Influence of the Purkinje-muscle junction on transmural repolarization heterogeneity

Walton, Richard D.; Martinez, M.; Bishop, Martin J.; Hocini, Mélèze; Haı̈ssaguerre, Michel; Plank, Gernot; Bernus, Olivier; Vigmond, Edward J.

doi:10.1093/cvr/cvu165

Cited by 35 publications

(35 citation statements)

References 33 publications

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“…These islands of prolonged action potential duration did not resemble the 'M'-cell layer as it was originally described and may rather reflect sites where intramural Purkinje fibers connect to the ventricular myocardium, the Purkinje-muscle junction (Fig. 4, see section 4.2) (Walton et al, 2014). Taken together, there is no evidence for a coherent midmyocardial region with long action potential in the human ventricular wall (Janse et al, 2012).…”

Section: Transmural Gradients In Repolarization: Where Are the M-cells?mentioning

confidence: 76%

“…These were solely attributed to a myocardial cell phenotype, the M-Cell (Yan and Antzelevitch, 1999), until it was recently shown by Walton et al that Purkinje fibers also had a role in providing sources of repolarization heterogeneity (Fig. 4) (Walton et al, 2014). This is due to the distinct electrophysiological properties of Purkinje fibers in comparison to their myocardial counterparts, which include greater conduction velocity, augmented action potential upstroke, but a relatively repolarized plateau phase and a longer APD.…”

Section: Purkinje-muscle Interactions As a Source Of Arrhythmiasmentioning

confidence: 99%

“…Such changes therefore suggest a greater role for PMJ-related repolarization heterogeneity in disease. Computer simulations showed it is it likely that local APD heterogeneity at the PMJ persist in a model of heart failure (Walton et al, 2014), although experimental data of the transmural heterogeneity at sufficient spatial resolution is currently lacking. Also clinically, Purkinje fibers may serve as a trigger for focal ectopic activity (Weerasooriya et al, 2003).…”

Section: Purkinje-muscle Interactions As a Source Of Arrhythmiasmentioning

confidence: 99%

See 2 more Smart Citations

Transmural electrophysiological heterogeneity, the T-wave and ventricular arrhythmias

Boukens

Walton

Meijborg

et al. 2016

Progress in Biophysics and Molecular Biology

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Section: Transmural Gradients In Repolarization: Where Are the M-cells?mentioning

confidence: 76%

Section: Purkinje-muscle Interactions As a Source Of Arrhythmiasmentioning

confidence: 99%

Section: Purkinje-muscle Interactions As a Source Of Arrhythmiasmentioning

confidence: 99%

See 1 more Smart Citation

Transmural electrophysiological heterogeneity, the T-wave and ventricular arrhythmias

Boukens

Walton

Meijborg

et al. 2016

Progress in Biophysics and Molecular Biology

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“…; Walton et al. ). The latter would make the observation of M cells a matter of chance, since not every plane within the transmural wall includes these junctions, which would explain why M cells are reported in one study in the canine wedge, but not in the other.…”

Section: Discussionmentioning

confidence: 99%

Local transmural action potential gradients are absent in the isolated, intact dog heart but present in the corresponding coronary-perfused wedge

et al. 2017

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The left ventricular (LV) coronary‐perfused canine wedge preparation is a model commonly used for studying cardiac repolarization. In wedge studies, transmembrane potentials typically are recorded; whereas, extracellular electrical recordings are commonly used in intact hearts. We compared electrically measured activation recovery interval (ARI) patterns in the intact heart with those recorded at the same location in the LV wedge preparation. We also compared electrically recorded and optically obtained ARIs in the LV wedge preparation. Five Langendorff‐perfused canine hearts were paced from the right atrium. Local activation and repolarization times were measured with eight transmural needle electrodes. Subsequently, left ventricular coronary‐perfused wedge preparations were prepared from these hearts while the electrodes remained in place. Three electrodes remained at identical positions as in the intact heart. Both electrograms and optical action potentials were recorded (pacing cycle length 400–4000 msec) and activation and repolarization patterns were analyzed. ARIs found in the subepicardium were shorter than in the subendocardium in the LV wedge preparation but not in the intact heart. The transmural ARI gradient recorded at the cut surface of the wedge was not different from that recorded internally. ARIs recorded internally and at the cut surface in the LV wedge preparation, both correlated with optically recorded action potentials. ARI and RT gradients in the LV wedge preparation differed from those in the intact canine heart, implying that those observations in human LV wedge preparations also should be extrapolated to the intact human heart with caution.

