Relation Between Repolarization and Refractoriness During Programmed Electrical Stimulation in the Human Right Ventricle

Koller, Bettina S.; Karasik, Pamela; Solomon, Allen J.; Franz, Michael R.

doi:10.1161/01.cir.91.9.2378

Cited by 77 publications

(84 citation statements)

References 29 publications

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“…As expected from previous studies, 13,14,29 PRR was not observed in the absence of sodium channel-blocking drugs. On the contrary, during baseline, repetitive extrastimulation caused the ERP to shorten by a greater extent than the concomitant APD 90 .…”

Section: Postrepolarization Refractorinesssupporting

confidence: 90%

“…14 In this isolated heart study, as in the previous human heart study, 14 encroachment of repetitive extrastimuli, or burst stimuli, onto the repolarization phase of the preceding action potential was associated with tachyarrhythmia induction (Figure 6). This may be explained by the fact that these most premature responses originated during the phase of relative refractoriness and therefore had slower conduction velocities (Table 2), resulting in shortened excitation wavelengths and subsequently functional reentry arrhythmias.…”

Section: Postrepolarization Refractorinesssupporting

confidence: 60%

“…[11][12][13] Although the ionic mechanisms resulting in this drug-induced postrepolarization refractoriness (PRR) are not yet well defined, PRR has been suggested to have an antiarrhythmic effect, based on the rationale and previous observations that PRR shields the myocardium against very premature excitation with its associated conduction slowing and wavelength shortening. [12][13][14] This study was designed to distinguish the antiarrhythmic and proarrhythmic potential of two clinically used drugs with sodium channel-blocking properties: procainamide, which has relatively fast dissociation kinetics and is known to prolong the action potential, and propafenone, which has slow dissociation kinetics 14 and divergent action potential duration effects. Specifically, we tested the hypotheses that drug-induced PRR is antiarrhythmic and that persistent sodium channel block producing conduction slowing even during regular stimulation is proarrhythmic.…”

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confidence: 99%

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Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

1998

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Background-Conduction block may be both antiarrhythmic and proarrhythmic. Drug-induced postrepolarization refractoriness (PRR) may prevent premature excitation and tachyarrhythmia induction. The effects of propafenone and procainamide on these parameters, and their antiarrhythmic or proarrhythmic consequences, were investigated. Methods and Results-In 11 isolated Langendorff-perfused rabbit hearts, monophasic action potentials (MAPs) were recorded simultaneously from six to seven different right and left ventricular sites, along with a volume-conducted ECG. All recordings were used to discern ventricular tachycardia (VT) or ventricular fibrillation (VF) induced by repetitive extrastimulation (S2-S5) or 10-second burst stimulation at 25 to 200 Hz at baseline and after addition of procainamide (20 mol/L) or propafenone (1 mol/L) to the perfusate. MAPs were analyzed for action potential duration at 90% repolarization (APD 90 ), conduction times (CT) between the pacing site and the other MAPs, and PRR (effective refractory periodϪAPD 90 ϭPRR) and related to the induction of VT or VF. During steady-state pacing, procainamide and propafenone prolonged APD 90 by 12% and 14%, respectively. Procainamide slowed mean CT by 40% during S2-S5 pacing, whereas propafenone slowed mean CT by up to 400% (PϽ0.001 versus baseline and procainamide). Wavelength was not changed significantly by procainamide but was shortened fourfold by propafenone at S5. Both drugs produced PRR, which was associated with a 70% decrease in VF inducibility with procainamide and elimination of VF with propafenone. Despite this protection from VF, monomorphic VT was induced with propafenone in 57% of burst stimulations. Conclusions-Drug-induced PRR protects against VF induction. Propafenone promotes slow monomorphic VT, probably by use-dependent conduction slowing and wavelength shortening. (Circulation. 1998;97:2567-2574.)

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Section: Postrepolarization Refractorinesssupporting

confidence: 90%

Section: Postrepolarization Refractorinesssupporting

confidence: 60%

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confidence: 99%

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Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

1998

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“…20, 36 The amplitude of the MAP recording declines gradually over the study. 37 However, the APD restitution curve recorded with the MAP electrode closely resembles the APD restitution curve obtained by the microelectrode technique. 38 A second limitation is that only APD restitution from the RVOT was measured, making determination of spatial heterogeneity of APD restitution inapplicable.…”

Section: Study Limitationssupporting

confidence: 66%

Abnormal Action Potential Duration Restitution Property in the Right Ventricular Outflow Tract in Brugada Syndrome

