Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.

Akhtar, Masood; Jazayeri, Mohammad; Sra, Jasbír; Blanck, Zalmen; Deshpande, Sanjay; Dhala, Anwer

doi:10.1161/01.cir.88.1.282

Cited by 189 publications

(79 citation statements)

References 81 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.

112

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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.

112

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“…The prevalence of PSVT is approximately 2-3 per 1,000 persons and the incidence is 35 per 100,000 personyears in the general population. 31, 32 There are 2 main causes Based on these findings, the CHADS2 score has been used for risk stratification of stoke, and AF patients with a CHADS2 score ≥2 should be treated with anticoagulation therapy. In the Framingham Heart Study, subjects with AF had markedly reduced survival compared with subjects without AF, with multivariate-adjusted ORs for death of 1.5 in men and 1.9 in women.…”

Section: Supraventricular Tachyarrhythmiasmentioning

confidence: 99%

Epidemiology of Arrhythmias and Sudden Cardiac Death in Asia

Murakoshi

Aonuma

2013

Circ J

125

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“…[1][2][3][4] It predominantly includes two forms of tachycardia (atrioventricular (AV) nodal re-entry and AV re-entry) and occurs in 35 out of 100,000 person years, with a prevalence of 2.29 per 1,000 people. 5 It is sometimes possible for patients to terminate the tachycardia themselves by simple manoeuvres that change the properties of the AV node.…”

Section: Introductionmentioning

confidence: 99%

Are patients admitted to emergency departments with regular supraventricular tachycardia (SVT) treated appropriately?

et al. 2013

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-Regular supraventricular tachycardia (SVT) is frequently encountered in clinical practice. Guidelines are available from the National Service Framework (NSF) for the treatment of patients attending emergency departments (ED) with SVT. These recommend a thyroid-function test (TFT) and arrhythmia electrocardiography (ECG), and referral to a heartrhythm specialist on discharge. Hospital admission is rarely required. In our multicentre study, we examined the implementation of these guidelines among patients attending the ED with SVT. Only 34% of patients had specialist referrals, with an average wait of 50.3 days (the majority of delays resulted from referral requests from general practitioners). A history of previous SVT, the mode of tachycardia termination, patient age and/or comorbidities were similar for the 27 (23.5%) patients who were admitted overnight. Of these, 15 (13%) of the total 115 patients who attended ED with regular SVT were referred for Holter monitoring despite having ECGs demonstrating arrhythmia. Low referral rates, unnecessary investigations and admissions indicate a need for improvement for better patient care and to minimise healthcare costs. We have formulated a standard operating procedure, which will be available via the College of Emergency Medicine website.

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Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.

Cited by 189 publications

References 81 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

Epidemiology of Arrhythmias and Sudden Cardiac Death in Asia

Are patients admitted to emergency departments with regular supraventricular tachycardia (SVT) treated appropriately?

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