Treatment of Supraventricular Tachycardia Due to Atrioventricular Nodal Reentry by Radiofrequency Catheter Ablation of Slow-Pathway Conduction

Jackman, Warren M.; Beckman, Karen J.; McClelland, James H.; Wang, X; Friday, Karen J.; Román, Carlos Agustín León; Moulton, Kriegh; Twidale, Nicholas; Hazlitt, H A; Prior, Michael

doi:10.1056/nejm199207303270504

Cited by 1,072 publications

(515 citation statements)

References 18 publications

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“…Nevertheless, disturbances of AV-nodal conductivity are of pathophysiological and clinical relevance, such as in the formation of dual pathways with different conduction velocities (slow and fast conducting areas of the AV node) (31). Different conduction properties of AV-nodal tissue with such division into slow (short refractory period) and fast (long refractory period) pathways facilitate development of local reentry and, thus, are the pathophysiological substrate for AV-nodal reentry tachycardia, the most common congenital supraventricular tachycardia in humans (32,33). Despite the high incidence of this tachycardia, little is known about the ultrastructural and cellular changes of the AV-nodal tissue leading to these differences in conduction velocity.…”

Section: Discussionmentioning

confidence: 99%

Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node

Kreuzberg

Schrickel

Ghanem

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

111

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In the mammalian heart, gap junction channels between electrically coupled cardiomyocytes are necessary for impulse propagation and coordinated contraction of atria and ventricles. Recently, mouse connexin30.2 (Cx30.2) was shown to be expressed in the cardiac conduction system, predominantly in sinoatrial and atrioventricular (AV) nodes. The corresponding gap junctional channels expressed in HeLa cells exhibit the lowest unitary conductance (9 pS) of all connexin channels. Here we report that Cx30.2 slows down the propagation of excitation through the AV node. Mice expressing a LacZ reporter gene instead of the Cx30.2 coding region (Cx30.2 LacZ/LacZ ) exhibit a PQ interval that is Ϸ25% shorter than in WT littermates. By recording atrial, His, and ventricular signals with intracardiac electrodes, we show that this decrease is attributed to significantly accelerated conduction above the His bundle (atrial-His interval: 27.9 ؎ 5.1 ms in Cx30.2 LacZ/LacZ versus 37.1 ؎ 4.1 ms in Cx30.2 ؉/؉ mice), whereas HV conduction is unaltered. Atrial stimulation revealed an elevated AV-nodal conduction capacity and faster ventricular response rates during induced episodes of atrial fibrillation in Cx30.2 LacZ/LacZ mice. Our results show that Cx30.2 contributes to the slowdown of impulse propagation in the AV node and additionally limits the maximum number of beats conducted from atria to ventricles. Thus, it is likely to be involved in coordination of atrial and ventricular contraction and to fulfill a protective role toward pathophysiological states such as atrial tachyarrhythmias (e.g., atrial fibrillation) by preventing rapid conduction to the ventricles potentially associated with hemodynamic deterioration.atrial fibrillation ͉ cardiac connexins ͉ conductive myocardium ͉ coordinated cardiac contraction G ap junctions are intercellular conduits that allow direct communication between neighboring cells. Two hemichannels, one contributed by each adjacent cell, form a pore that permits diffusion of ions, metabolites, and peptides Ͻ1.8 kDa molecular mass (1, 2). The protein subunits of these channels are the connexins (Cx) that are encoded by a multigene family, including 20 members in mice (3).It has been known for several years that three different connexins, i.e., Cx40, Cx43, and Cx45, are expressed by cardiac myocytes. The corresponding gap junctional channels are involved in electrical impulse propagation and coordinated contraction of the heart (4). The expression of these connexins is restricted to specialized compartments: Cx43 is the major connexin in the working myocytes of atria and ventricles (5, 6); Cx40 is detected in the atrioventricular (AV) conduction system and in atrial working myocytes (7,8). Cx45 is abundantly expressed in the sinoatrial (SA) node and the AV conduction system (9-11).Generation of Cx-deficient mice for Cx40, Cx43, and Cx45 helped to elucidate the involvement of these connexins in proper heart function. Targeted deletion of Cx40 in mice resulted in right bundle branch block and impaired left bu...

