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S M Dillon

Publications and source records attributed to S M Dillon.

28 records · Page 2Linked to original sources
PubMed1993

Reentrant circuits and the effects of heptanol in a rabbit model of infarction with a uniform anisotropic epicardial border zone.

INTRODUCTION: The purpose was to study reentry in a rabbit model of infarction. METHODS AND RESULTS: A model of an infarct epicardial border zone was produced in Langendorff perfused rabbit hearts by freezing the inner two thirds of the left ventricular wall, allowing only a thin epicardial muscle layer to survive. Reentrant circuits causing stable ventricular tachycardia occurred in the surviving rim of epicardial muscle as shown by mapping impulse propagation with a 196-electrode array. The circuits were functional, and reentry did not occur around an anatomical obstacle. Slow conduction in the circuits was caused by the anisotropic properties of the epicardial muscle. Activation in the circuits was slow transverse to the long axis of the fiber bundles and rapid parallel to the long axis. Other features of the circuits, including orientation of the central functional line of block parallel to the fiber long axis, and an oval shape are also characteristic of anisotropic reentry. Since the slow conduction causing reentry is a result of poor transverse intercellular coupling, we determined whether the "uncoupler" heptanol would cause block in the circuits and terminate tachycardia. Heptanol in concentrations up to 1.2 mM slowed conduction in the transverse and longitudinal directions in the circuits and sometimes extended the central line of functional block. It did not, however, stop reentry because the reentrant impulse was still able to conduct around the ends of the block line. CONCLUSION: Drugs that decrease intercellular coupling may not be effective antiarrhythmic agents when uniform anisotropy causes functional reentry.

Alcohols↗
PubMed1993

Effects of overdrive stimulation on functional reentrant circuits causing ventricular tachycardia in the canine heart: mechanisms for resumption or alteration of tachycardia.

INTRODUCTION: The purpose of the experiments described in this article was to investigate the effects of overdrive stimulation on functional anisotropic reentrant circuits causing ventricular tachycardia in infarcted canine ventricles. We determined how overdrive stimuli affect reentrant circuits to alter characteristics of the tachycardia. METHODS AND RESULTS: Activation patterns were determined by mapping excitation with a 192 bipolar electrode array. We found that overdrive stimuli could activate the circuits with the same pattern as the reentrant wavefront and that after overdrive stopped either the last or the next to last stimulated wavefront continued propagating through the circuit as a new reentrant impulse and tachycardia continued. When the circuit was not altered after overdrive, the exit route that the stimulated wavefront took from the circuit to activate the rest of the ventricles was also not altered and the tachycardia after overdrive had the same cycle length and QRS morphology as prior to overdrive. In some experiments, however, the overdrive stimuli did not follow the original reentrant pathway but led to the formation of a different circuit with a different exit route to the ventricles. As a result, after overdrive stimulation tachycardia had a different QRS morphology and cycle length than prior to stimulation. When the new circuit after overdrive was small and the revolution time of the reentrant impulse around the circuit was short, fibrillation occurred. CONCLUSION: Functional reentrant circuits can either be maintained or altered after a period of overdrive stimulation. The results explain many of the effects that have been seen during overdrive stimulation of clinical ventricular tachycardia.

Animals↗
PubMed1993

Overdrive stimulation of functional reentrant circuits causing ventricular tachycardia in the infarcted canine heart. Resetting and entrainment.

BACKGROUND: Clinical electrophysiology studies have used, for the most part, models of anatomic reentrant circuits to explain entrainment of ventricular tachycardia. Our studies use activation maps to directly determine mechanisms of entrainment of functional circuits that cause tachycardia. METHODS AND RESULTS: Electrograms were recorded from 192 sites on reentrant circuits in the epicardial border zone of canine myocardial infarcts during sustained ventricular tachycardia. Overdrive stimulation from different sites and at different cycle lengths was investigated. The reentrant circuits were shown to be functional, yet stimulated impulses could enter and repetitively reset the circuits (entrainment), demonstrating the presence of an excitable gap. Entrainment could occur from different stimulation sites with the stimulated impulses from each site activating the circuit with a different pattern. Entrainment, however, did not occur when the stimulated wave fronts obliterated the lines of functional block in the circuit. Fusion on the ECG occurred during entrainment when the stimulated impulses activated the ventricles concurrently with a previous stimulated impulse leaving the reentrant circuit at a different site. The first postpacing QRS was captured but not fused because it was caused by the last stimulated impulse emerging from the circuit. The first postpacing cycle length on the ECG was either equal to or longer than the overdrive cycle length depending on whether there was a fusion QRS during overdrive. The first postpacing cycle length at sites in the reentrant circuit equaled the pacing cycle length. At an appropriately short overdrive cycle length, stimulated impulses blocked in the circuit to terminate reentry. CONCLUSIONS: Functional reentrant circuits causing ventricular tachycardia can be reset and entrained. Activation maps directly show the mechanisms.

