenesis.

Abstract

Keywords

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A Virtual Cohort of Twenty-four Left-ventricular Models of Ischemic Cardiomyopathy Patients

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