Mechanisms that initiate ventricular tachycardia in the infarcted human heart

Segal, Oliver R.; Chow, Anthony; Peters, Nicholas S.; Davies, D. Wyn

doi:10.1016/j.hrthm.2009.09.025

Cited by 39 publications

(29 citation statements)

References 29 publications

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Section: Discussionmentioning

confidence: 74%

“…Previous studies of postinfarct VT initiation mechanisms in both animals 25 and humans 26 have confirmed that VT induction is dependent on unidirectional block. Furthermore, it has been suggested that the site of unidirectional block may be close to the exit of a subsequently induced VT. 26 In this study, Figures 2 and 3 demonstrate how decrement can lead to different modes of VT initiation using the same diastolic path. In Figure 2C, if sufficiently delayed conduction occurred in an impulse traveling in the direction from bipoles K to A so that the myocardium was not refractory when the impulse exited at bipole A (assuming the diastolic isthmus had no retrograde invasion), then reentrant VT could be initiated where bipole A was the exit site (as in Figure 3).…”

Section: Discussionmentioning

confidence: 74%

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Decrement Evoked Potential Mapping

Jackson

Gizurarson

Viswanathan

et al. 2015

Circ: Arrhythmia and Electrophysiology

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Background-Substrate-based mapping for ventricular tachycardia (VT) ablation is hampered by its inability to determine critical sites of the VT circuit. We hypothesized that those potentials, which delay with a decremental extrastimulus (decrement evoked potentials or DEEPs), are more likely to colocalize with the diastolic pathways of VT circuits. Methods and Results-DEEPs were identified in intraoperative left ventricular maps from 6 patients with ischemic cardiomyopathy (total 9 VTs) and were compared with late potential (LP) and activation maps of the diastolic pathway for each VT. Mathematical modeling was also used to further validate and elucidate the mechanisms of DEEP mapping. All patients demonstrated regions of DEEPs and LPs. The mean endocardial surface area of these potentials was 18±4% and 21±6%, respectively (P=0.13). The mean sensitivity for identifying the diastolic pathway in VT was 50±23% for DEEPs and 36±32% for LPs (P=0.31). The mean specificity was 43±23% versus 20±8% for DEEP and LP mapping, respectively (P=0.031). The electrograms that displayed the greatest decrement in each case had a sensitivity and specificity for the VT isthmus of 29±10% and 95±1%, respectively. Mathematical modeling studies recapitulated DEEPs at the VT isthmus and demonstrated their role in VT initiation with a critical degree of decrement. Conclusions-In this preliminary study, DEEP mapping was more specific than LP mapping for identifying the critical targets of VT ablation. The mechanism of DEEPs relates to conduction velocity restitution magnified by zigzag conduction within scar channels.

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Section: Discussionmentioning

confidence: 74%

Section: Discussionmentioning

confidence: 74%

Decrement Evoked Potential Mapping

Jackson

Gizurarson

Viswanathan

et al. 2015

Circ: Arrhythmia and Electrophysiology

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“…The MI border with normal tissue at the periphery of the infarct territory may also play an important role in these arrhythmias. Noncontact mapping in human hearts has suggested that functional reentry at the periphery of the MI may play a role in early reentry formation and the initiation of these arrhythmias (13,58). The electrophysiology at this junction of normal and infarcted tissue at this periphery is not as well studied.…”

Section: Discussionmentioning

confidence: 99%

A novel, minimally invasive, segmental myocardial infarction with a clear healed infarct borderzone in rabbits

