Characteristics and possible mechanism of ventricular arrhythmia dependent on the dispersion of action potential durations.

Abstract

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...

Arrhythmogenic cardiomyopathy of the right ventricle. Predictive value of QT interval dispersion to assess arrhythmogenic risk and sudden death

“…In the '60s, Han and Moe 17 pointed out that the nonuniform recovery of the myocardial excitability represented an important factor triggering ventricular tachyarrhythmias, leaving the ventricles more vulnerable to ventricular fibrillation. These findings were later confirmed by other authors, such as Vassalo et al 18 , who analyzed the nonuniform recovery of left ventricular excitability, and Kuo et al 19 , who assessed the mechanisms involved in the genesis of ventricular arrhythmias related to dispersion of ventricular repolarization. Hii et al 20 pointed out that the degree of dispersion of ventricular repolarization in precordial leads represents an important marker for the development of torsades de pointes in patients using drugs of the IA group, being also a relevant factor in acute myocardial infarction.…”

Effects of bepridil on ventricular depolarization and repolarization of rabbit isolated hearts with particular reference to its possible proarrhythmic properties

“…Allessie et al (1976) demonstrated in their experiments, using rabbit isolated atria, that a certain degree of dispersion of repolarization is required to induce circus movement tachycardia by premature stimuli. Also, Kuo et al (1983) showed in dog hearts that a critical level of dispersion in ventricular repolarization is necessary for the induction of arrhythmia by premature stimuli. The present results suggest that the critical level of dispersion in ventricular repolarization can be attained at high bepridil concentrations through a combination of regionally different APD prolongation and conduction delay.…”

Determination of Human Ventricular Repolarization by Noncontact Mapping

“…Substantial experimental evidence supports its role in the initiation and maintenance of reentrant ventricular arrhythmias. [1][2][3] Monophasic action potential (MAP) catheters may be used to directly measure endocardial repolarization in a variety of disease states. 4 -7 Although it is possible to determine global endocardial repolarization patterns with electroanatomic mapping, 8,9 contact measurement is still limited by the small area of coverage, need for sequential measurements, and technical requirement for good myocardial contact.…”