Vagal modulation of the rate-dependent properties of the atrioventricular node.

Nayebpour, Mohsen; Talajic, Mario; Villemaire, Christine; Nattel, Stanley

doi:10.1161/01.res.67.5.1152

Cited by 34 publications

(23 citation statements)

References 77 publications

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“…Compared with previous studies, these tachycardia-dependent AV nodal depressant properties could apply to calcium channel-blocking agents and vagal stimulation. 13,14,36 The intravenous bolus dose of adenosine used in this study was relatively small. Therefore, there were no significant negative dromotropic effects of adenosine at a slow heart rate.…”

Section: Rate Dependency Of Adenosine Effectsmentioning

confidence: 99%

Rate-dependent properties of adenosine-induced negative dromotropism in humans.

Lai

Lee

1994

Circulation

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BACKGROUND The antiarrhythmic effects of sodium channel and calcium channel blockers are known to be rate dependent. Little is known about the rate-dependent effect of adenosine on human atrioventricular (AV) nodal conduction. The purpose of this study was to determine whether the negative dromotropic effect of adenosine is dependent on heart rate. METHODS AND RESULTS Atrial pacing at 20-millisecond increments decreasing stepwise was performed, and the curves that relate the AH interval to the atrial pacing cycle length were analyzed. The change in AV nodal function was evaluated in three protocols: (1) In 8 group 1A and 6 group 1B patients, an intravenous infusion of adenosine at a dose of 140 and 320 micrograms.kg-1.min-1 was given, respectively; (2) a bolus injection of a fixed dose of adenosine was given to 12 group 2A patients without and 6 group 2B patients with propranolol (0.1 mg/kg) treatment; and (3) in 12 group 3 patients, the AV nodal function was evaluated after intravenous propranolol (0.05 mg/kg) and after subsequent intravenous aminophylline (loading dose, 5 mg/kg; maintenance dose, 0.9 mg.kg-1.h-1). No significant depression of AV nodal function could be demonstrated during intravenous infusion of adenosine. The bolus injection of adenosine could prolong the AH interval, which was dependent on heart rate and more significant at a shorter pacing cycle length. Intravenous propranolol significantly depressed the AV nodal conduction and shifted the curves of the AH interval versus the pacing cycle length to the right. Subsequent intravenous aminophylline shortened the AV nodal conduction time, however, in a rate-independent manner. CONCLUSIONS The negative dromotropic effects induced by intravenous bolus injection of adenosine became more pronounced at fast atrial pacing rates. These results indicate that adenosine causes rate-dependent prolongation of AV nodal conduction in humans.

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Section: Rate Dependency Of Adenosine Effectsmentioning

confidence: 99%

Rate-dependent properties of adenosine-induced negative dromotropism in humans.

Lai

Lee

1994

Circulation

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“…Atrial impulses at premature recovery (HA) intervals show less conduction slowing when preceded by a premature atrial activation.1 '22 This process, termed facilitation, reaches steady state after one cycle at a new rate22 and leads to a parallel shift of the recovery curve toward shorter recovery intervals. 23 In addition to these intrinsic AV nodal properties, tachycardias may also cause reflex changes in autonomic tone that alter AV nodal properties over time. 24 The relation between individual functional AV nodal properties (like recovery, facilitation, and fatigue) and complex AV nodal conduction patterns is unclear.…”

Section: A Unified Model Of Atrioventricular Nodal Conduction Predictmentioning

confidence: 99%

A unified model of atrioventricular nodal conduction predicts dynamic changes in Wenckebach periodicity.

