Characteristics of Ischemic and Peri‐Ischemic Regions During Ventricular Fibrillation in the Canine Heart

Ranković, Vladimir; Patel, Nikhil; Jain, Sandeep; Robinson, Nikki; Goldberger, J.; Horvath, George; Kadish, Alan H.

doi:10.1111/j.1540-8167.1999.tb00282.x

Cited by 11 publications

(7 citation statements)

References 22 publications

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“…Anchoring of reentry in areas of spatial electrophysiological heterogeneity is well-described 31,32. In the intact heart, wavebreak also occurred frequently in the IZ 33,34, although also in the BZ 35. Consistent with observations in intact heart,36 this created a “mother rotor” fibrillation pattern until the central IZ became inexcitable, after which fibrillation converted to macroreentry around the inexcitable IZ.…”

Section: Discussionsupporting

confidence: 55%

Electrophysiological Consequences of Acute Regional Ischemia/Reperfusion in Neonatal Rat Ventricular Myocyte Monolayers

et al. 2008

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Background-Electrophysiological changes promoting arrhythmias during acute regional ischemia/reperfusion are challenging to study in intact cardiac tissue because of complex 3-dimensional myocardial and vascular geometry. We characterized electrophysiological alterations and arrhythmias during regional ischemia/reperfusion in a simpler 2-dimensional geometry of cultured neonatal rat ventricular myocyte monolayers. Methods and Results-Optical mapping of intracellular Ca (Ca i ) and voltage was performed with the use of Rhod 2-AM and Rh-237, respectively. Regional ischemia was mimicked by covering the central portion of monolayer with a glass coverslip, and reperfusion was mimicked by removing the coverslip. Monolayers were stained with fluorescent antibodies to detect total and dephosphorylated connexin-43 at various time points. During coverslip ischemia, action potential duration shortened, Ca i transient duration was prolonged, and local conduction velocity (CV) slowed progressively, with loss of excitability after 10.6Ϯ3.6 minutes. CV slowing was accompanied by connexin-43 dephosphorylation. During ischemia, spontaneous reentry occurred in 5 of 11 monolayers, initiated by extrasystoles arising from the border zone or unidirectional conduction block of paced beats. On reperfusion, excitability recovered within 1.0Ϯ0.8 minutes, but CV remained depressed for 9.0Ϯ3.0 minutes, promoting reentry in the reperfused zone. As connexin-43 phosphorylation recovered in the reperfused zone, CV normalized, and arrhythmias resolved. Conclusions-Acute regional ischemia/reperfusion in neonatal rat ventricular myocyte monolayers recapitulates electrophysiological alterations and arrhythmias similar to those observed during acute coronary occlusion/reperfusion in intact hearts. During early reperfusion, slow recovery from connexin-43 dephosphorylation leads to persistent CV slowing, creating a highly arrhythmogenic substrate.

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Section: Discussionsupporting

confidence: 55%

Electrophysiological Consequences of Acute Regional Ischemia/Reperfusion in Neonatal Rat Ventricular Myocyte Monolayers

et al. 2008

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“…A common mechanism may be responsible for VF initiation in the two settings, as indicated by previous studies in ischemia [27][28][29] and resistive-heating [13] models. Within seconds of coronary occlusion, ischemia results in marked changes in the resting membrane potential, producing ionic current flow [27]; thus, phase IA VT/VF is triggered by focal mechanisms arising from numerous areas [27][28][29], mainly at the normal side of the ischemic border [27]. Similarly, abnormal automaticity was previously recorded at temperatures > 45.0°C in excised guinea-pig right ventricular papillary muscle in vitro [13].…”

Section: Phase I Ventricular Arrhythmogenesismentioning

confidence: 88%

“…Previous studies have indicated that VT/VF during phase IA is maintained by rotating spiral waves in both ischemic and normal myocardium [35], but their relative importance remains unclear; VF was initially thought to perpetuate by macro-and micro-reentry circuits arising mainly in the ischemic zone [27], but this view was challenged by findings of decreased wave break [36], suggesting that this area does not actively participate in VF maintenance [28]. Our results can be viewed as supportive of the latter notion, as arrhythmogenesis was enhanced in the presence of myocardium (of similar size to that produced after ischemia) with homogenously irreversible loss of cellular excitability [13] that is unlikely to participate in VF maintenance.…”