Animals↗
PubMed1992

Synchronized repolarization after defibrillation shocks. A possible component of the defibrillation process demonstrated by optical recordings in rabbit heart.

BACKGROUND: It is currently believed that defibrillation shocks act primarily by stimulating excitable myocardium to abolish wave fronts. Recent studies have shown that shocks applied during pacing not only stimulate excitable myocardium but also prolong the depolarization and refractoriness of myocardium already in a depolarized state. This study investigates the effects of shocks on fibrillation action potentials. METHODS AND RESULTS: Recordings of membrane action potentials free of shock artifact were obtained using the voltage-sensitive dye WW781 during defibrillation of isolated rabbit hearts. These records showed that the shocks caused an additional phase of depolarization beginning with an initial rapid depolarization of the optical signal followed by a slow phase of repolarization. This occurred throughout all phases of the fibrillation action potential from just after completion of the upstroke to a time of near maximal repolarization. Defibrillation shocks, however, had the additional effect of causing the myocardium to repolarize at a constant time after the shock regardless of its prior electrical activity--the constant repolarization time response. This effect was not dependent on the presence of D600 (methoxyverapamil) or continuous coronary perfusion. It was accompanied by a similar constancy in the return of myocardial excitability. Recordings taken from multiple adjacent recording sites also showed a constant repolarization time among them. CONCLUSIONS: A simple model of reentry is used to illustrate how the constant repolarization response, in addition to wave front termination and refractoriness extension, could play a role in the successful termination of fibrillation by electrical shock.

Animals↗
PubMed1991

Optical recordings in the rabbit heart show that defibrillation strength shocks prolong the duration of depolarization and the refractory period.

The present data were obtained using the technique of optical recording with the voltage-sensitive dye WW781. This technique, unlike electrical methods, was able to provide uninterrupted recordings free of artifacts during defibrillation shocks. Optical recordings were made from sites on the ventricular epicardium of perfused rabbit hearts during electrical pacing. Continuous recordings of the electrophysiological responses of an intact heart to defibrillation threshold-strength shocks were made. It was shown that these shocks were able to stimulate normal-appearing action potentials in nonrefractory myocardium. A new and unexpected finding was that defibrillation threshold-strength shocks were also able to evoke a sustained, depolarizing response from myocardium already undergoing an action potential. This prolonged the time that the myocardium remained in the depolarized state. Prolongation of the depolarized state was accompanied by an equal prolongation of the refractory period. There was no indication that this depolarizing shock response was due to damage of the myocardium by the shock, to heterogeneous electrical responses in the optical recording area, or to the methods used in this study. It is hypothesized that these shocks were able to elicit a new action potential in already depolarized myocardium by hyperpolarizing portions of the myocardium's cellular membranes and, in so doing, to reactivate the fast sodium current. This effect, if prevalent in a fibrillating ventricle, could play a role in the defribillation process by effectively resynchronizing electrical activity.

Action Potentials↗
PubMed1988

Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts.

Excitation in the epicardial border zone of 3-5-day-old canine infarcts was mapped with an array of 192 bipolar electrodes during sustained ventricular tachycardia. Reentrant circuits were found in which activation occurred around long lines of apparent conduction block based on the criterion that excitation on opposite sides of the lines occurred with marked disparity in time. When the lines of apparent block were functional (i.e., occurred only during tachycardia and not during sinus rhythm or ventricular pacing) they were oriented parallel to the long axis of epicardial muscle fiber bundles. Isochrones distal to the lines were oriented parallel to them because widely separate sites within these isochrones were activated nearly simultaneously. This suggested that excitation not only occurred around the lines of block but also slowly across them. This slow activation occurred transverse to the long axis of the myocardial fibers and therefore might result because of the anisotropic tissue properties. To test this hypothesis, the epicardial border zone was stimulated during sinus rhythm through electrodes around its margin and at the center of the recording array. Activation transverse to the myocardial fibers in regions where lines of block occurred during tachycardia was slow, whereas it was rapid parallel to fibers' orientation. During tachycardia electrograms along the lines of apparent block had long durations and were fractionated, a characteristic that can also result from activation transverse to the myocardial fiber long axis. Therefore, we propose that the parallel orientation of the muscle bundles in the epicardial border zone is an important cause of ventricular tachycardia because activation transverse to myocardial fibers is sufficiently slow to permit the occurrence of reentry.

Animals↗