Talajic

Papadatos

Villemaire

et al. 1991

Circulation Research

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The atrioventricular (AV) node responds in a complex fashion to changes in activation rate. A variety of approaches have been used to explain these dynamic AV nodal responses, but none has been able to account fully for AV nodal behavior. Three specific rate-dependent properties of the AV node have been described: 1) time-dependent recovery after excitation, 2) an effect of short cycles to advance recovery ("facilitation"), and 3) a gradual slowing of conduction in response to sustained, high-frequency activation ("fatigue"). We hypothesized that a model incorporating quantitative descriptors of all three processes might be able to account for a wide variety of AV nodal behaviors. Quantitative descriptors of AV nodal recovery, facilitation, and fatigue were developed based on AV nodal conduction changes during selective pacing protocols in seven autonomically blocked dogs. These descriptors were incorporated into a set of mathematical equations that define AV nodal conduction of any beat based on activation history. The equations were then applied to predict pacing-induced Wenckebach periodicity in each dog. Experimental data were obtained after nine to 19 step decreases in atrial cycle length into the Wenckebach zone in each animal. Observed behaviors included complex patterns of block, a progressive increase in the level of block over 5 minutes of rapid pacing, and periods of alternating patterns of block. The model accurately predicted the onset of AV block at each cycle length, the relation between conduction ratio and cycle length as a function of time, and the changing patterns of Wenckebach periodicity during sustained atrial pacing. All three terms of the model equation (describing recovery, facilitation, and fatigue) were essential to account fully for the observed behaviors. Elimination of AV nodal fatigue from the model resulted in failure to account for time-dependent changes in Wenckebach patterns, whereas exclusion of facilitation led to consistent overestimation of the degree of AV block at each cycle length. We conclude that a mathematical model incorporating terms to describe recovery, facilitation, and fatigue accurately predicts a wide range of Wenckebach-type behavior and that complex conduction patterns of the AV node can be fully accounted for by simple functional AV nodal properties. (Circulation Research 1991;68:1280-1293 Preliminary results from this study have been presented in abstract form (JAm Coll Cardiol 1990;15:201A

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“…To understand the potential direct effects of SV on ionic currents, we should consider the inability of SV to significantly change the recovery time constant. The slow inactivation kinetics of calcium channels determines the time constant of the recovery process Nayebpour et al 1990). In addition, medications with major inhibitory effects on calcium channels alter the recovery time constant in a frequency-dependent manner.…”

Section: Sv Effects On Basic Av Nodal Propertiesmentioning

confidence: 99%

Protective role of simvastatin on isolated rabbit atrioventricular node during experimental atrial fibrillation model: role in rate control of ventricular beats

Khori

Najafi

Alizadeh

et al. 2012

Naunyn-Schmiedeberg's Arch Pharmacol

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The purpose of the present study was to determine (1) whether simvastatin (SV) modifies the rate-dependent conduction time and refractoriness of the atrioventricular (AV) node and (2) how it can change the protective mechanism of the AV node during atrial fibrillation (AF). Predefined stimulation protocols were applied to detect the electrophysiological parameters of the AV node, including atrial-His conduction time, effective refractory period (ERP), functional refractory period (FRP), concealed conduction, excitable index, and fatigue in two groups of isolated, perfused rabbit AV nodal preparations (N=16). The stimulation protocols (fatigue, recovery) were carried out during control and in the presence of SV (0.5, 0.8, 3, and 10 μM). Simulated AF was executed in a separate group (N=8), and specific indexes, including H-H mean, zone of concealment (ZOC), and concealed beats were recorded. SV, in a concentration-dependent manner, prolonged ERP, FRP, and Wenckebach cycle lengths. It (10 μM) significantly increased fatigue and the excitable index. In addition, SV elicited prolongation of ZOC and H-H mean at 3 and 10 μM. SV-evoked prolongation of nodal refractoriness and concealed conduction caused rate-dependent ventricular slowing effects during AF. The ability of simvastatin to decrease the excitable gap by its heterogeneous effects on nodal dual pathways proposes its protective role in AF.

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Vagal modulation of the rate-dependent properties of the atrioventricular node.

Cited by 34 publications

References 77 publications

Rate-dependent properties of adenosine-induced negative dromotropism in humans.

Rate-dependent properties of adenosine-induced negative dromotropism in humans.

A unified model of atrioventricular nodal conduction predicts dynamic changes in Wenckebach periodicity.

Protective role of simvastatin on isolated rabbit atrioventricular node during experimental atrial fibrillation model: role in rate control of ventricular beats

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