Overdrive suppression of conduction in the canine His-Purkinje system after occlusion of the anterior septal artery.

Takahashi, Naomi; Gilmour, Robert F.; Zipes, D P

doi:10.1161/01.cir.70.3.495

Cited by 16 publications

(12 citation statements)

References 30 publications

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“…Post-pacing conduction block has been reported in the atrioventricular node, bundle branch, and His-Purkinje system, and has been called a fatigue phenomenon or overdrive suppression of conduction. [1][2][3][4][5] Similar findings were reported in accessory pathways as well. [6][7][8] However, in earlier studies, overdrive suppression of preexcitation was observed in the accessory pathway lacking retrograde conduction 6) or that affected by pharmacological treatment.…”

supporting

confidence: 67%

“…10,11) The mechanism responsible for direction-dependency is not clear but is probably related to the geometry of the conduction properties and the antegrade versus the retrograde activation sequence. 4) Because neither tachycardia nor rapid pacing generally yield this phenomenon, some unknown concomitant factor must have participated in creating a particular electrophysiologic property of the accessory pathway in the present case. If such a factor functions at a slower heart rate, the mechanism of overdrive sup-pression of conduction may explain intermittent preexcitation in some patients.…”

Section: Discussionmentioning

confidence: 80%

“…The same dependencies were demonstrated in the atrioventricular node, bundle branch and His-Purkinje system. [1][2][3][4][5] Faster pacing rates or longer durations of pacing in conduction properties increases cytosolic sodium and calcium concentrations as well as the extracellular potassium level, and subsequently mitigates cellular excitability. 10,11) The mechanism responsible for direction-dependency is not clear but is probably related to the geometry of the conduction properties and the antegrade versus the retrograde activation sequence.…”

Section: Discussionmentioning

confidence: 99%

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Overdrive Suppression of Antegrade Conduction over the Accessory Pathway.

et al. 2000

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SUMMARYIn a patient with Wolff-Parkinson-White syndrome whose accessory pathway was primarily capable of bidirectional conduction, antegrade conduction over the accessory pathway was transiently inhibited after rapid atrial or ventricular pacing or after spontaneous termination of atrioventricular reentrant tachycardia. Pacing rate and duration of tachycardia were related to the duration of the suppression of preexcitation, while the coupling interval of the first sinus beat to the last driven or tachycardia beat was irrelevant to the phenomenon. Thus, overdrive suppression of conduction may be the most likely mechanism of this phenomenon. (Jpn Heart J 2000; 41: 767-772)

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supporting

confidence: 67%

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

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Overdrive Suppression of Antegrade Conduction over the Accessory Pathway.

et al. 2000

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“…It has been demonstrated that pacing proximal to the His bundle lesion (atrial or direct His bundle pacing) may not trigger fatigue phenomenon, whereas direct pacing of the left bundle branch just distally to the lesion does. 3 The underlying mechanisms of these anisotropic specific properties of disease HPS remain unclear, but in our case one may also suppose that relatively slow conduction through the AV node may have initially protected the diseased HPS from overdrive suppression. The persistent AF did not allow us to assess further more anterograde properties of AV conduction in this patient.…”

Section: Mechanism 1: Overdrive Suppressionmentioning

confidence: 78%

“…3 In patients with a narrow baseline QRS complex, the block always occurs within the common His bundle, whereas in those with pre-existing bundle-branch block, the location of block may be in the remaining fascicle.…”

Section: Clementy Et Al Unusual Tachycardia-bradycardia Syndrome E43mentioning

confidence: 99%

Unusual Tachycardia-Bradycardia Syndrome During Atrial Fibrillation

Clémenty

Andrade²,

Babuty³

et al. 2013

Circ: Arrhythmia and Electrophysiology

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A 60-year-old man with a history of remote myocarditis and residual mild left ventricular dysfunction presented with syncope. Before admission, the patient was not taking any regular medications. Medical history was otherwise unremarkable. Examination at presentation was unremarkable, apart from slow atrial fibrillation (AF). ECG on presentation demonstrated AF with slow ventricular response and a complete left bundle-branch block (Figure 1). Inpatient telemetry demonstrated episodes of nonsustained ventricular tachycardia (VT). Cardiac catheterization with coronary angiography was normal. Echocardiogram demonstrated mild left ventricular dysfunction (ejection fraction 50%) but was otherwise unremarkable.An electrophysiological study showed a hisioventricular interval of 75 ms during AF at a rate of 75 beats per minute. No spontaneous pauses or infranodal phase 4 atrioventricular (AV) block was spontaneously observed. Programmed stimulation from the right ventricular apex was unremarkable at a 600-ms cycle length. At a 400-ms cycle length, a sustained monomorphic VT at 165 beats per minute with left bundlebranch block morphology and an inferior axis ( Figure 2) was induced with a single extrastimulus (S2=270 ms). After 35 seconds, the VT spontaneously terminated. Despite the persistence of AF, the termination of VT was followed by a prolonged complete infrahisian AV block (Figure 3). After 8.5 seconds of ventricular asystole, AV conduction resumed. In addition, spontaneous premature ventricular complexes were observed (Figure 4). Those originating from the left anterior septum were associated with transient infrahisian AV block ( Figure 4A). In contrast, those originating from the right ventricular apex were not associated with AV block, despite an identical coupling interval ( Figure 4B). A single-chamber cardioverter-defibrillator was successfully implanted, and the patient subsequently remained asymptomatic. DiscussionThis case demonstrates an uncommon cause of syncope in a patient with persistent AF and mild cardiomyopathy. Although paroxysmal infrahisian AV block may be observed in patients with underlying conduction disease, the mechanism of block in this case is fairly unique. Specifically, fatigue phenomenon of a diseased His-Purkinje system (HPS) is a rarely observed mechanism of infranodal atrioventricular AV block, whereby transient but sustained anterograde AV block, which is not inducible by rapid anterograde stimulation, occurs after rapid retrograde stimulation (either by ventricular burst pacing or by spontaneous ventricular arrhythmias). 1,2Irrespective of the underlying cause, a depression of infranodal conduction is a prerequisite, usually as a result of ischemic injury, but also nonischemic (as in this case) or idiopathic fibrosis, and once established acts as the substrate for high-degree by guest on

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