Considerations in phase plane analysis for nonstationary reentrant cardiac behavior

Bray, Mark-Anthony; Wikswo, John P.

doi:10.1103/physreve.65.051902

Cited by 94 publications

(91 citation statements)

References 14 publications

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“…20 The dominant frequency (DF) was defined as the frequency corresponding to the highest peak in the power spectrum. Phase movies 21 were generated by applying the Hilbert transform 5,22 to the AP fluorescent signal. Singularity point (SP) was defined as a point where all phases converge.…”

Section: Discussionmentioning

confidence: 99%

Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

Warren

Huízar

Shvedko

et al. 2007

Circulation Research

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Abstract-Normal "master-slave" relationship between the action potential (AP) and intracellular Ca 2ϩ transient (Ca i T) is sometimes altered during ventricular fibrillation (VF). The nature of AP/Ca i T dissociation during VF and its role in inducing wavebreaks (WBs) remain unclear. We simultaneously mapped AP (RH237) and Ca i T (Rhod-2) during VF in blood-perfused pig hearts. We computed AP and Ca i T dominant frequency (DF) and Ca i T delay in each AP cycle. We identified WBs as singularity points in AP phase movies and sites of conduction block (CB) as sites where an AP wavefront failed to propagate. We analyzed spatiotemporal relationship between abnormal AP/Ca i T sequences and CB sites. We used a calcium chelator (BAPTA-AM) to abolish Ca i T and test its involvement in WB formation. During VF, the DF difference between AP and Ca i T was Ͻ10% of the respective values in 95% of pixels, and 80% of all Ca i T upstrokes occurred during the initial 25% of the excitation cycle. Aberrant sequences of AP and Ca i T occurred almost exclusively near CB sites but could be traced to normal wavefront sequences away from CB sites. Thus, apparent AP/Ca i T dissociation was largely attributable to spatial uncertainty of the absolute position of block of each wave. BAPTA-AM reduced Ca i T amplitude to 30.5Ϯ12.9% of control and the DF of AP from 12.2Ϯ1.6 to 10.4Ϯ1.3Hz (PϽ0.01), but did not significantly alter WB incidence (0.76Ϯ0.19 versus 0.72Ϯ0.19SP/mm 2 ). These results do not support presence of spontaneous, non-voltage-gated Ca i Ts during VF and suggest that AP/Ca i T dissociation is a consequence rather than a cause of wave fragmentation. (Circ Res. 2007;101:e90-e101.) Key Words: ventricular fibrillation Ⅲ pig heart Ⅲ action potential Ⅲ calcium transient Ⅲ wavebreak R ecurrent wave fragmentation, or wavebreak (WB), is a hallmark of ventricular fibrillation (VF). 1,2 Wavebreak occurs when a propagating wavefront encounters an obstacle which may result from electrophysiological heterogeneities, [3][4][5][6] intrinsic repolarization instabilities, 7,8 anatomic structures, 9 or regional ischemia. 10 Repolarization instabilities in the form of action potential duration (APD) alternans are at least in part mediated by beat-to-beat changes in L-type Ca 2ϩ current (I Ca,L ) and Na ϩ -Ca 2ϩ exchanger (NCX). 2,11 These currents are bidirectionally coupled to intracellular Ca 2ϩ (Ca i ) cycling, so that Ca 2ϩ influx via I Ca,L triggers Ca 2ϩ release from the sarcoplasmic reticulum (SR), whereas an increase in Ca i modulates inactivation of I Ca,L and the transsarcolemmal current generated by NCX. 12 SR Ca 2ϩ cycling can exhibit intrinsic dynamics in the form of Ca i transient (Ca i T) alternans (even when the AP waveform is fixed under voltage clamp) 13 and in the form of spontaneous, non-voltage-gated Ca 2ϩ releases. 12 It was hypothesized that such intrinsic dynamics of Ca i T can promote APD fluctuations at high excitation rates and thus contribute to mechanisms of WB during VF. 2,13 To test this hypothesis, Omichi et al 14...

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Section: Discussionmentioning

confidence: 99%

Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

Warren

Huízar

Shvedko

et al. 2007

Circulation Research

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“…Therefore, the comparison of the average RV and LV values of APD80 between groups was performed between 3 and 8 min of ischemia. For analysis of VF, we applied the Hilbert Transform to movies of voltage-sensitive fluorescence and identified singularity points and rotors as points where all OAP phases converged (20) (9). Timespace plots were created by stacking intensity profiles along a selected line of pixels in consecutive frames of the voltagesensitive fluorescence (39).…”

