Focal Initiation of Sustained and Nonsustained Ventricular Tachycardia in a Canine Model of Ischemic Cardiomyopathy

Johnson, Carolyn M.; Pogwizd, Steven M.

doi:10.1111/j.1540-8167.2011.02239.x

Cited by 3 publications

(3 citation statements)

References 37 publications

(107 reference statements)

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“…Our model shows several mechanisms of ischemic VT/VF with the most common being endocardial focal as well as epicardial reentry, as also described by others in ischemic models [ 5 ]. Endocardial mechanisms are particularly interesting because of clinical results of ablation [ 6 , 7 ] prevent induction of VT and implantable defibrillator shocks.…”

Section: Discussionsupporting

confidence: 73%

“…There is no arbitrary exclusion based on voltage of electrograms, but short cycle lengths indicating refractory block are manifest by >75% reduction of voltage. Additionally, unidirectional block is associated with circuitous activation in adjacent sites and increased voltage of the subsequent activation on the electrogram showing block [ 5 ]. Refractory periods during tachycardia are assumed to be shorter in epicardium (80 ms) than endocardium (100 ms); these values are utilized by algorithm to consider reentry when present.…”

Section: Methodsmentioning

confidence: 99%

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Role of NADPH Oxidase and Xanthine Oxidase in Mediating Inducible VT/VF and Triggered Activity in a Canine Model of Myocardial Ischemia

Martins

Chaudhary

Jiang

et al. 2014

IJMS

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Background: Ventricular tachycardia or fibrillation (VT/VF) of focal origin due to triggered activity (TA) from delayed afterdepolarizations (DADs) is reproducibly inducible after anterior coronary artery occlusion. Both VT/VF and TA can be blocked by reducing reactive oxygen species (ROS). We tested the hypothesis that inhibition of NADPH oxidase and xanthine oxidase would block VT/VF. Methods: 69 dogs received apocynin (APO), 4 mg/kg intraveneously (IV), oxypurinol (OXY), 4 mg/kg IV, or both APO and OXY (BOTH) agents, or saline 3 h after coronary occlusion. Endocardium from ischemic sites (3-D mapping) was sampled for Rac1 (GTP-binding protein in membrane NADPH oxidase) activation or standard microelectrode techniques. Results (mean ± SE, * p < 0.05): VT/VF originating from ischemic zones was blocked by APO in 6/10 *, OXY in 4/9 *, BOTH in 5/8 * or saline in 1/27; 11/16 VT/VFs blocked were focal. In isolated myocardium, TA was blocked by APO (10−6 M) or OXY (10−8 M). Rac1 levels in ischemic endocardium were decreased by APO or OXY. Conclusion: APO and OXY suppressed focal VT/VF due to DADs, but the combination of the drugs was not more effective than either alone. Both drugs inhibited ischemic Rac1 with inhibition by OXY suggesting ROS-induced ROS. The inability to totally prevent VT/VF suggests that other mechanisms also contribute to ischemic VT.

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Section: Discussionsupporting

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Role of NADPH Oxidase and Xanthine Oxidase in Mediating Inducible VT/VF and Triggered Activity in a Canine Model of Myocardial Ischemia

Martins

Chaudhary

Jiang

et al. 2014

IJMS

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“…Finally, focal nonre-entrant mechanisms like triggered activity, also inducible by PES, may play a role. 7 To date, there is insufficient data on the clinical relevance, (re)inducibility, and specific substrate requirements for these arrhythmia mechanisms. In this context, the results of a recently conducted ablation study, using the combined end point of noninducibility and late potential ablation, are noteworthy.…”

Section: Article See P 677mentioning

confidence: 99%

The Ideal End Point for Ablation in Postinfarction Ventricular Tachycardia

Zeppenfeld

2014

Circ: Arrhythmia and Electrophysiology

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T he end point of ventricular tachycardia (VT) ablation studies should ideally predict the target outcome-freedom from VT recurrence. VT in patients with previous myocardial infarction is often due to scar-related re-entry. This is supported, although not proven, by the fact that VT can be initiated by programmed electric stimulation (PES). Entrainment and resetting with fusion are strong arguments for re-entry but can be only performed during hemodynamically tolerated VT. Article see p 677The substrate for re-entry is characterized by regions of slow conduction, unidirectional conduction block that allows initiation of re-entry, and areas of conduction block that can define parts of the re-entry circuit. Conduction block can be anatomically fixed but also functional and thus only present during VT or at rapid rates. Catheter ablation aims to transect the critical isthmus of the re-entry circuit.The ideal ablation candidate is inducible for the clinically documented, hemodynamically tolerated VT. This allows for detailed analysis of the mechanism involved and accurate delineation of the underlying substrate. Unfortunately, this scenario applies only to a minority (albeit an important number) of patients.This first patient category was accepted for ablation in the early 1990s. Only the clinical VT was targeted and of importance, was, without exception reproducibly inducible from the right ventricle.1 Outcome was favorable if the clinical VT was abolished, a result achieved in 75% of the patients. Remarkably, 82% of them were noninducible for any VT after ablation. In 16% of these noninducible patients, ventricular arrhythmia (VA) recurred; in half of the patients early and often with the same VT morphology, perhaps due to lesion recovery. Patients presenting with a late recurrence either died suddenly, presumably (but not definitively) arrhythmic, or had a not previously documented VT. Patients with VA recurrence were more likely to be inducible for nonclinical VT.The second patient category was patients presenting with stable VTs but had multiple inducible VTs, of which all tolerated VTs were targeted.2 In 85%, the clinical VT could be abolished, but only 31% were rendered uninducible, despite a more extensive ablation approach. The difference in acute outcome may be partly explained by the more impaired ejection fraction (EF) in this second category. VT recurred in only 9% of noninducible patients but in 47% of patients with inducible nonclinical VTs after ablation. The latter had more inducible VTs, and the remaining VTs were faster than the ablated VTs.With the widespread use of implantable cardioverter defibrillators (ICDs), a third patient category has entered the electrophysiology laboratory. The majority have advanced heart failure and not tolerated VTs. For unstable VTs and for VTs that are documented but not inducible, it is impossible to verify the mechanism and to prove a causal relationship between the arrhythmia and the targeted substrate. It is important to remember that much of our knowledge about...

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Reassessing Noninducibility as Ablation Endpoint of Post-Infarction Ventricular Tachycardia

Riva

Piers

Kapel

et al. 2015

Circ: Arrhythmia and Electrophysiology

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Focal Initiation of Sustained and Nonsustained Ventricular Tachycardia in a Canine Model of Ischemic Cardiomyopathy

Abstract: Thus, initiation of SuVT in a model of ischemic HF is due to a focal mechanism. However, subsequent acceleration of this focal mechanism can ultimately lead to functional conduction delay and development of intramural reentry.

Cited by 3 publications

References 37 publications

Role of NADPH Oxidase and Xanthine Oxidase in Mediating Inducible VT/VF and Triggered Activity in a Canine Model of Myocardial Ischemia

Role of NADPH Oxidase and Xanthine Oxidase in Mediating Inducible VT/VF and Triggered Activity in a Canine Model of Myocardial Ischemia

The Ideal End Point for Ablation in Postinfarction Ventricular Tachycardia

Reassessing Noninducibility as Ablation Endpoint of Post-Infarction Ventricular Tachycardia

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