A mathematical model of parasystole and its application to clinical arrhythmias.

Moe, Gordon K.; Jalife, José; Mueller, William J.; Moe, B

doi:10.1161/01.cir.56.6.968

Cited by 188 publications

(72 citation statements)

References 20 publications

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“…It has been shown that if the impedance of the communication between the ectopic focus and the surrounding ventricle is low, locking of the ectopic pacemaker could be nearly fixed to give the appearance of a reciprocating bigeminy. 18 This is substantiated by Figure 2 in our case, wherein after infusion of amiodarone there is partial suppression of focus A resulting in occasional ectopic beats during sustained monomorphic VT because of focus B. Measurement of B-B intervals shows that there is doubling of the rate from 0.88 s during BVT as seen in Figure 1, compared with 0.44 s in Figure 2 suggesting a parasystole as the mechanism of arrhythmia.…”

Section: Discussionsupporting

confidence: 73%

“…This results in the occurrence of modulated parasystole. 17,18 This means that nonparasystolic beats falling close to the parasystolic beats can cause (1) maximal delay, (2) maximal acceleration, (3) lesser effects, (4) practically no effect, or (5) pacemaker annihilation of the parasystolic focus. 16,19 Nonparasystolic beats falling during the first half of the parasystolic interval induce a prolongation of this interval, those occurring during the second half of the parasystolic cycle length cause an abbreviation of this interval.…”

Section: Discussionmentioning

confidence: 99%

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Unusual Incessant Ventricular Tachycardia

Shenthar

2015

Circ: Arrhythmia and Electrophysiology

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V entricular tachycardia (VT) is defined as a tachycardia with a rate of >100 per minute, with ≥3 consecutive beats that originates from the ventricles, and is independent of atria or atrioventricular nodal conduction. Of all the VTs, 10% occurs in those with structurally normal heart and these are called as idiopathic VTs, and the rest 90% occurs in patients with structural heart disease. VTs may be classsified based on the clinical characteristic (clinical VT, hemodynamically stable or unstable, repetitive, incessant, etc.), morphology (monomorphic, multiple morphologies, pleomorphic, polymorphic, bidirectional, etc.) or mechanisms (scar-related reentry, automaticity, and triggered activity). Incessant VT is defined as continuous sustained VT during several hours, which recurs promptly despite repeated intervention for termination. VT storm is considered as ≥3 separate episodes of sustained VT within 24 hours, each requiring termination by an intervention. Monomorphic VT has a uniformly similar QRS configuration from beat-to-beat, with either right or left bundle configuration depending on whether the dominant deflection in lead V1 is R or S wave. Multiple monomorphic VTs refer to >1 morphologically distinct monomorphic VT, occurring as different episodes, or induced at different times. Polymorphic VT has continuously changing QRS configuration from beat-to-beat indicating a changing ventricular activation sequence. Pleomorphic VT has >1 morphologically distinct QRS complex occurring during the same episode of VT, but the QRS is not continuously changing. Bidirectional VT (BVT) is characterized by beat-to-beat alternation of the QRS axis on the ECG and is usually regular. Editor's Perspective see p 1512Here, we describe unusual incessant VT in a young male and discuss evaluation, management, and the possible mechanism. Case ReportA 33-year-old male, nondiabetic, nonhypertensive, presented with history of palpitation, chest discomfort, and fatigue of 6 hours duration. He had been otherwise healthy, not on any medications with no history of tobacco, alcohol, or drug use. At presentation, pulse rate was 144 beats per minute, irregular, blood pressure 96/60 mm Hg, and the rest of physical examination was unremarkable. Twelve-lead ECG revealed a wide complex regularly irregular tachycardia at a rate of 144 beats per minute, right bundle morphology, QRS duration of 200 to 220 ms, QRS axis alternating between +160° and −40°, QRS transition alternating from V3 to V6, and evidence of atrioventricular dissociation (Figure 1). Tachycardia was unresponsive to intravenous lignocaine, esmolol, amiodarone (300 mg during 1 hour), and 2 attempts of biphasic direct current (DC) cardioversion of 200 J. Because the tachycardia was incessant, patient was sedated, intubated, ventilated, and continued on intravenous amiodarone (900 mg/24 hours) with further 4 unsuccessful attempts at DC cardioversion. Tachycardia converted to monomorphic VT with occasional VT complexes of the 2nd morphology (Figure 2), which terminated 6 hours late...

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Unusual Incessant Ventricular Tachycardia

Shenthar

2015

Circ: Arrhythmia and Electrophysiology

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“…In a series of mathematical simulations and experimental studies the investigators showed that the effect of modulation could frequently mask the parasystolic nature of a VEA focus (Moe 1977;Antzelevitch , 1983b. At certain heart rates the timing and coupling intervals of the PVCs appeared to conform to a fixed coupled, reentry-like pattern.…”

Section: Patterns In the Grouding Of Pvcsmentioning

confidence: 99%

A stochastic characterization of chronic ventricular ectopic activity

Albrecht

Cohen

Mark

1988

IEEE Trans. Biomed. Eng.

