The Role of the Purkinje System in Defibrillation

Role of His-Purkinje System in the Initiation of Orthodromic Tachycardia in Wolff-Parkinson-White Syndrome

Cardiac Preexcitation Syndromes ◽

10.1007/978-1-4684-7526-5_7 ◽

1986 ◽

pp. 141-150

Author(s):

Masood Akhtar ◽

Michael H. Lehmann ◽

Stephen Denker ◽

Rehan Mahmud

Keyword(s):

White Syndrome ◽

Purkinje System ◽

Wolff Parkinson White Syndrome

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Role of Purkinje system in cardiac arrhythmias

2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society ◽

10.1109/iembs.2008.4649112 ◽

2008 ◽

Author(s):

Makarand Deo ◽

Patrick Boyle ◽

Gernot Plank ◽

Edward Vigmond

Keyword(s):

Cardiac Arrhythmias ◽

Purkinje System

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Purkinje involvement in arrhythmias after coronary artery reperfusion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00227.2001 ◽

2002 ◽

Vol 282 (4) ◽

pp. H1189-H1196 ◽

Cited By ~ 16

Author(s):

David O. Arnar ◽

James B. Martins

Keyword(s):

Ventricular Tachycardia ◽

Coronary Artery ◽

Ventricular Fibrillation ◽

Cycle Length ◽

Ischemic Myocardium ◽

Risk Zone ◽

Purkinje System ◽

Mean Cycle

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 ± 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.

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Role of the His-Purkinje system in the genesis of cardiac arrhythmia

Heart Rhythm ◽

10.1016/j.hrthm.2009.03.011 ◽

2009 ◽

Vol 6 (7) ◽

pp. 1050-1058 ◽

Cited By ~ 60

Author(s):

Melvin M. Scheinman

Keyword(s):

Cardiac Arrhythmia ◽

Purkinje System

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Role of the Purkinje System in Spontaneous Ventricular Tachycardia During Acute Ischemia in a Canine Model

Circulation ◽

10.1161/01.cir.96.7.2421 ◽

1997 ◽

Vol 96 (7) ◽

pp. 2421-2429 ◽

Cited By ~ 58

Author(s):

David O. Arnar ◽

John R. Bullinga ◽

James B. Martins

Keyword(s):

Ventricular Tachycardia ◽

Canine Model ◽

Acute Ischemia ◽

Purkinje System

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Arrhythmogenesis by single ectopic beats originating in the Purkinje system

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01237.2009 ◽

2010 ◽

Vol 299 (4) ◽

pp. H1002-H1011 ◽

Cited By ~ 35

Author(s):

Makarand Deo ◽

Patrick M. Boyle ◽

Albert M. Kim ◽

Edward J. Vigmond

Keyword(s):

Ventricular Myocytes ◽

Conduction System ◽

Cardiac Conduction ◽

Ectopic Beat ◽

Tissue Conductivity ◽

Purkinje System ◽

Ectopic Beats ◽

Reentrant Arrhythmia ◽

Underlying Mechanisms

Cells in the Purkinje system (PS) are known to be more vulnerable than ventricular myocytes to secondary excitations during the action potential (AP) plateau or repolarization phases, known as early afterdepolarizations (EADs). Since myocytes have a lower intrinsic AP duration than the PS cells to which they are coupled, EADs occurring in distal branches of the PS are more likely to result in propagating ectopic beats. In this study, we use a computer model of the rabbit ventricles and PS to investigate the consequences of EADs occurring at different times and places in the cardiac conduction system. We quantify the role of tissue conductivity and excitability, as well as interaction with sinus excitation, in determining whether an EAD-induced ectopic beat will establish reentrant activity. We demonstrate how a single ectopic beat arising from an EAD in the distal PS can give rise to reentrant arrhythmia; in contrast, EADs in the proximal PS were unable to initiate reentry. Clinical studies have established the PS as a potential substrate for reentry, but the underlying mechanisms of these types of disorder are not well understood, nor are conditions leading to their development clearly defined; this work provides new insights into the role of the PS in such circumstances. Our findings indicate that simulated EADs in the distal PS can induce premature beats, which can lead to the tachycardias involving the conduction system due to interactions with sinus activity or impaired myocardial conduction velocity.

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