Studies on overdrive stimulation of canine cardiac purkinje fibers: Maximal diastolic potential as a determinant of the response

Dangman, Kenneth H.; Hoffman, Brian F.

doi:10.1016/s0735-1097(83)80349-0

Cited by 72 publications

(14 citation statements)

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“…In some instances, only subthreshold electrotonic responses occurred ( figure 12, A); in other instances, one or two secondary premature responses occurred during the electrotonic pulse ( figure 12, B to E). 820 Discussion These data indicate that automatic rhythms in (1) false tendon Purkinje fibers with normal automaticity occurring from the high level of membrane potential, (2) in partially depolarized Purkinje fibers in bariumtreated false tendon preparations, or (3) in surviving subendocardial Purkinje fibers from the central regions of 24-hr-old infarct zones all respond to single premature stimuli in a similar way. That is, each type of preparation examined usually showed reset of the rhythm so that the return cycle following the premature impulse was + 40% of the control spontaneous cycle length.…”

Section: Resultsmentioning

confidence: 81%

“…We have previously reported that short periods of overdrive stimulation can be used to determine the approximate maximum diastolic potential of the pacemaker fibers of a preparation of cardiac Purkinje fibers; preparations with pacemakers with high (> -70 mV) maximum diastolic potentials (and "high potential automaticity") show postoverdrive suppression, whereas pacemaker fibers with low (-60 to -40 mV) maximum diastolic potentials (which we have referred to as "low potential automaticity" or "abnormal automaticity") show postoverdrive enhancement or no change in automaticity after a short period of overdrive stimulation. 2 In this study, we report on the effects of single premature impulses on automatic and triggered activity in isolated canine Purkinje fiber bundles and ventricular muscle preparations.…”

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confidence: 99%

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The effects of single premature stimuli on automatic and triggered rhythms in isolated canine Purkinje fibers.

Dangman¹,

Hoffman²

1985

Circulation

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We studied the effects of single premature stimuli on automatic and triggered rhythms occurring in preparations of isolated canine Purkinje fibers. Preparations were made from false tendons, the subendocardial right bundle branch, and infarct zone Purkinje fibers 24 hr after occlusion of the left anterior descending coronary artery, and were studied by standard microelectrode techniques. Single premature impulses almost always produced reset of automatic rhythms, whether the pacemaker had a low (< -60 mV), intermediate (-61 to -70 mV), or high (> -70 mV) maximum diastolic potential. In contrast, single premature impulses imposed on triggered rhythms sometimes were found to alter these rhythms; often, early premature impulses (i.e., during phase 3) resulted in either a shortened first return cycle or a short period of arrest of the rhythm. The results of this study indicate that it may be possible to design simple electrophysiologic tests using single premature stimuli to determine whether an arrhythmia is being caused by an automatic focus or by triggered activity. Circulation 71, No. 4, 813-822, 1985. IT IS THOUGHT that ventricular ectopic activity can be caused by a variety of mechanisms at the cellular level, including normal automaticity, abnormal automaticity, triggering, and reentrant activation. ' However, at this time there are no precise tests available to determine which of these mechanisms is causing a particular arrhythmia of the heart in situ. To develop such tests, it will be necessary to better understand the response of automatic and triggered foci in preparations in vitro to stimulus regimens such as those that can be applied to the heart in situ. We have previously reported that short periods of overdrive stimulation can be used to determine the approximate maximum diastolic potential of the pacemaker fibers of a preparation of cardiac Purkinje fibers; preparations with pacemakers with high (> -70 mV) maximum diastolic potentials (and "high potential automaticity") show postoverdrive suppression, whereas pacemaker fibers with low (-60 to -40 mV) maximum diastolic potentials (which we have referred to as "low potential automaticity" or "abnormal automaticity") show postoverdrive enhancement or no change in automaticity after

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Section: Resultsmentioning

confidence: 81%

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confidence: 99%

The effects of single premature stimuli on automatic and triggered rhythms in isolated canine Purkinje fibers.

