Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: Role of the accessory pathway

Waspe, Lawrence E.; Brodman, Richard; Kim, Soo G.; Fisher, John D.

doi:10.1016/0002-8703(86)90342-x

Cited by 69 publications

(19 citation statements)

References 28 publications

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“…This condition can result in life-threatening ventricular tachycardias and sudden arrhythmic cardiac death due to fast conduction of supraventricular arrhythmias to the ventricles (34,35). In analogy, induction of ventricular tacharrhythmias can be observed under accelerated AV-nodal conduction (36).…”

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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“…Fre quent atrioventricular reciprocating tachycar dia may result in ischemia of the atrium and changes in the structure of the atrial wall. Sev eral investigators reported that surgical or catheter ablation of accessory pathways abol ished atrioventricular reciprocating tachycar dia and reduced the incidence of paroxysmal AF [13,19]. This observation supports the concept that atrioventricular reciprocating tachycardia contributes to the pathogenesis of AF.…”

Section: Discussionmentioning

confidence: 70%

Electrophysiological Properties in Paroxysmal Atrial Fibrillation Complicated with the Wolff-Parkinson-White Syndrome: Comparison with Paroxysmal Atrial Fibrillation Alone

et al. 1994

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Electrophysiological studies were performed in 26 patients with atrial fibrillation (AF). Thirteen patients had the Wolff-Parkinson-White (WPW) syndrome (group A), and another 13 patients did not have the WPW syndrome (group B). The right atrium effective refractory period was significantly shorter in group A than in group B. The wavelength index which was defined as the ratio of the refractory period to the conduction delay was significantly lower in group A than in group B. Accordingly, patients in group A had a greater tendency to produce atrial reentry than those in group B.

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“…Es wird angenommen, daB bei der Mehrzahl der Patienten mit WPW-Syndrom das Vorhoffiimmern aus einer orthodromen AV-Reentry-Tachykardie hervorgeht [39]. Nach erfolgreicher Ablation einer akzessorischen Leitungsbahn liegt das Risiko des Wiederauftretens von Vorhoffiimmern bei 6 bis 10% [14,37,46] Tachykardie, einer AV-Reentry-Tachykardie auf dem Boden einer akzessorischen Leitungsbahn, von typischem Vorhofflattern oder einer ektopen atrialen Tachykardie gefahndet werden. Jais et al [17] …”

Section: Derzeitige M6glichkeiten Der Katheterablation Ron Vorhofflimunclassified

Radiofrequenz-Katheterablation von Vorhofflattern und Vorhofflimmern

Reithmann

Hoffmann

Steinbeck

1998

Herz

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Radiofrequency catheter ablation is now considered as a curative approach in patients with typical atrial flutter. Typical atrial flutter is due to a macrore-entrant circuit within the right atrium and it can be eliminated by a linear lesion in the isthmus between the tricuspid annulus and the vena cava inferior. The electrophysiological criterion of a bidirectional isthmus block has been shown to reduce the recurrence rate of atrial flutter after catheter ablation, thus achieving long-term cure of typical atrial flutter. Acute success rates of 85 to 90% and recurrence rates of 10 to 15% have been reported. The risk of paroxysmal atrial fibrillation continues to be clinically relevant in patients who underwent successful ablation of atrial flutter, in particular in patients with previously documented atrial fibrillation. The incidence of a new onset of atrial fibrillation after ablation of atrial flutter seems to be approximately 20%. Isthmus ablation has also been shown to be beneficial for the majority of patients with typical atrial flutter and atrial fibrillation: In addition to an elimination of typical atrial flutter the isthmus ablation apparently reduces the incidence of paroxysmal atrial fibrillation. At present, atrial fibrillation can only be treated by catheter ablation as a curative approach in the rare cases where an accessory pathway, an AV nodal re-entrant tachycardia, typical atrial flutter or an ectopic atrial tachycardia is the induction mechanism of the atrial fibrillation. The majority of patients with atrial fibrillation is apparently not amenable to a curative local ablation. While AV junction ablation and AV node modification can palliate some of the symptoms of atrial fibrillation by a control of ventricular rate, the arrhythmia persists with the loss of AV synchrony and continued risk of thromboembolism. The surgical MAZE procedure implies a compartimentation of the atria by surgical incisions resulting in areas to small to sustain the arrhythmia. Based on this procedure experimental and clinical studies are currently performed in order to develop catheter ablation cure of atrial fibrillation.

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Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: Role of the accessory pathway

Cited by 69 publications

References 28 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 Properties in Paroxysmal Atrial Fibrillation Complicated with the Wolff-Parkinson-White Syndrome: Comparison with Paroxysmal Atrial Fibrillation Alone

Radiofrequenz-Katheterablation von Vorhofflattern und Vorhofflimmern

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