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 degrees C) and regional warm blood (38-43 degrees 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 less than 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 less than 0.001). The maximal difference between activation times was not significantly changed while QRS duration increased from 47 +/- 6 to 52 +/- 7 ms (P less than 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 less than 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.(ABSTRACT TRUNCATED AT 250 WORDS)