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“…In addition, novel factors influencing local APD, such as Purkinje fiber--myocyte junctions have been described and merit further investigation. 26 From the clinical perspective, the human data on QT interval shortening during continuous ventricular pacing 14,15 are most consistent with reciprocal changes in APD between early (prolongation) and late-activated (shortening) areas.…”

Section: Electrophysiology Molecular Mechanisms and Triggers Of CM mentioning

confidence: 86%

Cardiac Memory

Shvilkin

Huang

Josephson

2015

Circ: Arrhythmia and Electrophysiology

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C lassic definition of the term cardiac memory (CM) refers to the persistent T-wave changes on the ECG after a period of wide QRS rhythms that become evident once normal ventricular activation pattern is restored. It is related to the term ventricular electric remodeling sometimes used in basic science literature. Although CM itself is considered as an adaptive reaction to the change in the ventricular activation sequence, its manifestations (usually T-wave inversions, TWIs) are often confused with pathological conditions manifesting with TWI, such as myocardial ischemia or infarction. Although originally CM was described after restoration of the normal ventricular activation (narrow QRS), recently it was described and studied in wide QRS rhythms significantly expanding the clinical relevance of this phenomenon. Although complex molecular mechanisms of CM have been previously reviewed extensively, practical clinical application of this phenomenon received much less attention. In this article, we will focus on the clinically relevant aspects of CM including its diagnostic use in narrow and wide QRS rhythms. We will also examine how the fundamental CM property of being initiated by the changes in the geometry of the ventricular contraction might open new perspectives in wide QRST morphology analysis by establishing parallels between electric and mechanical functions of the heart. History, Properties, and Adaptive Nature of Cardiac MemoryIn 1915, White 1 was the first to observe the phenomenon of transient TWI after single ventricular premature beats. Later in the 1940s, TWIs after conversion to sinus rhythm were described after paroxysmal tachycardias.2 Since then abnormal T waves of various duration have been documented after intermittent ventricular pre-excitation, 3-5 ventricular pacing, 6,7 intermittent left bundle branch block (LBBB), 8,9 ventricular tachycardia, 10 and even QRS widening associated with sodium channel blocker toxicity. 11In 1982, Rosenbaum et al 10 introduced the term heart memory and presented the first unified hypothesis of how abnormal ventricular activation could lead to the development of T-wave abnormalities regardless of the wide QRS cause by a process he referred to as electrotonic modulation. In this seminal article, 3 principles of CM were formulated: (1) the direction of the T waves in sinus rhythm follows (remembers) the direction of the QRS complex during preceding episode of abnormal activation; (2) the amplitude of memory T waves increases the longer abnormal conduction continues, and (3) repeat episodes of abnormal activation after complete normalization of T waves result in more rapid and prominent accumulation of T-wave changes (hence the term memory). The authors hypothesized that CM represents adaptation of myocardial repolarization to the new activation sequence.The adaptive nature of CM was subsequently confirmed in both animal and human studies. Costard-Jäckle et al 12 and later Sosunov et al 13 in an isolated rabbit heart demonstrated the presence of an inverse relatio...

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Influence of the Purkinje-muscle junction on transmural repolarization heterogeneity

Abstract: The Purkinje network has the potential to influence myocardial AP morphology and rate-dependent behaviour, and furthermore to underlie enhanced transmural APD heterogeneities and spatial gradients of APD in non-failing and failing myocardium.

Cited by 35 publications

References 33 publications

Transmural electrophysiological heterogeneity, the T-wave and ventricular arrhythmias

Transmural electrophysiological heterogeneity, the T-wave and ventricular arrhythmias

Local transmural action potential gradients are absent in the isolated, intact dog heart but present in the corresponding coronary-perfused wedge

Cardiac Memory

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