Induction and termination of triggered activity by pacing in isolated canine Purkinje fibers.

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Premature escape beats induced in conscious dogs with chronic complete atrioventricular block have been defined as escape beats occurring on cessation of overdrive pacing and having a coupling interval to the last paced beat shorter than the coupling interval between the premature escape beat and the second postpacing beat. Triggered activity has been proposed as the primary underlying mechanism. We used standard microelectrode techniques to study the effects of overdrive pacing on normal automatic canine Purkinje fibers to determine if premature escape beats could be induced and if so, to define the underlying cellular mechanism(s). For this purpose, we overdrive-paced Purkinje fibers for 10 and 50 seconds and for 10 and 50 beats at a pacing cycle length (PCL) of 1,000-200 msec. In addition, to help distinguish among major arrhythmogenic mechanisms, we used a matrix of drugs consisting of propranolol, nadolol, lidocaine, ethmozin, and doxorubicin. Fifty-second stimulation trains induced "classic"1 overdrive suppression of the first three postpacing impulses, whereas 10-second overdrive pacing induced significant overdrive suppression only at a PCL of 200 msec. With 50-beat overdrive pacing and a PCL of 1,000-600 msec, there was overdrive suppression of postpacing impulses, whereas reduced overdrive suppression was observed at a PCL of 400-200 msec. Ten-beat stimulation trains induced a "flat response" of postpacing impulses. Ten-and 50-beat overdrive pacing provoked premature escape beats in 66% of the fibers, with the higher incidence at a PCL of 200 msec for 50-beat stimulation trains. No shortening of the coupling interval of premature escape beats was observed at faster pacing rates. Only lidocaine (which suppresses normal automaticity) abolished premature escape beats. We conclude that normal automaticity is the most likely mechanism underlying premature escape beats in Purkinje fibers with high levels of membrane potential. (Circulation 1990;82:234-243) O verdrive suppression, the quiescent period after rapid stimulation of a pacemaker cell, "qk.owl was well characterized during the 1960s and 1970s. In vivo and in vitro experiments demonstrated the duration of suppression to depend on the rate and duration of the period of overdrive pacing.1-' This property of automatic rhythms has been used to distinguish them from other mechanisms underlying normal and abnormal cardiac rhythms.Recently, Gorgels et al6,7 studied the effects of ventricular pacing in conscious dogs one week after From the

Section: Discussioncontrasting

confidence: 50%

Premature escape beats induced by overdrive pacing in canine Purkinje fibers. Evidence for the role of normal automaticity as an underlying cellular mechanism.

Viamonte

Rosen

1990

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“…In vitro, the occurrence of a triggered rhythm is facilitated by rapid pacing. 12,13,17,19,26 This was evident in all of these preparations, although the frequency of occurrence at all cycle lengths was higher in the presence of digitalis toxicity. In vitro, the coupling interval of the first beat of a triggered rhythm is directly related to the pacing cycle length, with a tendency toward overdrive acceleration after fast pacing.…”

Section: Methodsmentioning

confidence: 89%

The response to overdrive pacing of triggered atrial and ventricular arrhythmias in the canine heart.

Malfatto

Rosen

1988

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Although triggered activity has been identified in isolated atrial tissue with the use of cellular electrophysiologic techniques, there has been no identification of triggered atrial arrhythmias in situ. Moreover, it is unclear whether triggered rhythms of different causes and sites of origin in the heart exhibit uniform responses to pacing that might aid in their identification. We therefore studied arrhythmias induced by overdrive pacing in three canine preparations, and based the analysis of our results on guidelines derived from microelectrode studies. We studied ventricular tachycardias induced by ouabain or by anterior wall myocardial infarction and atrial (coronary sinus) arrhythmias induced by the infusion of epinephrine into the great cardiac vein. In the ouabain and postinfarction preparations, right ventricular epicardial pacing induced ventricular premature beats or tachycardias whose recovery intervals after cessation ofpacing shortened and showed overdrive acceleration as pacing rate increased. The first postpacing beat displayed progressive fusion with the paced beats but transient entrainment could not be induced. In the coronary sinus, the recovery intervals of impulses induced by epinephrine and pacing decreased as the drive rate increased, and inducibility of the paced rhythms increased at faster drive rates. Thus, the recovery intervals of triggered activity induced in the coronary sinus are phenomenologically similar to those of infarct-and digitalis-induced triggered rhythms. This is the first demonstration of consistent behavior in response to pacing of diverse types of triggered activity. Considered in light of the failure to induce transient entrainment, the results emphasize the potential utility of pacing in clinical identification of triggered rhythms and their differentiation from reentry. Circulation 77, No. 5, 113977, No. 5, -114877, No. 5, , 1988 ALTHOUGH much has been done to characterize delayed afterdepolarization-induced triggered rhythms in isolated cardiac tissues`8 and in intact animals,9' 10 it remains difficult to identify triggered arrhythmias clinically and to distinguish them from reentry. 11-16 The cellular electrophysiologic "rules" that have been applied to the identification of triggered rhythms in the intact heart are derived largely from studies of digitalistoxic Purkinje fibers.

“…The return cycle length was divided by the average cycle length of the preceding 3 beats and plotted as a function of the premature coupling interval divided by the average cycle length of the rhythm. 28 In addition, we studied the responses of these rhythms to overdrive pacing at cycle lengths of 1000. 800.…”

Section: Methodsmentioning

confidence: 99%

Effects of pacing on triggered activity induced by early afterdepolarizations.

Damiano¹,

Rosen²

1984

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250

Early afterdepolarizations (EADs) are depolarizing potentials that occur during phase 2 or phase 3 of repolarization. They can induce triggered activity and have been proposed as a cause for arrhythmias in the heart in situ. To determine the response of EADs and triggered activity to interventions analogous to those used in the clinic for identifying arrhythmogenic mechanisms, we used a pacing protocol to study the response of EADs to sustained drive and extrastimuli. Cesium chloride (5 to 20 mM), which induces triggered arrhythmias in the intact dog, was used to induce EADs in isolated canine Purkinje fibers, and these were studied by microelectrode techniques. Cesium prolonged action potential duration and induced two types of EADs. At a potassium concentration of 4 mM, EADs occurred at membrane potentials of -3 to -30 mV. They were initiated 240 to 680 msec after the action potential upstroke and were 2 to 30 mV in amplitude. Their amplitude increased as drive cycle length increased, but their coupling interval to the action potential did not change with drive cycle length. These EADs did not induce triggered action potentials. At a potassium concentration of 2 mM, EADs usually occurred at higher membrane potentials (-50 to -70 mV) and longer coupling intervals (470 to 1360 msec) and were manifested as a delay.of phase 3 repolarization. These EADs induced triggered action potentials. When the triggered rhythms became sustained, premature stimuli either reset or terminated them, depending on the maximum diastolic potential. Termination occurred more frequently as the maximum diastolic potential increased. The extent of overdrive suppression induced by pacing for 15 sec to 3 min also increased as the maximum diastolic potential increased. In summary, cesium induced EADs at low or high membrane potentials. The former did not induce triggered activity, but the latter did. The triggered rhythms that occurred were similar to abnormal automatic mechanisms in their response to overdrive pacing and extrastimuli.