Dispersion of ventricular repolarization and arrhythmia: Study of two consecutive ventricular premature complexes

The effect of two consecutive ventricular premature stimuli (S₁S₂) during atrial pacing on dispersion of repolarization and inducibility of ventricular arrhythmias was studied in 16 dogs under control conditions and in four dogs in the presence of an increased dispersion of repolarization during atrial pacing induced by general hypothermia and regional warm blood perfusion via selective cannulation of the distal branch of left anterior decending coronary artery. Dispersion of repolarization was measured as the maximal difference between the ends of six simultaneously recorded monophasic action potentials (MAPs) from anterior ventricular surface, and consisted of MAP duration difference and activation time difference. Dispersion of repolarization during atrial pacing at control was 29 ± 7 msec (activation time difference 4 ± 6 msec, MAP duration difference 25 ± 8 msec), that after S₁ at paraseptal the site was 81 ± 8 msec (activation time difference 73 ± 12 msec, MAP duration difference 8 ± 5 msec), and that after S₁S₂ was 148 ± 27 msec (activation time difference 103 ± 21, MAP duration difference 44 ± 26 msec). Neither S₁ nor S₁S₂ induced ventricular arrhythmia. Hypothermia and regional warm blood reperfusion increased dispersion of repolarization during atrial pacing to 70 ± 22 msec (activation time difference 9 ± 3 msec, MAP duration difference 61 ± 19 msec). During hypothermia and regional warm blood reperfusion, S₁ produced a dispersion of repolarization of 149 ± 29 msec (activation time difference 85 ± 8 msec, MAP duration difference 64 ± 23 msec) and did not induce ventricular arrhythmia. However, S₁S₂ at the paraseptal site induced ventricular fibrillation in all four dogs. At the time of induction of fibrillation, the S₂-induced activation time difference increased while the MAP duration difference decreased. Our results show the following: (1) S₁S₂ of 2 msec duration and up to 10 times diastolic threshold strength does not induce ventricular arrhythmia in normal myocardium, but does induce arrhythmia in the presence of increased dispersion of repolarization during atrial pacing; (2) S₁ does not induce ventricular arrhythmia but facilitates induction of arrhythmia by S₂ by increasing activation time difference distal to the stimulation site; (3) Increased MAP duration difference facilitates induction of ventricular arrhythmia by increasing activation time difference, but is no longer essential in perpetuation of ventricular arrhythmia after the onset of arrhythmia. Our results imply that S₁S₂, i.e., an equivalent of a ventricular couplet, does not create sufficient MAP duration difference and activation time difference for induction of ventricular arrhythmia in normal ventricular myocardium.