Ashino

Watanabe

Kofune

et al. 2010

Circ J

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Background: Although patients with Brugada syndrome (BS) are at risk of ventricular fibrillation (VF) and ensuing death, the action potential duration (APD) restitution properties of the right ventricular outflow tract (RVOT) in patients with BS remain undetermined. Methods and Results:Endocardial monophasic action potentials (MAPs) were obtained from 16 patients with BS and 17 control patients. MAPs were recorded from the RVOT in all patients. The MAP duration at 90% repolarization (MAPD90), effective refractory period (ERP), and maximum slope of the APD restitution curve were obtained. VF was induced with up to 3 extrastimuli from the RV apex or RVOT. There was no difference in MAPD90 between the 2 groups, but the ERP was significantly shorter in patients with BS than in control patients (210.7±10.5 vs 223.8±13.4 ms, P=0.008). MAPD at the shortest diastolic interval was significantly shorter in patients with BS than in control patients (149.9±19.9 vs 179.8±13.7 ms, P<0.001). The maximum slope of the APD restitution curve was steeper in patients with BS than in control patients (2.90±1.29 vs 1.38±0.41, P<0.001). Conclusions:The shorter ERP, shorter MAPD at the shortest diastolic interval and steeply sloped APD restitution curve in the RVOT appear to be related to the inducibility of VF in patients with BS. (Circ J 2010; 74: 664 - 670)

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“…A substantial proportion of sudden cardiac arrests, approximately half in a recent study,2 are associated with ventricular tachycardia (VT) or ventricular fibrillation (VF). It has been observed clinically that sustained VT and VF are often preceded by several irregularly timed premature complexes,3, 4 and studies conducted to explore this phenomenon have shown that specific coupling interval patterns of premature complexes, such as short‐long‐short5 and short‐short‐short,6 tend to lead to reentry and VT. Various researchers have examined the mechanism by which premature complexes or pacing history can interact with electrical restitution properties, including the dependence of action potential duration (APD) and conduction velocity (CV) on the preceding diastolic interval (DI) to produce dynamical heterogeneity of refractoriness, wave break, reentry, and VF7, 8, 9, 10, 11 (see elsewhere12, 13 for reviews).…”

Section: Introductionmentioning

confidence: 99%

Discordant Alternans as a Mechanism for Initiation of Ventricular Fibrillation In Vitro

Muñoz

Gelzer

Fenton

et al. 2018

JAHA

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BackgroundVentricular tachyarrhythmias are often preceded by short sequences of premature ventricular complexes. In a previous study, a restitution‐based computational model predicted which sequences of stimulated premature complexes were most likely to induce ventricular fibrillation in canines in vivo. However, the underlying mechanism, based on discordant‐alternans dynamics, could not be verified in that study. The current study seeks to elucidate the mechanism by determining whether the spatiotemporal evolution of action potentials and initiation of ventricular fibrillation in in vitro experiments are consistent with model predictions.Methods and ResultsOptical mapping voltage signals from canine right‐ventricular tissue (n=9) were obtained simultaneously from the entire epicardium and endocardium during and after premature stimulus sequences. Model predictions of action potential propagation along a 1‐dimensional cable were developed using action potential duration versus diastolic interval data. The model predicted sign‐change patterns in action potential duration and diastolic interval spatial gradients with posterior probabilities of 91.1%, and 82.1%, respectively. The model predicted conduction block with 64% sensitivity and 100% specificity. A generalized estimating equation logistic‐regression approach showed that model‐prediction effects were significant for both conduction block (P<1×10−15, coefficient 44.36) and sustained ventricular fibrillation (P=0.0046, coefficient, 1.63) events.ConclusionsThe observed sign‐change patterns favored discordant alternans, and the model successfully identified sequences of premature stimuli that induced conduction block. This suggests that the relatively simple discordant‐alternans‐based process that led to block in the model may often be responsible for ventricular fibrillation onset when preceded by premature beats. These observations may aid in developing improved methods for anticipating block and ventricular fibrillation.

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Relation Between Repolarization and Refractoriness During Programmed Electrical Stimulation in the Human Right Ventricle

Cited by 77 publications

References 29 publications

Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

Postrepolarization Refractoriness Versus Conduction Slowing Caused by Class I Antiarrhythmic Drugs

Abnormal Action Potential Duration Restitution Property in the Right Ventricular Outflow Tract in Brugada Syndrome

Discordant Alternans as a Mechanism for Initiation of Ventricular Fibrillation In Vitro

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