Does increased dispersion of repolarization facilitate the induction of ventricular arrhythmia in an open-chest dog model?
23 open-chest dogs
Increased dispersion of repolarization induced by generalized hypothermia (29 degrees C) and regional warm blood (38-43 degrees C) perfusion through a coronary artery branch, with programmed ventricular premature stimulation (VPS)
Baseline state (before hypothermia/warm blood perfusion) and comparison between stimulation sites (region with short vs long monophasic action potentials)
Induction of ventricular arrhythmiasurrogate
Large dispersion of repolarization facilitates the development of a conduction delay necessary to induce sustained ventricular arrhythmia by an early premature stimulus applied at the site with a short action potential.
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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C S Kuo
Rutgers, The State University of New Jersey
Kazuo Munakata
Tsurumi University
C.A. Reddy
Cleveland Clinic
Circulation
Dr. Reddy's Laboratories (United States)
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Kuo et al. (Wed,) studied this question.
synapsesocial.com/papers/69f14b962811130d0cde222f — DOI: https://doi.org/10.1161/01.cir.67.6.1356