Physiologic Evidence for a Dual A-V Transmission System

Moe, Gordon K.; Preston, James B.; Burlington, H.

doi:10.1161/01.res.4.4.357

Cited by 459 publications

(127 citation statements)

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“…It is now possible to extend our observations in man by recording extracellular action potentials from several specialized areas along the A-V conduction system." 1 The results of the present study relate closely to the reports of Moe and co-workers,3 Hoffman and associates,2 and Moore,4 despite the fact that obvious differences in methodology exist between this clinical report and their animal experiments. Among these differences is the fact that in the aforementioned studies the basic driving rate of the atrium was controlled while in this study premature atrial stimulation was performed during sinus rhythm.…”

Section: Discussionsupporting

confidence: 90%

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A Study of Atrioventricular Conduction in Man Using Premature Atrial Stimulation and His Bundle Recordings

et al. 1969

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SUMMARYIn 20 subjects the effects of controlled premature atrial stimulation on atrioventricular conduction was studied using an electrode catheter technic for recording electrical activity of specialized conducting fibers. recording the electrical activity of the specialized conduction system.10' 1 Methods Right heart catheterization was performed on 20 subjects in the post-absorptive, nonsedated state. All subjects were in normal sinus rhythm at the time of study. Using local anesthesia, a tripolar electrode catheter* was percutaneously introduced into the right femoral vein and fluoroscopically positioned across the tricuspid valve. This catheter was used to record A-V nodal, His bundle, and right bundle-branch potentials as described in previous communications.10' 11 The proximal terminals of the electrode catheter were plugged into a multichannel distribution switch boxt which permitted the selection of any two electrodes for bipolar recordings, Each channel of the distribution switch box was led into the AC input of an ECG preamplifier. The filter frequencies of the ECG preamplifier were set at 40

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Section: Discussionsupporting

confidence: 90%

“…The filter frequencies of the ECG preamplifier were set at 40 and 500 cps. In most studies three simultaneous bipolar electrograms were recorded using electrodes 1 .p '4 ,. P'I…”

mentioning

confidence: 99%

A Study of Atrioventricular Conduction in Man Using Premature Atrial Stimulation and His Bundle Recordings

et al. 1969

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“…The reason for this finding in our mouse model remains to be clarified. Faster AV-nodal conduction properties and unchanged or even elevated AV-nodal refractory period are not a necessarily contradictory finding, but a common pathophysiological phenomenon in arrhythmias involving fast-conducting AV-nodal pathways (27,28).…”

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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“…1940 sonrasında reentry mekanizmasının atriyoventrilüer (AV) nodda yerleştiği tespit edildi [6]. İlerleyen yıllarda yapılan hayvan çalışmaları sayesinde AV nodda ikili yolak olduğu ortaya konuldu [7,8]. İnsanlarda yapılan elektrofiyolojik çalışmalarda, oluşturulan bazı atriyal erken vuruların His demetini depolarize etmeden, AV nod refrakter durumda iken sürekli taşikardilere neden olduğu tespit edildi [9].…”

Section: Tarihçeunclassified

Atriyoventriküler nodal reenteran taşikardi: Patofizyolojiden tedaviye

Yontar¹,

Tandoğan²

2012

CMJ

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ÖzetSupraventriküler taşikardiler; tüm yaş gruplarını etkileyebilen, yaşam kalitesini kayda değer derecede kötüleştirebilen bir hastalık grubudur. Bu grupta sınıflandırılan taşikardi tipleri arasında en sık gözleneni Atriyoventriküler Nodal Reenteran Taşikardi olarak tespit edilmiştir. Derlememizin amacı, sık gözlenen bu aritminin oluş mekanizmalarını ve tedavisini kısa ancak anlaşılır bir şekilde özetleyebilmektir.Anahtar sözcükler: Supraventriküler taşikardi, yeniden giriş, ikili AV yolak Abstract Supraventricular tacycardias are a group of arrhytmias which may affect all age groups and cause remarkable recession in life quality. Atrioventricular nodal reentry tachycardia is the most common observed arrhythmia in this group. Aim of current review is to summarize the pathophysiologial basis and treatment methods in a brief and perceptible way. GirişSupraventriküler taşikardiler (SVT); tüm yaş gruplarını etkileyebilen, yaşam kalitesini kayda değer derecede kötüleştirebilen bir hastalık grubudur. Genellikle eşlik eden diğer hastalığı ve yapısal kalp hastalığından yoksun kişilerde ortaya çıkarlar [1]. Amerika Birleşik Devletleri'nde yapılan bir araştırmaya göre [2] SVT insidansı 36/100.000 kişi/yıl, prevalansı ise 2,29/1000 kişidir. Buna göre sadece Amerika Birleşik Devletleri'nde; yaklaşık 570.000 SVT hastası varken bu hastalara yılda 89.000 kişinin daha eklendiği tahmin edilmektedir. SVT başlığı altında incelenen taşikardilerin prevalansı değişkenlik göstermektedir. 1991 ve 2003 yılları arasında kateter ablasyonu yapılan hastaların tarandığı bir çalışmada [3]; atriyal fibrilasyon, atriyal flutter ve uygunsuz sinüs taşikardisi dışlandığında, en sık gözlenen taşikardi %56 sıklıkla atriyoventriküler nodal reenteran taşikardi (AVNRT), ikincisi ise %27 sıklıkla atriyoventriküler reenteran taşikardi (AVRT) olmuştur. TarihçeAVNRT, dar QRS kompleksli, düzenli taşikardinin en sık sebebidir. Bu aritminin altında yatan "reentry" (yeniden giriş) mekanizması ilk olarak 1900'lü yılların başında ortaya atılmış ve bir çok araştırmacı bunun üzerinde çalışmıştır [4,5]. 1940 sonrasında reentry mekanizmasının atriyoventrilüer (AV) nodda yerleştiği tespit edildi [6]. İlerleyen yıllarda yapılan hayvan çalışmaları sayesinde AV nodda ikili yolak olduğu ortaya konuldu [7,8]. İnsanlarda yapılan elektrofiyolojik çalışmalarda, oluşturulan bazı atriyal erken vuruların His demetini depolarize etmeden, AV nod refrakter durumda iken sürekli taşikardilere neden olduğu tespit edildi [9].

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Physiologic Evidence for a Dual A-V Transmission System

Cited by 459 publications

References 0 publications

A Study of Atrioventricular Conduction in Man Using Premature Atrial Stimulation and His Bundle Recordings

A Study of Atrioventricular Conduction in Man Using Premature Atrial Stimulation and His Bundle Recordings

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

Atriyoventriküler nodal reenteran taşikardi: Patofizyolojiden tedaviye

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