Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks

Dosdall, Derek J.; Cheng, Kang An; Huang, Jian; Allison, J. Scott; Allred, James; Smith, William M.; Ideker, Raymond E.

doi:10.1016/j.hrthm.2007.02.017

Cited by 33 publications

(30 citation statements)

References 45 publications

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“…This different distribution of earliest postshock activation in the two species draws our attention to the Purkinje fibers involved in the creation and propagation of earliest activation, because in the pig the Purkinje fibers extend from the endocardium almost to the epicardium, while in dogs the Purkinje fibers are limited to the subendocardium. Dosdall et al [28] demonstrated that the Purkinje system is active during the early postshock activation cycles following DFT level shocks with the same shock electrode configuration as ours. Therefore, the endocardial basket in the LV is capable of detecting the earliest activation pattern after the defibrillation shock in the canine model.…”

Section: Alteration Of Apd and Qt Interval By Pinacidilsupporting

confidence: 61%

The effect of pinacidil on postshock activation and ventricular defibrillation threshold in canine hearts

Zhang

Zhou

et al. 2012

Acta Pharmacol Sin

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Aim: To determine the postshock activation patterns with both successful and failed shocks in a canine model of ventricular fibrillation, and whether piniacidil, an early after-depolarization (EAD) inhibitor, altered the defibrillation threshold (DFT) and postshock activation patterns. Methods: In 6 beagles, a basket catheter with 64 unipolar electrodes was placed in the LV for global endocardial mapping, a monophasic action potential catheter was inserted into the LV apex, and a catheter with the negative electrode in the right ventricle and the positive electrode in the superior vena cava was inserted for defibrillation. The DFT, 90% action potential duration (APD 90 ) and activation recovery interval (ARI) were evaluated before and after pinacidil administration (loading dosage 0.5 mg/kg and maintenance dosage 0.5 mg·kg -1 ·h -1, iv). Electrical heterogeneities were defined with the dispersion of ARI. After successful and failed shocks with near-DFT strength, the earliest postshock activation patterns (focal or nonfocal endocardial activation), interval and location were detected. Results: Pinacidil significantly decreased APD 90 (from 178±16 ms to 168±18 ms) and ARI from (152±10 ms to 143±10 ms) at pacing cycle length of 300 ms. The drug significantly increased VF activation rate (from 10.0±1.9 Hz to 10.8±2.0 Hz). The drug did not affect the dispersion of ARI, neither it changed DFT (baseline: 480±110 V; pinacidil: 425±55 V, P>0.05). The earliest postshock activation arose locally on the LV apical endocardium before and after the drug treatment. Pinacidil significantly prolonged the postshock cycle length of cycles 2 to 5 for the successful episodes but not for the failed episodes. Conclusion: Pinacidil increases the postshock cycle length suggesting that EAD may play a role in postshock activation, while it fails to alter DFT suggesting that EAD produced by shock does not determine a defibrillation success or failure.

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Section: Alteration Of Apd and Qt Interval By Pinacidilsupporting

confidence: 61%

The effect of pinacidil on postshock activation and ventricular defibrillation threshold in canine hearts

Zhang

Zhou

et al. 2012

Acta Pharmacol Sin

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“…Furthermore, patterns of postshock propagation on the epicardium of the rabbit model match well these determined experimentally, 15 with no evidence of micro-VE contribution. Finally, the ventricular model did not include Purkinje network; depolarization-induced automaticity from Purkinje fibers could be a different mechanism for PA origin 29 in addition to those presented here. …”

Section: Study Limitationsmentioning

confidence: 89%

Tunnel Propagation of Postshock Activations as a Hypothesis for Fibrillation Induction and Isoelectric Window

