The transition to ventricular fibrillation induced by reperfusion after acute ischemia in the dog: a period of organized epicardial activation.

Ideker, Raymond E.; Klein, George J.; Harrison, Lura; Smith, William M.; Kasell, J; Reimer, Keith A.; Wallace, Andrew G.; Gallagher, J J

doi:10.1161/01.cir.63.6.1371

Cited by 117 publications

(35 citation statements)

References 32 publications

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“…Previously, Janse et al (6) have shown that, whereas complete and incomplete reentrant waveforms were seen during transition of reperfusion VT to VF, no evidence of reentry was seen during the initiation of VT in isolated canine and porcine hearts. Ideker et al (5) suggested that during transition of reperfusion VT to VF the complexes were initiated by a focal source in the ischemic border zone in the dog. These studies were somewhat limited in that the number of recording sites did not allow for exact delineation of the mechanism of the arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

Purkinje involvement in arrhythmias after coronary artery reperfusion

Arnar

Martins

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Previous studies have indicated that the endocardium may be responsible for a large portion of ventricular tachycardia (VT) seen with reperfusion of ischemic myocardium. To evaluate the role of the Purkinje system in nonreentrant VT arising from the endocardium after reperfusion, the anterior descending coronary artery was occluded for 20 min and then reperfused in 23 dogs after instrumentation of the risk zone with 21 multipolar plunge needles. VT with focal Purkinje origin was defined as a focal endocardial VT with Purkinje potentials recorded before the earliest endocardial myopotential. A total of 19 VTs (mean cycle length 214 Ϯ 2 ms) were observed with 11 (58%) having focal Purkinje origin. Fifty-eight percent of the VTs degenerated to ventricular fibrillation, with occurrences of two or more independent foci per complex (seen in 7 of 11 compared with 1 of 8 nonsustained VTs). In conclusion, these data show that Purkinje tissue may be important in the genesis of reperfusion VT. mapping; ventricles REPERFUSION OF ACUTELY ISCHEMIC myocardium can result in the development of ventricular tachycardia (VT) within seconds (7,10,17). This VT can degenerate rapidly to ventricular fibrillation (VF) and this may be more commonly associated with reperfusion than with coronary artery occlusion (16). There appears to be an important relationship between the time of ischemia and the development of reperfusion arrhythmia, with the incidence of VT being highest when the ischemia duration is ϳ20 min (8).Although evidence for slow conduction in the epicardium (3) indirectly suggests that conditions for reentry may be present during reperfusion, a study by Pogwizd and Corr (12), using a high-resolution mapping system, showed that nonreentrant mechanisms may account for the majority of reperfusion VT. In that study, nonreentrant mechanisms arising in the area of the endocardium were responsible for 75% of all reperfusion VT. Pogwizd and Corr, however, did not record signals from Purkinje tissue. It is unknown whether the Purkinje system contributes to genesis or maintenance of reperfusion VT. On the other hand, we (1) reported that Purkinje tissue may be important in the genesis of spontaneous VT when it occurs acutely after coronary artery occlusion. The goal of this study was to evaluate the contribution of the Purkinje system to the initiation and maintenance of early reperfusion VT, given the previous implications that the endocardium appears to be of significant importance in this type of VT. METHODSTwenty-three healthy adult mongrel dogs were used for this study. The protocol was approved by the University of Iowa Animal Use and Care committee and conforms to the position of the American Physiological Society on research animal use.Surgical preparation. Anesthesia was induced with the use of thiopental sodium (500 mg) and ␣-chloralose (100-200 mg/kg iv) as a bolus and maintained with a continuous intravenous infusion of ␣-chloralose dissolved in polyethylene glycol at 8 mg ⅐ kg Ϫ1 ⅐ h Ϫ1 . The animals were intubated and v...

