The Amplitude-Normalized Area of a Bipolar Electrogram as a Measure of Local Conduction Delay in the Heart
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The Amplitude-Normalized Area of a Bipolar Electrogram as a Measure of Local Conduction Delay in the Heart. / Mendonca Costa, Caroline; Anderson, Grace C.; Meijborg, Veronique M.F.; O’Shea, Christopher; Shattock, Michael J.; Kirchhof, Paulus; Coronel, Ruben; Niederer, Steven; Pavlovic, Davor; Dhanjal, Tarvinder; Winter, James.
In: FRONT PHYSIOL, Vol. 11, 465, 19.05.2020.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - The Amplitude-Normalized Area of a Bipolar Electrogram as a Measure of Local Conduction Delay in the Heart
AU - Mendonca Costa, Caroline
AU - Anderson, Grace C.
AU - Meijborg, Veronique M.F.
AU - O’Shea, Christopher
AU - Shattock, Michael J.
AU - Kirchhof, Paulus
AU - Coronel, Ruben
AU - Niederer, Steven
AU - Pavlovic, Davor
AU - Dhanjal, Tarvinder
AU - Winter, James
N1 - Funding Information: JW (FS/16/35/31952) is supported by the British Heart Foundation. DP and CO’S are supported by the (Sci-Phy-4-Health Center for Doctoral Training L016346) EPSRC, (109604/Z/15/Z) Wellcome Trust and (PG/17/55/33087, FS/16/35/31952, FS/19/16/34169, FS/19/12/34204) British Heart Foundation. RC, VM are supported by a Transatlantic Network of Excellence grant from the Leducq Foundation (16CVD02, RHYTHM). GA and MS are supported by the British Heart Foundation (RG/12/4/29426 and FS/15/66/32037). CM is supported by the British Heart Foundation (PG/15/91/31812). This work was further supported by European Union (grant agreement No 633196 [CATCH ME]), European Union BigData@Heart (grant agreement EU IMI 116074), British Heart Foundation (FS/13/43/30324; PG/17/30/32961, and AA/18/2/34218), and Leducq Foundation (genomic topology of AF to PK). Publisher Copyright: © Copyright © 2020 Mendonca Costa, Anderson, Meijborg, O’Shea, Shattock, Kirchhof, Coronel, Niederer, Pavlovic, Dhanjal and Winter.
PY - 2020/5/19
Y1 - 2020/5/19
N2 - Background: Re-entrant ventricular tachycardia may be non-inducible or haemodynamically compromising, requiring assessment of the electrophysiological properties of the myocardium during sinus rhythm (i.e., substrate mapping). Areas of heart tissue with slow conduction can act as a critical isthmus for re-entrant electrical excitation and are a potential target for ablation therapy. Aim: To develop and validate a novel metric of local conduction delay in the heart, the amplitude-normalized electrogram area (norm_EA). Methods: A computational model of a propagating mouse action potential was used to establish the impact of altering sodium channel conductance, intracellular conductivity, fibrosis density, and electrode size/orientation on bipolar electrogram morphology. Findings were then validated in experimental studies in mouse and guinea pig hearts instrumented for the recording of bipolar electrograms from a multipolar linear mapping catheter. norm_EA was calculated by integrating the absolute area of a bipolar electrogram divided by the electrogram amplitude. Electrogram metrics were correlated with the local conduction delay during sodium channel block, gap junction inhibition, and acute ischemia. Results: In computational simulations, reducing sodium channel conductance and intracellular conductivity resulted in a decrease in signal amplitude and increase in norm_EA (reflecting a broadening of electrogram morphology). For larger electrodes (3 mm diameter/7.1 mm2 area), the change in norm_EA was essentially linear with the change in local conduction delay. Experimental studies supported this finding, showing that the magnitude of change in norm_EA induced by flecainide (1–4 μM), carbenoxolone (10–50 μM), and low-flow ischemia (25% of initial flow rate) was linearly correlated with the local conduction delay in each condition (r2 = 0.92). Qualitatively similar effects were observed in guinea pig hearts perfused with flecainide. Increasing fibrosis density in the computational model also resulted in a decrease in signal amplitude and increase in norm_EA. However, this remains to be validated using experimental/clinical data of chronic infarct. Conclusion: norm_EA is a quantitative measure of local conduction delay between the electrode pair that generates a bipolar electrogram, which may have utility in electrophysiological substrate mapping of non-inducible or haemodynamically compromising tachyarrhythmia.
AB - Background: Re-entrant ventricular tachycardia may be non-inducible or haemodynamically compromising, requiring assessment of the electrophysiological properties of the myocardium during sinus rhythm (i.e., substrate mapping). Areas of heart tissue with slow conduction can act as a critical isthmus for re-entrant electrical excitation and are a potential target for ablation therapy. Aim: To develop and validate a novel metric of local conduction delay in the heart, the amplitude-normalized electrogram area (norm_EA). Methods: A computational model of a propagating mouse action potential was used to establish the impact of altering sodium channel conductance, intracellular conductivity, fibrosis density, and electrode size/orientation on bipolar electrogram morphology. Findings were then validated in experimental studies in mouse and guinea pig hearts instrumented for the recording of bipolar electrograms from a multipolar linear mapping catheter. norm_EA was calculated by integrating the absolute area of a bipolar electrogram divided by the electrogram amplitude. Electrogram metrics were correlated with the local conduction delay during sodium channel block, gap junction inhibition, and acute ischemia. Results: In computational simulations, reducing sodium channel conductance and intracellular conductivity resulted in a decrease in signal amplitude and increase in norm_EA (reflecting a broadening of electrogram morphology). For larger electrodes (3 mm diameter/7.1 mm2 area), the change in norm_EA was essentially linear with the change in local conduction delay. Experimental studies supported this finding, showing that the magnitude of change in norm_EA induced by flecainide (1–4 μM), carbenoxolone (10–50 μM), and low-flow ischemia (25% of initial flow rate) was linearly correlated with the local conduction delay in each condition (r2 = 0.92). Qualitatively similar effects were observed in guinea pig hearts perfused with flecainide. Increasing fibrosis density in the computational model also resulted in a decrease in signal amplitude and increase in norm_EA. However, this remains to be validated using experimental/clinical data of chronic infarct. Conclusion: norm_EA is a quantitative measure of local conduction delay between the electrode pair that generates a bipolar electrogram, which may have utility in electrophysiological substrate mapping of non-inducible or haemodynamically compromising tachyarrhythmia.
KW - bipolar electrogram
KW - cardiac arrhythmia
KW - cardiac mapping
KW - conduction delay
KW - electrophysiology
KW - substrate mapping
UR - http://www.scopus.com/inward/record.url?scp=85085874596&partnerID=8YFLogxK
U2 - 10.3389/fphys.2020.00465
DO - 10.3389/fphys.2020.00465
M3 - SCORING: Journal article
C2 - 32508676
AN - SCOPUS:85085874596
VL - 11
JO - FRONT PHYSIOL
JF - FRONT PHYSIOL
SN - 1664-042X
M1 - 465
ER -