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Section: Discussionmentioning

confidence: 99%

Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node

Kreuzberg

Schrickel

Ghanem

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

111

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“…14 Also, it was shown that RF energy application near the CSOS inferior to the AV node can selectively eliminate the slow pathway conduction. 1,15 In addition, Keim et al 16 demonstrated the location of the site of the antegrade slow pathway using ice mapping techniques. Histological findings in patients also have provided evidence that the AV node itself does not participate in the slow pathway conduction.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 However, the exact boundaries of the reentry circuit in AVNRT have not been convincingly defined. The purpose of the present study was to define the tachycardia circuit in AVNRT.…”

mentioning

confidence: 99%

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

et al. 1999

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Background-The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined. Methods and Results-To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368Ϯ52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356Ϯ51, 356Ϯ51, 355Ϯ52, 357Ϯ51, 318Ϯ47, 305Ϯ53, 311Ϯ56, and 312Ϯ56 ms, respectively, and the following return cycles at these sites were 368Ϯ52, 368Ϯ53, 367Ϯ53, 367Ϯ53, 407Ϯ66, 431Ϯ73, 415Ϯ55, and 412Ϯ56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (PϽ0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (PϽ0.0001). Conclusions-The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway. (Circulation. 1999;100:621-627.)

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“…[1][2][3][4][5] Mapping of the cardiac chambers is performed with relatively stiff manually deflectable catheters with unidirectional or bidirectional deflection radius. Steering of those electrodes is performed via a pull-wire mechanism integrated in the handle of the catheter, allowing a reliable and reproducible deflection.…”

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confidence: 99%

Initial Experience With Remote Catheter Ablation Using a Novel Magnetic Navigation System

et al. 2004

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Background-Catheters are typically stiff and incorporate a pull-wire mechanism to allow tip deflection. While standing at the patient's side, the operator manually navigates the catheter in the heart using fluoroscopic guidance. Methods and Results-A total of 42 patients (32 female; mean age, 55Ϯ15 years) underwent ablation of common-type (slow/fast) or uncommon-type (slow/slow) atrioventricular nodal reentrant tachycardia (AVNRT) with the use of the magnetic navigation system Niobe (Stereotaxis, Inc). It consists of 2 computer-controlled permanent magnets located on opposite sides of the patient, which create a steerable external magnetic field (0.08 T). A small magnet embedded in the catheter tip causes the catheter to align and to be steered by the external magnetic field. A motor drive advances or retracts the catheter, enabling complete remote navigation. Radiofrequency current was applied with the use of a remote-controlled 4-mm, solid-tip, magnetic navigation-enabled catheter (55°C, maximum 40 W, 60 seconds) in all patients. The investigators, who were situated in the control room, performed the ablation using a mean of 7.2Ϯ4.7 radiofrequency current applications (mean fluoroscopy time, 8.9Ϯ6.2 minutes; procedure duration, 145Ϯ43 minutes). Slow pathway ablation was achieved in 15 patients, whereas slow pathway modulation was the end point in the remaining patients. There were no complications. Conclusions-The Niobe magnetic navigation system is a new platform technology allowing remote-controlled navigation of an ablation catheter. In conjunction with a motor drive unit, this system was used successfully to perform completely remote-controlled mapping and ablation in patients with AVNRT.

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Treatment of Supraventricular Tachycardia Due to Atrioventricular Nodal Reentry by Radiofrequency Catheter Ablation of Slow-Pathway Conduction

Abstract: Catheter ablation of the atrial end of the slow pathway using radiofrequency current, guided by ASP potentials, can eliminate AVNRT with very little risk of atrioventricular block.

Cited by 1,072 publications

References 18 publications

Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node

Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

Initial Experience With Remote Catheter Ablation Using a Novel Magnetic Navigation System

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