SUMMARY 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°C) and regional warm blood (38430C) perfusion through a coronary artery branch. Hypothermia and regional warm blood perfusion increased maximum dispersion from 13 + 10 to 111 ± 16 msec (p < 0.001), predominantly because of the increased MAP duration difference (10 15 vs 97 ± 16 msec, p < 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 < 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/mm 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 < 0.05). In six dogs, we compared the stimulation sitedependent 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.STRONG experimental evidence links the vulnerability of ventricular myocardium to arrhythmia with increased temporal dispersion of refractoriness. '-5 Conversely, it is believed that one of the beneficial effects of antiarrhythmic drugs relates to their ability to decrease dispersion. ed predominantly from differences in MAP duration. MethodsWe studied 23 mongrel dogs that weighed 19.1-32.7 kg and were anesthetized with i.v. sodium pentobarbital, 30 mg/kg. The chest was opened by a midsternal incision, and the dogs were ventilated with a Harvard respirator. The heart was suspended in a pericardial cradle. The sinus node was crushed and a bipolar Grass E2B platinum electrode was attached to the right atrial appendage for pacing at 100-1 58 beats/min (mean 119 + 13 beats/min). In 13 dogs, the pacing rate was maintained constant throughout the entire experiment at an average of 116 ± 10 beats/min (range 100-140 beats/min), and in 10 dogs the pacing rate during hypothermia (see below) was slower than control, averaging 113 ± 7 beats/min (range 100-120 beats/min).Six suction electrodes were applied to record MAPs using the technique described prev...

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The sources of error in determination of the beginning of QRS and the end of T during measurement of the Q-T duration are analyzed. An important error is confusion of an elevated U wave with the T wave, resulting in the diagnosis of a prolonged Q-T. In such cases, some of the precordial leads usually show a notch or kink between T and U which indicates approximately the end of T. If these criteria are used, the true corrected Q-T duration in hypopotassemia without hypocalcemia is not prolonged, but normal or shortened, corresponding to an earlier appearance of the second heart sound.

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Electrical restitution of action potential duration (APD) was determined in Purkinje (n = 8) and ventricular muscle (n = 6) fibers at two different basic cycle lengths (BCL, 1,500 and 500 ms). Restitution curves, normalized for the longest APD (the plateau of restitution), fitted the sum of a fast (T1) and a slow (T2) exponential component. The T1 was shorter in ventricular muscle than Purkinje fibers (89 +/- 5 and 143 +/- 9; mean +/- SE, P less than 0.05), whereas the T2 did not differ (1,448 +/- 231 and 1,439 +/- 211). The BCL altered the APD value during the plateau of restitution but did not change the two exponential components. In both fiber types, the relation between APD and BCL during steady state fitted a hyperbolic curve that predicts the achievement of the maximum APD at long BCL. The restitution curves crossed the steady-state curve at two points outlining three different zones of APD intervals: early premature, late premature, and postmature. The APD during restitution was longer than the steady state in the late premature zone and shorter than the steady-state APD in the post-mature and early premature zones. The APD per se, independent of BCL, did not influence the kinetics of restitution in Purkinje fibers.