Ashihara

Constantino

Trayanova

2008

Circulation Research

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Abstract-Comprehensive understanding of the ventricular response to shocks is the approach most likely to succeed in reducing defibrillation threshold. We propose a new theory of shock-induced arrhythmogenesis that unifies all known aspects of the response of the heart to monophasic (MS) and biphasic (BS) shocks. The central hypothesis is that submerged "tunnel" propagation of postshock activations through shock-induced intramural excitable areas underlies fibrillation induction and the existence of isoelectric window. We conducted simulations of fibrillation induction using a realistic bidomain model of rabbit ventricles. Following pacing, MS and BS of various strengths/timings were delivered. The results demonstrated that, during the isoelectric window, an activation originated deep within the ventricular wall, arising from virtual electrodes; it then propagated fully intramurally through an excitable tunnel induced by the shock, until it emerged onto the epicardium, becoming the earliest-propagated postshock activation. Differences in shock outcomes for MS and BS were found to stem from the narrower BS intramural postshock excitable area, often resulting in conduction block, and the difference in the mechanisms of origin of the postshock activations, namely intramural virtual electrode-induced phase singularity for MS and virtual electrode-induced propagated graded response for BS. This study provides a novel analysis of the 3D mechanisms underlying the origin of postshock activations in the process of fibrillation induction by MS and BS and the existence of isoelectric window. Comprehensive knowledge and appreciation of the mechanisms by which a shock interacts with the heart is the approach most likely to succeed in reducing shock energy.The presence of an isoelectric window (IW) following unsuccessful defibrillation attempts 3-5 led to the understanding that an electric shock terminates ongoing fibrillation but then reinitiates it; hence the mechanisms of fibrillation induction and its reinitiation (unsuccessful defibrillation) are the same. Indeed, striking similarities between these mechanisms have been found, particularly with regard to propagation of the first global postshock activation (PA) and IW duration. 4 -6 The similarity is supported by the significant correlation between upper limit of vulnerability (ULV) and DFT. 7,8 Therefore, elucidating the origin of PAs resulting in fibrillation induction is expected to provide invaluable insight into the mechanisms of defibrillation failure and could contribute significantly to the effort to find novel ways to appreciably lower DFT.Although numerous hypotheses 9 -12 exist for the mechanisms of PA origin, none provides comprehensive mechanistic explanation of the following findings:1. Earliest PA following near-ULV (or near-DFT) shocks occurred after the epicardium recovered completely from shock-induced direct excitation. 3,5 2. IW increased as shock strength increased. 4,6,13 3. For both monophasic (MS) and biphasic (BS) shock waveforms, earliest PAs a...

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“…In fact, here we observed in the simulations that postshock propagation within the LV midmyocardium was strongly dependent on preshock state. However, the concepts proposed here do not limit the origin of the initiating PAs; these might have alternative origins, such as Purkinje fibers (Dosdall et al, 2007). The tunnel hypothesis is independent of the origin of wavefronts that propagate through it.…”

Section: Implications Of the Tunnel Propagation Hypothesismentioning

confidence: 92%

“…Understanding the origins of the isoelectric window is thus of great importance for uncovering the mechanisms of defibrillation failure. Various hypothesis have been proposed for the existence of the isoelectric window, including virtual electrodeinduced propagated graded response (Trayanova et al, 2003), calcium sinkholes (Hwang et al, 2006), and activations emanating from Purkinje fibers (Dosdall et al, 2007); however, the mechanisms responsible for it remain inconclusive. In this context, we hypothesized that submerged "tunnel propagation" of postshock activation (PA) through shock-induced intramural excitable areas underlies both fibrillation induction and failed defibrillation by shocks as well as the existence of an isoelectric window.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Defibrillation Failure

Ashihara¹,

Constantino²,

Trayanova³

2011

Cardiac Defibrillation - Mechanisms, Challenges and Implications

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Transmural and endocardial Purkinje activation in pigs before local myocardial activation after defibrillation shocks

Abstract: Background-Earliest recorded post-shock myocardial activations in pigs originate in the subepicardium of the apex and lateral free wall of the left ventricle (LV) 30−90 ms after the shock.

Cited by 33 publications

References 45 publications

The effect of pinacidil on postshock activation and ventricular defibrillation threshold in canine hearts

The effect of pinacidil on postshock activation and ventricular defibrillation threshold in canine hearts

Tunnel Propagation of Postshock Activations as a Hypothesis for Fibrillation Induction and Isoelectric Window

Mechanisms of Defibrillation Failure

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