Section: Insights On the Pathophysiology Of Ischemia-related Arrhythmiasmentioning

confidence: 98%

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

Kolettis¹,

Kontonika²,

Valenti³

et al. 2013

Journal of Basic and Clinical Physiology and Pharmacology

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“…Rankovic et al 10 Zaitsev et al 11 Liu et al 6 reflexes and is not subject to stretch because it has been paralyzed with an electromechanical uncoupler, it is not obvious why the activation rate is increased and the APD restitution curve slope is increased more than a short distance past the boundary of the ischemic region, beyond where the nonischemic myocardium is subject to electrotonic influences from the ischemic zone. One possibility mentioned in the Discussion section of the article is that, because the perfusate is recirculated, substances released from the acutely ischemic region may have altered the activation rate in the nonischemic myocardium.…”

Section: Comparison Of Three Studies On the Effects Of Acute Ischemiamentioning

confidence: 99%

“…9 Although it should be possible to analyze optical mapping results for this behavior, no study has yet reported attempts to do so.A third issue is that several of the study findings differ from findings in other studies in which activation mapping was performed during VF in the presence of acute regional ischemia. 10,11 The important similarities and differences among those two studies and the study by Liu et al are listed in the Table 1. Although all three studies found that the activation rate, obtained either by direct identification of individual activation times 10 or by estimation from the peak in the power spectrum, 6,11 was decreased in the ischemic zone, the activation rate in the nonischemic zone was unchanged after induction of ischemia in the studies by Rankovic et al and Zaitsev et al but was increased in the study by Liu et al Because the isolated heart is dissociated from autonomic…”

mentioning

confidence: 94%

Types of Ventricular Fibrillation:

Ideker

Rogers

Huang³

2004

Cardiovasc electrophysiol

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Editorial CommentVentricular fibrillation (VF) has been considered to be caused by totally disorganized electrical activity, 1 but evidence accumulating for over half a century suggests different degrees and types of organization exist during VF. As VF continues, it progresses through different stages. Wiggers divided this time course into four stages based on high-speed cinematography 1,2 while Huang et al. divided it into five stages based on electrical activation mapping. 3 In addition to changes in VF over time, the Cedar Sinai-UCLA group has reported two distinct types of VF. [4][5][6] In type I VF, the activation rate is rapid, reentry is uncommon and short lived, and activation wavefronts follow constantly changing pathways with little repetition. Although the conduction velocity (CV) restitution curve is flat and the action potential duration (APD) restitution curve determined by pacing is steep, the authors believe this steep APD restitution curve is responsible for conduction block during type I VF. In type II VF, the activation rate is slower and many of the activation fronts are large and follow similar pathways. Whereas the APD restitution slope is flat, excitability is reduced and the CV restitution curve is broad. The authors believe this broad CV restitution is responsible for conduction block in type II VF.The same authors state that type I VF is consistent with VF Maintenance by wandering wavelets, whereas type II VF is consistent with VF maintenance by a mother rotor. 5 They also reported that the two types of VF can occur at different times in the same heart, either through reducing excitability by giving a high dose of the drug D600, which causes type II VF in a heart that exhibited type I VF before the drug, 4 or through changes in VF over time with the first two of Wiggers' stages representing type I VF and the later stages type II VF. 5 In this issue of the Journal, the same group reports that both types of VF can coexist simultaneously in different regions of the same heart. 6 They performed optical mapping in isolated, perfused rabbit hearts in which a region of ischemia was created by coronary occlusion. The ischemic zone was identified by shortening of the APD, whereas the APD was normal or lengthened in the nonischemic zone. These investigators found that type I VF was present in the nonischemic zone, whereas type II VF was present simultaneously in the ischemic zone. They reported that, after occlusion, the slope of the APD restitution curve decreased in the ischemic region consistent with type II VF, whereas the slope increased in the nonischemic region, consistent with type I VF. They also found that the incidence of conduction block was increased in all portions of the mapped myocardium after occlusion, i.e., in the ischemic zone, in the nonischemic zone, and in the border zone encompassing the boundary between these two zones. Based on these findings, the authors concluded that changes in both the ischemic and the nonischemic zones are proarrhythmic and that these two zones play ...

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Characteristics of Ischemic and Peri‐Ischemic Regions During Ventricular Fibrillation in the Canine Heart

Cited by 11 publications

References 22 publications

Electrophysiological Consequences of Acute Regional Ischemia/Reperfusion in Neonatal Rat Ventricular Myocyte Monolayers

Electrophysiological Consequences of Acute Regional Ischemia/Reperfusion in Neonatal Rat Ventricular Myocyte Monolayers

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

Types of Ventricular Fibrillation:

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