Mechanism of ventricular arrhythmias caused by increased dispersion of repolarization

To explain the mechanism of arrhythmias dependent predominantly on increased dispersion of repolarization, we created a model in which increased dispersion was induced by means of generalized hypothermia (29° C) and regional warm blood (38-43°C) perfusion (RWBP) via a coronary artery branch. In 23 open-chest dogs, hypothermia plus RWBP increased maximum dispersion of repolarization from 13 ± 10 to 111 ± 16 ms (P < 0.001) due predominantly to the increased monophasic action potential duration (MAP) difference of six simultaneously recorded MAP's from the ventricular surface, from 10 ± 15 to 97 ± 16 ms (P < 0.001). The maximal difference between activation times was not significantly changed while QRS duration increased from 47 ± 6 to 52 ± 7 ms (P < 0.01). Ventricular arrhythmia (VA) did not occur spontaneously but was induced by a single ventricular premature stimulus (VPS) in all 23 dogs during hypothermia plus RWBP when dispersion reached a critical magnitude. The requirement of this critical magnitude of dispersion for the induction of VA was documented in 16 dogs by means of stepwise increments or decrements of dispersion. In four dogs an increase in atrial pacing rate by 24 beats/min^-1 prevented induction of VA by decreasing dispersion from a critical magnitude of 103 ± 5 ms to a nonarrhythmogenic value of 86 ± 9 ms (P < 0.05). In six dogs, we compared the stimulation-site dependent effects of VPS applied in the region with short and long MAPD. In all dogs VA was inducible only by VPS from the region with short MAPD. Premature impulses from this region propagated slower than those from the region with long MAPD. Our results show that the large dispersion of repolarization creates an environment which facilitates the development of a conduction delay necessary for the induction of sustained arrhythmia by an early premature stimulus applied at the site with a short MAPD.