Ziv

Schofield

Lau

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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G. A novel, minimally invasive, segmental myocardial infarction with a clear healed infarct borderzone in rabbits. Am J Physiol Heart Circ Physiol 302: H2321-H2330, 2012. First published March 23, 2012 doi:10.1152/ajpheart.00031.2012.-Ventricular arrhythmias in the setting of a healed myocardial infarction have been studied to a much lesser degree than acute and subacute infarction, due to the pericardial scarring, which results from the traditional open-chest techniques used for myocardial infarction (MI) induction. We sought to develop a segmental MI with low perioperative mortality in the rabbit that allows optimal visualization and therefore improved study of the infarction borderzone. Rabbits underwent MI using endovascular coil occlusion of the first obtuse marginal artery. Three weeks postprocedure, we evaluated our model by echocardiography and electrophysiology studies, optical mapping of isolated hearts, and histological studies. Seventeen rabbits underwent the protocol (12 MI and 5 sham) with a 92% survival to completion of the study (11 MI and 5 sham). MI rabbits demonstrated wall motion abnormalities on echocardiography while shams did not. At electrophysiological study, two MI rabbits had inducible ventricular tachycardia and one had inducible ventricular fibrillation. Isolated hearts demonstrated no pericardial scarring with a smooth, easily identifiable infarct borderzone. Optical mapping of the borderzone region showed successful mapping of peri-infarct reentry formation, with ventricular fibrillation inducible in 11 of 11 MI hearts and 1 of 5 sham hearts. We demonstrate successful high resolution mapping in the borderzone, showing delayed conduction in this region corresponding to late deflections in the QRS on ECG. We report the successful development of a minimally invasive MI via targeted coil delivery to the obtuse marginal artery with an exceptionally high rate of procedural survival and an arrhythmogenic phenotype. This model mimics human post-MI on echocardiography, gross pathology, histology, and electrophysiology.arrhythmia; optical mapping; ventricular tachycardia SUDDEN CARDIAC DEATH (SCD) remains a major public health issue constituting an estimated 20% of deaths in industrialized countries (31,40,49). In autopsy series, nearly 50% of SCD victims have had healed myocardial infarction (MI; Refs. 24, 69). The majority of sudden deaths after MI occur due to ventricular tachyarrhythmias (26). Post-MI ventricular arrhythmias have been studied extensively in animal models. The animal studies suggest the epicardial borderzone as a key player in the formation of reentrant ventricular tachyarrhythmias due to changes in tissue structure, ion channels, and gap junctions that slow conduction and generate anisotropy (6,21,22,35,47,65,67). While these studies have greatly enhanced our understanding of post-MI arrhythmias, our understanding of the arrhythmia mechanisms in healed infarct remains limited because most of studies used 5 days postinfarction, not a fully healed post-MI heart. In additio...

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“…Indeed, experimental data showed increase in stimulation magnitude for infarcted cardiac tissue (Meesmann and Marchlinski 1990). On the other hand, uni-directional blocks that are common in infarcted tissue border zones (Segal et al 2010) are known to be arrhythmogenic, and may theoretically work to either increase or decrease the needed stimulation magnitude, similarly to patches of fibroblasts with varying coupling coefficients.…”

Section: Discussionmentioning

confidence: 99%

Subthreshold Parameters of Cardiac Tissue in a Bi-Layer Computer Model of Heart Failure

Zlochiver

2010

Cardiovasc Eng

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Current density threshold and liminal area are subthreshold parameters of the cardiac tissue that indicate its susceptibility to external and internal stimulations. Extensive experimental and theoretical research has been conducted to quantify these two parameters in normal conditions for both animal and human models. Here we employed a 2D numerical model of human cardiac tissue to assess these subthreshold parameters under the pathological conditions of heart failure and fibrosis. Stimuli were applied over an area ranging from 0.04 to 1 mm² using various pulse durations. The current density threshold decreased with increasing stimulation area or pulse duration. No significant changes were found in both parameters between control conditions and heart failure in the atrial tissue, while in the ventricular tissue, heart failure resulted in significantly reduced excitability with higher stimulation current magnitudes needed for excitation and larger liminal areas. This results from the specific ionic remodeling in ventricular heart failure that affects both subthreshold active currents such as I(K₁) and connexin 43 conductance. In fibrosis, increased fibroblast to myocyte coupling coefficient had a non-linear influence on current density thresholds, with an initial increase of current magnitude followed by a relaxation phase down to the current magnitude threshold for the control condition with no fibrosis. The results show that subthreshold excitation properties of the myocardium are influenced in a complex, non-linear manner by cardiac pathologies. Such observations may contribute to our understanding of impulse capturing properties, relevant, for example, for the generation of ectopic foci-originated arrhythmias and for the efficient design of cardiac stimulating electrodes.

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Mechanisms that initiate ventricular tachycardia in the infarcted human heart

Cited by 39 publications

References 29 publications

Decrement Evoked Potential Mapping

Decrement Evoked Potential Mapping

A novel, minimally invasive, segmental myocardial infarction with a clear healed infarct borderzone in rabbits

Subthreshold Parameters of Cardiac Tissue in a Bi-Layer Computer Model of Heart Failure

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