Electrophysiologic mechanisms for modification and abolition of atrioventricular junctional tachycardia with simultaneous and sequential atrial and ventricular pacing.

Akhtar, Masood; Gilbert, Carol J.; Al-Nouri, Mamoun B.; Schmidt, Donald H.

doi:10.1161/01.cir.60.7.1443

Cited by 28 publications

(2 citation statements)

References 33 publications

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“…Since concomitant retrograde A2 activation in most instances took place exclusively via the AP, the collision of the two impulses via the normal pathway and AP must have occurred in the AV node rather than the atrium (7,17). Retrograde penetration and concealed conduction in the AV node was most probably responsible for preventing the forward progress of the A2 impulse.…”

Section: Discussionmentioning

confidence: 98%

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

Akhtar¹,

Shenasa²,

Schmidt³

1981

J. Clin. Invest.

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A B S T R A C T The precise mechanisms for paroxysmal reentrant supraventricular tachycardia (PSVT) initiation during right ventricular premature stimulation (V2 method) were analyzed in 14 consecutive patients with Wolff-Parkinson-White Syndrome in whom the PSVT was inducible during retrograde refractory period studies. 9 patients had left-sided and the remaining 5 of 14 had right-sided ventriculo-atrial (VA) accessory pathway (AP). At the basic cycle lengths (V,V1) ranging from 550 to 900 ms (mean, 657.1+139.5), closely coupled V2 (mean V,V2, 357.3+59.2 ms, range 320-500) produced retrograde His bundle (H2) activation via the bundle branches and retrograde atrial (A2) activation via the AP. As the V1V2 were further shortened, the V2 showed a retrograde block in the His Purkinje system (HPS) and conducted to the atria via AP in 9 of 14 cases. Subsequently, the A2 impulse conducted anterograde over the atrioventricular node-HPS to initiate a PSVT or an atrial echo response in all nine cases. In none of the patients was a PSVT induced by V2 when the latter produced retrograde H2 activation via the bundle branches. In 10 of 14 cases, however, the retrograde H2 was followed by a V3, due to macroreentry in the HPS. The V3 in turn blocked retrogradely in the HPS while producing A3 via the AP to initiate a PSVT or an atrial echo response in 9 of 10 cases. Retrograde block of V2 and/or V3 in the HPS resulted in PSVT initiation in 13 of 14 cases, whereas in the remaining 1 case the exact mechanism was not clear. In none ofthe patients in this series was the PSVT initiated with a retrograde block of

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Section: Discussionmentioning

confidence: 98%

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

Akhtar¹,

Shenasa²,

Schmidt³

1981

J. Clin. Invest.

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“…Twenty-six patients (12 males and 14 females), ages 15-82 years (mean 55.6 ± 16.3 years), were studied because of recurrent ventricular arrhythmias, dizziness or syncope. All were in sinus rhythm and none was taking cardioactive medications at the time of the study.…”

Section: Methodsmentioning

confidence: 99%

Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses.

et al. 1983

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SUMMARY Animal studies have suggested that spontaneous or programmed ventricular beats that occur simultaneously with atrial activation may facilitate atrioventricular (AV) nodal conduction during subsequent atrial impulses. However, this possibility has not been systematically studied in the human heart. In the present study the AV nodal conduction during a programmed atrial premature beat (S2) was analyzed.The S2 was delivered after a series of atrial drive beats (SjSj) of constant duration; this was termed stimulation method I. The results were compared with stimulation method II, which was similar to method I except that a single ventricular beat (Vs) was introduced simultaneously with the last Sl. The longest and shortest possible paced atrial cycle lengths (CLs) were scanned during both methods. Twenty-six patients were studied: 14 with a normal PR and normal intraventricular conduction (NIVC), four with first-degree AV nodal block and NIVC, three with a complete left bundle branch block (LBBB) pattern, three with a complete right bundle branch block (RBBB) pattern, and two with an incomplete RBBB pattern.At the same SlS2 intervals, the AV nodal conduction times (S2112 intervals) were consistently shorter with method II than with method I except in three patients, two with complete RBBB and one with complete LBBB. The magnitude of S2H2 shortening with method II was more pronounced at the shorter basic CLs and shorter SlS2 intervals. During method I, the effective refractory period (ERP) of the AV node was measured in 13 patients, eight with NIVC and five with preexisting bundle branch block. With method II, the ERP of the AV node shortened in all but three patients (one with complete RBBB, one with incomplete RBBB and one with complete LBBB pattern), in whom this variable did not change. The findings suggest that intranodal collison from antegrade and retrograde impulses facilitates AV nodal conduction and shortens the ERP. The magnitude of this change is greater at shorter atrial CLs and is probably related to deeper intranodal penetration of a Vs. The shortening in AV nodal conduction and refractoriness is not noted in patients with bundle branch block when retrograde conduction delay or block in the bundle branches coexists with the antegrade counterpart producing delayed or ineffective input of Vs into the AV node.ATRIOVENTRICULAR (AV) nodal conduction and refractoriness in the antegrade direction have been extensively investigated in both animals and man.'-'0 Although several studies have addressed the effects of programmed ventricular premature stimulation on subsequent AV nodal conduction in animals,9' 11 rarely has such a study been carried out systematically in the human heart. This study was designed to examine the effect of simultaneous AV stimulation on the functional properties of the AV node in man. Patients and MethodsTwenty-six patients ( ously introduced through the femoral and antecubital veins and were positioned under fluoroscopic guidance, in the region of the tricuspid valve to permit...

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Pacing therapy for atrial tachyarrhythmias

Zhu

Spencer

1996

Clinical Cardiology

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Summary:The use of pacing techniques for the treatment of atrial tachyarrhythmias has been advocated for more than 30 years. Although it has played a beneficial role in the management of paroxysmal supraventricular tachycardia (PSVT) in drug-refractory patients, tachycardia acceleration and development of atrial fibrillation has been the major drawback. With the availability of radiofrequency catheter ablation therapy, the use of implantable antitachycardia devices for PSVT is currently negligible. From retrospective and small control studies it has been shown that atrial or dual-chamber pacing in patients with sick sinus syndrome has been associated with a lower incidence of paroxysmal atrial flutter or fibrillation than in those who received a ventricular pacemaker. Furthermore, recent studies have reported the potential benefit of reducing frequency of paroxysmal atrial flutter and fibrillation with multisite atrial pacing. As a result, there is a resurgence of research interest in antitachycardia pacing for prevention of atrial tachyarrhythmias. This paper briefly describes the basic aspects of antitachycardia pacing, reviews the data on the use of implantable antitachycardia devices for PSVT and the selection of patients, and assesses the current status of research on atrial pacing for prevention of paroxysmal atrial flutter and fibrillation.

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Electrophysiologic mechanisms for modification and abolition of atrioventricular junctional tachycardia with simultaneous and sequential atrial and ventricular pacing.

Cited by 28 publications

References 33 publications

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

Role of Retrograde His Purkinje Block in the Initiation of Supraventricular Tachycardia by Ventricular Premature Stimulation in the Wolff-Parkinson-White Syndrome

Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses.

Pacing therapy for atrial tachyarrhythmias

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