Functional transverse interconnections within the His bundle and the bundle branches.
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Biomedical subjects
Publications and source records attributed to R Lazzara.
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The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)
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The long-term intracoronary infusion of ethanol was used to evaluate the potential of ethanol to produce myocardial injury and cardiac rhythm disturbances. In 22 dogs, electrophysiologic testing was performed 48 hr after cessation of alcohol administration. Multiple premature ventricular beats occurred spontaneously in 3 dogs with spontaneous sustained monomorphic ventricular tachycardia observed in 1 dog. Provocative ventricular pacing produced ventricular tachycardia lasting 20 or more beats in 13 animals with sustained tachycardia observed in 3 animals. Provocative ventricular pacing in the presence of lidocaine or epinephrine produced sustained ventricular tachycardia in an additional 4 dogs. The electrophysiologic properties of Purkinje fibers from the zone receiving ethanol were altered when compared to the control zone. The resting membrane potential was decreased (-76 +/- 2 mV vs. -85 +/- mV, p less than 0.001) with a decrease in action potential amplitude (91 +/- 4 vs. 109 +/- 2 mV, p less than 0.001) and phase 0 upstroke (231 +/- 27 vs. 456 +/- 25 V/sec, p less than 0.02). Prolonged refractoriness was observed in the ethanol zone without a prolongation of action potential duration. Intramural lesions observed within the left circumflex distribution varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The data suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histologic and electrophysiologic injury in the canine heart. The electrophysiologic ch changes provide a substrate sufficient for the induction and maintenance of ventricular arrhythmia.
The Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial was completed in 1992 and the primary results were reported in 1993. Since then, considerable discussion about this trial has taken place and new trial results have been reported. Trial analysis has yielded seven principal findings to date concerning treatment of patients with ventricular tachyarrhythmias, ie: (1) similar accuracy of electrophysiologic study (EPS), Holter monitoring (HM), and EPS combined with HM for predicting antiarrhythmic drug efficacy; (2) greater efficiency and lower cost of HM; (3) improved survival associated with predicted drug efficacy; (4) predictors of response to EPS and HM; (5) greater efficacy and lower cost of therapy with sotalol compared with drugs with class-l effects; (6) lack of a relationship between presenting and recurring arrhythmia; and (7) preponderance of nonarrhythmic deaths in trial participants. A number of additional specific findings of the trial are reviewed in this symposium. Several criticisms of the trial's enrollment, methods, and efficacy criteria are reviewed and discussed. Some criticisms are valid. Many are related to misunderstandings of ESVEM trial methodology and to bias of the individual critics. Some are simply incorrect. The importance of the ESVEM trial in the present day may be limited by the growing use of implanted devices rather than drugs for treatment of ventricular tachyarrhythmias. If clinical trials ultimately prove devices to be no more effective than drugs, the findings of the ESVEM investigators will grow in importance.
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