Literature DB >> 6851031

Characteristics and possible mechanism of ventricular arrhythmia dependent on the dispersion of action potential durations.

C S Kuo, K Munakata, C P Reddy, B Surawicz.   

Abstract

The arrhythmogenic role of increased dispersion of repolarization (dispersion) was studied in 23 open-chest dogs using six simultaneously recorded monophasic action potentials (MAPs) from the ventricular surface and programmed ventricular premature stimulation (VPS). Increased dispersion was induced by generalized hypothermia (29 degrees C) and regional warm blood (38-43 degrees C) perfusion through a coronary artery branch. Hypothermia and regional warm blood perfusion increased maximum dispersion from 13 +/- 10 to 111 +/- 16 msec (p less than 0.001), predominantly because of the increased MAP duration difference (10 +/- 15 vs 97 +/- 16 msec, p less than 0.001). The maximal difference between activation times was not significantly changed, but the QRS duration increased from 47 +/- 6 to 52 +/- 7 msec (p less than 0.01). Ventricular arrhythmia did not occur spontaneously but was induced by a single VPS in all 23 dogs during hypothermia and regional warm blood perfusion when dispersion reached a critical magnitude. The critical magnitude of dispersion required to induce ventricular arrhythmia was documented in 16 dogs by stepwise increments or decrements of dispersion. In four dogs, an increase in atrial pacing rate of 24 beats/min prevented induction of ventricular arrhythmia by decreasing dispersion from a critical magnitude of 103 +/- 5 msec to a nonarrhythmogenic value of 86 +/- 9 msec (p less than 0.05). In six dogs, we compared the stimulation site-dependent effects of VPS applied in the region with short and long MAPs. In all dogs, ventricular arrhythmia was inducible only by VPS from the region with a short MAP. Premature impulses from this region propagated more slowly than those from the region with a long MAP. Our results show that the large dispersion of repolarization facilitates the development of a conduction delay necessary to induce sustained arrhythmia by an early premature stimulus applied at the site with a short MAP.

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Year:  1983        PMID: 6851031     DOI: 10.1161/01.cir.67.6.1356

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  126 in total

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6.  A computer model study of the ventricular fibrillation vulnerable window: sensitivity to regional conduction depressions.

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Journal:  Ann Biomed Eng       Date:  1994 Nov-Dec       Impact factor: 3.934

7.  Electrocardiological profile and proarrhythmic effects of quinidine, verapamil and their combination: a mapping study.

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8.  Improving sudden cardiac death risk stratification by evaluating electrocardiographic measures of global electrical heterogeneity and clinical outcomes among patients with implantable cardioverter-defibrillators: rationale and design for a retrospective, multicenter, cohort study.

Authors:  Jonathan W Waks; Christopher Hamilton; Saumya Das; Ashkan Ehdaie; Jessica Minnier; Sanjiv Narayan; Mark Niebauer; Merritt Raitt; Christine Tompkins; Niraj Varma; Sumeet Chugh; Larisa G Tereshchenko
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9.  Monophasic action potentials in a patient with multiform ventricular tachycardia without QT prolongation.

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Journal:  Br Heart J       Date:  1993-04

10.  Bifurcation theory and cardiac arrhythmias.

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Journal:  Am J Cardiovasc Dis       Date:  2013-02-17
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