Section: This Investigation Conformed To the National Institutes Of Hmentioning

confidence: 99%

β-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart

Garg

Taylor

Warren

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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bayama J, Zaitsev A. ␤-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart. Am J Physiol Heart Circ Physiol 308: H1155-H1170, 2015. First published February 20, 2015 doi:10.1152/ajpheart.00768.2014.-Global ischemia, catecholamine surge, and rapid heart rhythm (RHR) due to ventricular tachycardia or ventricular fibrillation (VF) are the three major factors of sudden cardiac arrest (SCA). Loss of excitability culminating in global electrical failure (asystole) is the major adverse outcome of SCA with increasing prevalence worldwide. The roles of catecholamines and RHR in the electrical failure during SCA remain unclear. We hypothesized that both ␤-adrenergic stimulation (␤AS) and RHR accelerate electrical failure in the globally ischemic heart. We performed optical mapping of the action potential (OAP) in the right ventricular (RV) and left (LV) ventricular epicardium of isolated rabbit hearts subjected to 30-min global ischemia. Hearts were paced at a cycle length of either 300 or 200 ms, and either in the presence or in the absence of ␤-agonist isoproterenol (30 nM). 2,3-Butanedione monoxime (20 mM) was used to reduce motion artifact. We found that RHR and ␤AS synergistically accelerated the decline of the OAP upstroke velocity and the progressive expansion of inexcitable regions. Under all conditions, inexcitability developed faster in the LV than in the RV. At the same time, both RHR and ␤AS shortened the time to VF (TVF) during ischemia. Moreover, the time at which 10% of the mapped LV area became inexcitable strongly correlated with TVF (R 2 ϭ 0 .72, P Ͻ 0.0001). We conclude that both ␤AS and RHR are major factors of electrical depression and failure in the globally ischemic heart and may contribute to adverse outcomes of SCA such as asystole and recurrent/persistent VF.

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“…To overcome this dilemma, the Hilbert Transform (HT)-based approach was used by some of the recent studies in computing the instantaneous phase. 4,5 In simple terms, HT is another way of generating a phase-shifted signal from the original signal and using these 2 signals the instantaneous phase is computed. For interested readers, more details are provided in the methods supplemental section.…”

Section: Hilbert Transformmentioning

confidence: 99%

“…These points in the phase map are called phase singularity (PS) points. Bray et al 4 developed a procedure to locate PS points in a phase map. Nash et al 5 used phase mapping to study the entire ventricular epicardium of human hearts with a sock containing 256 unipolar contact electrodes.…”

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Phase Mapping of Cardiac Fibrillation

Umapathy

Nair

Massé

et al. 2010

Circ: Arrhythmia and Electrophysiology

156

140

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Phase is a descriptor that tracks the progression of a defined region of myocardium through the action potential and has been demonstrated to be an effective parameter in analyzing spatiotemporal changes during fibrillation. In this review, the basic principles behind phase mapping are presented mainly in the context of ventricular fibrillation (VF), atrial fibrillation (AF), and fibrillation from experimental monolayer data. During fibrillation, the phase distribution changes over time, depending on activation patterns. Analyzing these phase patterns provides us insight into the fibrillatory dynamics and helps clarify the mechanisms of cardiac fibrillation and modulation by interventions. Winfree 1 introduced the phase analysis to study cardiac fibrillation in the late eighties. This time-encoding technique deals with a scenario where the activation periods are the same over the surface being mapped. To deal with the scenario of varying activation period over the mapped surface (common in animal and human fibrillation models), Gray et al 2,3 introduced the state-space encoding concept from nonlinear dynamics.In analyzing spatiotemporal phase maps constructed from electric or optical mapping of the surface of heart during VF, points around which the phase progresses through a complete cycle from Ϫ to ϩ are of great interest. At these points, the phase becomes indeterminate and the activation wave fronts hinge to these points and rotate around them in an organized fashion. These points in the phase map are called phase singularity (PS) points. Bray et al 4 developed a procedure to locate PS points in a phase map. Nash et al 5 used phase mapping to study the entire ventricular epicardium of human hearts with a sock containing 256 unipolar contact electrodes. The development of this phase mapping tool has led to better understanding of fibrillation dynamics as evidenced by the use of phase mapping in detecting PS and their role in demonstrating organization during VF. Some of these works and their findings are (1) PS colocalize with anatomic heterogeneities, and their spatial meandering is modulated by these heterogeneities, 6 (2) PS correlates with the locations of wave breaks, 7 (3) in myopathic human hearts, phase maps were used to show that the organization of electric activity were characterized by wave fronts emanating from a few rotors, 8 and (4) phase mapping technique has also been applied to investigate the mechanism of fibrillation. 7-9 Clinical electrophysiologists innovating therapies for both AF and VF are commonly not aware of phase mapping. This review addresses this shortcoming with the hope that by introducing the basic concepts of phase mapping to a greater audience, there will be an opportunity to devise therapies for these arrhythmias on a mechanistic basis.

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Considerations in phase plane analysis for nonstationary reentrant cardiac behavior

Cited by 94 publications

References 14 publications

Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

β-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart

Phase Mapping of Cardiac Fibrillation

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Considerations in phase plane analysis for nonstationary reentrant cardiac behavior

Cited by 94 publications

References 14 publications

Spatiotemporal Relationship Between Intracellular Ca 2+ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

Spatiotemporal Relationship Between Intracellular Ca 2+ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

β-Adrenergic stimulation and rapid pacing mutually promote heterogeneous electrical failure and ventricular fibrillation in the globally ischemic heart

Phase Mapping of Cardiac Fibrillation

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Product

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Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts

Spatiotemporal Relationship Between Intracellular Ca ²⁺ Dynamics and Wave Fragmentation During Ventricular Fibrillation in Isolated Blood-Perfused Pig Hearts