C S Kuo

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.

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)

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.(ABSTRACT TRUNCATED AT 250 WORDS)

We studied dispersion of repolarisation and the components of dispersion during atrial pacing (AP), ventricular pacing (VP), and programmed ventricular premature stimulation (VPS) using six simultaneously recorded monophasic action potentials (MAP's) from ventricular surface in nine open-chest dogs. Varitions in MAP duration (MAPD) caused no changes in the configuration of strength-interval curves. During AP, maximum dispersion (MD) between any two of six sites averaged 32± 10 ms, consisting of 27 ± 10 ms MAPD and 4±9 ms activation time (AT) differences; during VP, MD averaged 77± 16 ms, consisting of 7± 15 ms MAPD and 70± 13 ms AT differences. Maximum dispersion in the earliest ventricular premature complexes (VPC) averaged 97 ± 16 ms: the difference between this value and the MD during VP was due to an increase in MAPD difference without significant change in AT difference. Dispersion during VPS exceeded dispersion during AP by 5 to 70 ms at 61 of 68 pairs of adjacent sites separated by 1.5 to 2.0 cm; the greatest increases were due to added contributions of MAPD and AT differences. Greatest dispersion between any two of six sites during VPS occurred in the early VPC, ie, at coupling intervals (CI) ≤30 ms following effective refractory period (ERP), but at the adjacent sites the timing of greatest dispersion during VPS varied, occurring at about one half of the sites at CI within 40 to 220 ms following ERP. Our results show that the MD during AP is due predominantly to MAPD difference, during VP predominantly to AT difference, and that prematurity increases the contribution of MAPD differences to dispersion from an average of 9% during VP to an average of 25%. No spontaneous repetitive activity occurred during VPS on the surface of the left ventricle using 2 ms stimuli of strength up to 40 mA.