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Section: Discussionmentioning

confidence: 99%

Purkinje involvement in arrhythmias after coronary artery reperfusion

Arnar

Martins

2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…It has indeed been found that in the initial phase of reperfusion-induced VF ͑i.e., when blood flow to an ischemic region is suddenly restored͒, the normal myocardium is rapidly excited by orderly wave fronts emerging from the reperfused myocardium. 32 In Fig. 2 epicardial activation maps of the first beats of VF, occurring spontaneously after 5 min of ischemia, are shown.…”

Section: Is the Purkinje System Necessary For The Transition Of Ventrmentioning

confidence: 99%

Vulnerability to ventricular fibrillation

Janse

1998

Chaos: An Interdisciplinary Journal of Nonlinear Science

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One of the factors that favors the development of ventricular fibrillation is an increase in the dispersion of refractoriness. Experiments will be described in which an increase in dispersion in the recovery of excitability was determined during brief episodes of enhanced sympathetic nerve activity, known to increase the risk of fibrillation. Whereas in the normal heart ventricular fibrillation can be induced by a strong electrical shock, a premature stimulus of moderate intensity only induces fibrillation in the presence of regional ischemia, which greatly increases the dispersion of refractoriness. One factor that is of importance for the transition of reentrant ventricular tachycardia to ventricular fibrillation during acute regional ischemia is the subendocardial Purkinje system. After selective destruction of the Purkinje network by lugol, reentrant tachycardias still develop in the ischemic region, but they do not degenerate into fibrillation. Finally, attempts were made to determine the minimal mass of thin ventricular myocardium required to sustain fibrillation induced by burst pacing. This was done by freezing of subendocardial and midmural layers. The rim of surviving epicardial muscle had to be larger than 20 g. Extracellular electrograms during fibrillation in both the intact and the ''frozen'' left ventricle were indistinguishable, but activation patterns were markedly different. In the intact ventricle epicardial activation was compatible with multiple wavelet reentry, in the ''frozen'' heart a single, or at most two wandering reentrant waves were seen. © 1998 American Institute of Physics. ͓S1054-1500͑98͒00201-8͔It has been known for a long time that the normal rhythmic activity of the heart can be upset by applying a single, strong electrical shock to the heart during a short part of the cardiac cycle, the so-called vulnerable period. The ensuing rhythm is called ventricular fibrillation, in which the different parts of the two main chambers of the heart "the ventricles… are rapidly and asynchronously activated so that a coordinated contraction of the heart no longer occurs. This is a lethal condition, unless another strong electrical shock causes this abnormal electrical activity to cease, allowing the normal pacemaker of the heart to resume control and to initiate the normal, regular heartbeat. In this paper the vulnerability to ventricular fibrillation is described in terms of the ''dispersion of refractoriness,'' indicating a time window during which some parts of the ventricles are inexcitable "refractory…, others partially excitable, and still others completely excitable. An electrical stimulus delivered during this time window will initially be unable to activate those parts that are inexcitable, but will cause a wave front of electrical activity that slowly travels around the area of inexcitable tissue, exciting it after a delay when excitability has returned, to finally reenter the site of origin. This so-called reentrant activity, which continues to reexcite tissue that just has recover...

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“…Experimental studies are generally restricted to mapping electrical activity on the ventricular surfaces [7,[10][11][12], and major advances have been achieved through the simultaneous mapping of endocardial and epicardial activity in a ventricular slice preparation [6] and the panoramic mapping of activity over the surface of the entire heart [13,14]. Theory, experiments and clinical studies all lead to a need to visualise, within the ventricular wall, the pattern of events occurring during VF.…”

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confidence: 99%

The Virtual Ventricular Wall: A Tool for Exploring Cardiac Propagation and Arrhythmogenesis

et al. 2006

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Methods for the experimental and clinical investigation of cardiac arrhythmias are limited to inferring propagation within the myocardium, from surface measurements, or from electrodes at a few sites within the cardiac wall. Biophysically and anatomically detailed computational models of cardiac tissues offer a powerful way for studying the electrical propagation processes and arrhythmias within the virtual heart. We use virtual tissues to study and visualise the effects of patho-and physiological conditions, and pharmacological interventions on transmural propagation in the virtual ventricular walls. Class III drug actions are quantitatively explained by changes induced in the transmural dispersion of action potential duration. We illustrate the automated construction of a virtual anisotropic ventricle from Diffusion Tensor MRI for individual hearts, and use it to explore mechanisms leading to ventricular fibrillation. The virtual ventricular wall provides an effective tool for exploring, evaluating and visualising processes during the initiation and maintenance of ventricular arrhythmias.

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The transition to ventricular fibrillation induced by reperfusion after acute ischemia in the dog: a period of organized epicardial activation.

Cited by 117 publications

References 32 publications

Purkinje involvement in arrhythmias after coronary artery reperfusion

Purkinje involvement in arrhythmias after coronary artery reperfusion

Vulnerability to ventricular fibrillation

The Virtual Ventricular Wall: A Tool for Exploring Cardiac Propagation and Arrhythmogenesis

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