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Ventricular ectopic beats are clinically important because of their association with the problem of sudden cardiac death. Ventricular ectopic activity (VEA) is most commonly evaluated using long-term ambulatory electrocardiographic (ECG) recordings. The results of these recordings are usually summarized in the form of hourly counts of VEA events.Although such hourly counts are useful, they are a nonspecific measure which, in effect, treats VEA generation as an unpredictable process.This thesis develops a new means for characterizing the activity of the VEA-generating mechanism using the beat type and timing information of the long-term ECG. The approach is founded on the hypothesis that the VEA mechanism is often stable over time, although its activity may be modulated by physiologic influences and by the timing of the sino-atrial node impulses.This hypothesis implies that there should be some relationship between the beat type and timing of preceding beats and the subsequent generation of ectopic beats.The VEA generation was characterized by a multi-dimensional conditional distribution which gives the probability that an ectopic beat will follow a specific conditioning sequence of beat types and intervals. Using this approach a three part study was performed. The first step examined the conditional distributions and tested the null hypothesis that the generation of ectopic beats is unpredictable.Using a database of half-hour ECG tapes from 66 patients, the null hypothesis was rejected at p=0.005 in 80% of the tapes.The second step developed a means of displaying the multidimensional distributions. By an appropriate transformation of the conditioning variables, the distributions could be represented as one-dimensional distributions. The resulting distributions were useful for. separating patients into groups and for finding characteristic, VEA-related events in the ECG data.The third step examined the reproducibility of the onedimensional distributions over time. Using ten-hour ECG tapes, it was found that in 7 of 10 patients the patient-specific distribution, although modulated in amplitude, maintained a similar shape over the ten hours.The VEA characterization which has been developed goes significantly beyond the simple counting of ectopic beats. The distributions can be considered a kind of "fingerprint" of the VEA-generating mechanism -a "fingerprint" which may be useful in the selection and evaluation of therapy.

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“…Inverse solution of some clinical records, however, yielded curves in which the delay phase was of considerably lower amplitude than the acceleration phase.4 6,7 To explain this anomaly, we considered the possibility that the position of the dominant ectopic pacemaker relative to Complete scans of the EP cycles in the experiment depicted in figure 3 are illustrated in figure 4. When the dominant pacemaker was close to the block, the EP firing was delayed by a maximum of 32% and accelerated by 22%/o.…”

Section: Position Of Pacemakermentioning

confidence: 99%

“…1-3 Electrotonic depolarizations that occur early during phase 4 of the spontaneous pacemaker cycle delay the next discharge; those that occur later in the cycle accelerate, or "capture," the pacemaker.3 Thus, the activity of an ectopic focus, "protected" but not insulated by an area of depressed excitability, may be modulated by activity in the surrounding tissue according to a biphasic electrotonic influence or phase-response relationship.…”

mentioning

confidence: 99%

Electrotonic metabolism of pacemaker activity. Further biological and mathematical observations on the behavior of modulated parasystole.

Antzelevitch¹,

Jalife²,

Moe³

1982

Circulation

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SUMMARY An in vitro biologic model of parasystole and a mathematical model of parasystole based on the phase-response relationships derived from the biologic model were used in tandem to further develop our understanding of the patterns of ectopic activity that might arise as a consequence of the interaction of two pacemakers across a zone of block. Superfusion of the central segment of a dog Purkinje fiber with an ion-free isotonic sucrose solution provided a narrow region of block. The modulation of pacemaker activity by electrotonic potentials transmitted across the area of block was shown to be importantly influenced by the position of the "ectopic" pacemaker relative to the site of block. Effects of repetitive electrotonic influences on a single pacemaker cycle, the degree of entrance block and capture of the pacemaker during a phase of supernormal excitability were also studied in both the biologic and mathematical models. Our results indicate that marked shifts in the incidence and pattern of manifest ectopic activity can occur as a result of slight changes in heart rate, ectopic pacemaker rate, level of block and the position of the parasystolic pacemaker relative to the block border.ELECTROTONIC POTENTIALS transmitted across an area of depressed conductivity may modulate the activity of a spontaneously beating pacemaker beyond the region of block. 1-3 Electrotonic depolarizations that occur early during phase 4 of the spontaneous pacemaker cycle delay the next discharge; those that occur later in the cycle accelerate, or "capture," the pacemaker.3 Thus, the activity of an ectopic focus, "protected" but not insulated by an area of depressed excitability, may be modulated by activity in the surrounding tissue according to a biphasic electrotonic influence or phase-response relationship.In a computer model programmed to imitate the modulation of an ectopic pacemaker, Moe and coworkers4 defined the patterns of entrainment and ectopic activity that may be expected to result from such interaction. Jalife and Moe' confirmed some of these predictions in a sucrose gap preparation of Purkinje tissue.Simplifying assumptions had been incorporated into the mathematical model, with the recognition that they would at least quantitatively warp the recorded patterns if not the basic rules of behavior: (1) made for supernormal excitability. In only a few runs was a relatively refractory period considered.In the present study, additional experiments were conducted in the sucrose gap preparation to assess the importance of these simplifications and to incorporate the biologic results into appropriately modified computer programs. Experiments were designed to test the effects of repetitive electrotonic influences on a single "ectopic" pacemaker cycle, the position of the ectopic pacemaker relative to the site of block, the degree of block between the two active segments and capture of the pacemaker during a phase of supernormal excitability. Methods Biologic ModelUnbranched free-running false tendons obtained from dog hear...

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A mathematical model of parasystole and its application to clinical arrhythmias.

Cited by 188 publications

References 20 publications

Unusual Incessant Ventricular Tachycardia

Unusual Incessant Ventricular Tachycardia

A stochastic characterization of chronic ventricular ectopic activity

Electrotonic metabolism of pacemaker activity. Further biological and mathematical observations on the behavior of modulated parasystole.

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