Dangman¹,

Hoffman²

1985

Circulation

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“…The Purkinje fibers were impaled with 3 M KCIfilled glass microelectrodes having tip resistances of [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] Mfl. Attempts were made to impale the site of earliest impulse initiation, at which the slope of phase 4 and phase 0 merged smoothly in the typical configuration of a pacemaker fiber.…”

Section: Methodsmentioning

confidence: 99%

“…To further study whether the mechanism underlying premature escape beats was automatic or triggered, we used a drug matrix consisting of suppresses normal automaticity22 and delayed afterdepolarizations,23 20 ,ug/ml doxorubicin abolishes delayed afterdepolarizations,10 and 2 ,ug/ml ethmozin suppresses abnormal automaticity and delayed afterdepolarizations. '218 We also used (3-blockers to test whether local release of catecholamines during pacing was related to the generation of premature escape beats.…”

Section: Mechanism Of Initiation Of Premature Escape Beatsmentioning

confidence: 99%

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

Circulation

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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

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“…To establish its value in differentiating between mechanisms of arrhythmias in the canine heart, the effect of flunarizine was investigated on ventricular tachycardia (VT) induced by ouabain intoxication or occurring [16][17][18][19][20][21][22][23][24] hours after occlusion of the left anterior descending coronary artery. Four groups of dogs were studied.…”

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confidence: 99%

Flunarizine allows differentiation between mechanisms of arrhythmias in the intact heart.

et al. 1990

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The calcium antagonist flunarizine suppresses pathologic accumulation of calcium intracellularly without affecting the fast sodium or the slow calcium channel. To establish its value in differentiating between mechanisms of arrhythmias in the canine heart, the effect of flunarizine was investigated on ventricular tachycardia (VT) induced by ouabain intoxication or occurring 16-24 hours after occlusion of the left anterior descending coronary artery. Four groups of dogs were studied. Group 1 consisted of 13 animals with VT induced by ouabain intoxication (triggered-activity group). Group 2 included nine dogs in whom VT developed 16-24 hours after occlusion of the left anterior descending coronary artery (abnormal automaticity group). Group 3 included six dogs with normally conducted sinus beats, whereas group 4 consisted of six animals having a ventricular escape rhythm. With the exception of group 3, all dogs had surgically induced complete atrioventricular block. All animals were studied while conscious and without premedication. In groups 1 and 2, 2-3 mg/kg flunarizine was given intravenously after VT had persisted for at least 20 minutes. In groups 3 and 4, 2 mg/kg flunarizine was given after the rhythm was registered for 20 minutes. The cycle lengths of the different rhythms were compared before and after flunarizine. In group 1, flunarizine increased the cycle length of the VT from 300±30 to 410+50 msec (pO.001). Termination of VT was seen in 11 out of 13 animals. In group 2, flunarizine resulted in a nonsignificant shortening of the RR interval from 450±60 to 440+60 msec. Persistent termination was observed in only one of nine dogs. A significant acceleration in rate was seen in groups 3 and 4. In conclusion, flunarizine slows and terminates ventricular arrhythmias resulting from triggered activity but accelerates rhythms based on normal and abnormal automaticity. These findings suggest that flunarizine can be used to differentiate between mechanisms of arrhythmias. (Circulation 1990;81:343-349) T wo decades ago, clinically occurring cardiac arrhythmias were thought to result from either automaticity, reentry, or a combination of these mechanisms.' In vitro, other mechanisms have been described, like triggered activity induced by early and delayed afterdepolarizations (DADs) and abnormal automaticity.2 While reentry has been proven to be responsible for a number of human supraventricular and ventricular arrhythmias,34 the clinical relevance of the other mechanisms is not known.

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Studies on overdrive stimulation of canine cardiac purkinje fibers: Maximal diastolic potential as a determinant of the response

Cited by 72 publications

References 10 publications

The effects of single premature stimuli on automatic and triggered rhythms in isolated canine Purkinje fibers.

The effects of single premature stimuli on automatic and triggered rhythms in isolated canine Purkinje fibers.

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

Flunarizine allows differentiation between mechanisms of arrhythmias in the intact heart.

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