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Journal of Cardiovascular... Jun 2019
Topics: Animals; Atrioventricular Node; Gonadal Steroid Hormones; Heart; Heart Rate; Incidence; Progesterone; Rabbits; Torsades de Pointes
PubMed: 31006915
DOI: 10.1111/jce.13939 -
Journal of Interventional Cardiac... Jan 2016In contrast to the current textbook model and the current clinical index of dual pathway atrioventricular (AV) nodal conduction, here we summarize the discovery and... (Review)
Review
BACKGROUND
In contrast to the current textbook model and the current clinical index of dual pathway atrioventricular (AV) nodal conduction, here we summarize the discovery and validation of Zhang's phenomenon (originally His electrogram alternans) as a new index of dual pathway conduction. We also describe the new findings of transverse-versus-longitudinal electrical propagation within the AV node as the electrophysiological basis underlining this new index. Thus, a new index and a new model of dual pathway AV conduction are being developed.
METHODS
We have reviewed current literature and provided evidence supporting a new index and a new model of dual pathway AV conduction.
RESULTS
Recent data revealed that during fast pathway conduction, electrical excitation in the AV node propagates in a superior to inferior direction across AV conduction axis and fiber orientation to reach first the superior His bundle fibers. However, this transverse conduction can fail easily within the superior nodal domain at fast rates. The failing of transverse propagation permits electrical excitation formed at the posterior/inferior nodal region to propagate longitudinally along fiber orientation in a posterior to anterior direction through the inferior nodal domain to reach the inferior His bundle (slow pathway conduction). This transverse-versus-longitudinal electrical propagation within the AV node results in a functional dissociation in the distal node and formation of dual inputs into the His bundle, providing the electrophysiological basis for the formation of Zhang's phenomenon (His electrogram alternans).
CONCLUSIONS
Based on strong experimental data, a new index and a new model of dual pathway AV nodal conduction are emerging, although they are still awaiting clinical validation.
Topics: Accessory Atrioventricular Bundle; Atrioventricular Node; Electrophysiologic Techniques, Cardiac; Heart Conduction System; Humans; Models, Cardiovascular; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 26614299
DOI: 10.1007/s10840-015-0079-0 -
Circulation. Arrhythmia and... Nov 2016
Topics: Atrioventricular Node; Bundle of His; Heart Conduction System; Heel
PubMed: 27906656
DOI: 10.1161/CIRCEP.116.004719 -
Journal of Cardiovascular... Jul 2021The complex electrophysiological phenomena related to the atrioventricular node (AVN) are due to its complex anatomical structures. Aside from the inferior nodal...
INTRODUCTION
The complex electrophysiological phenomena related to the atrioventricular node (AVN) are due to its complex anatomical structures. Aside from the inferior nodal extension (INE), other node-like tissues, such as the retroaortic node (RN), have been described less extensively and may also share the mechanism of normal conduction and abnormal conduction in AVN re-entrant tachycardia.
METHODS
High-density sections of the entire AVN were obtained from rats and rabbits. Fibrosis was analyzed by Masson's trichrome staining. Connexin (Cx43, Cx40, and Cx45) and ion channel (Na 1.5, Ca 3.1, and HCN4) proteins were immunohistochemically labeled for the analysis of tissue features. Three-dimensional (3D) reconstruction of the AV junction was performed to clarify the relationships among different structures.
RESULTS
The RN expressed the same connexin isoforms as the compact node (CN) and INE. Na 1.5 labeling was observed at low levels in the CN, RN, and INE, where Ca 3.1 and HCN4 were expressed. The CN connected with the RN in a narrow strip pattern at the start of the CN. The RN presented as a shuttle shape and was the only tissue directly connected with the atrium in the anterior septum.
CONCLUSION
The RN connects with the AVN anatomically, suggesting that direct electrical conduction occurs between them. The entrance of the atria into the AVN is distal to the RN, which may form the fast AVN pathway.
Topics: Animals; Atrioventricular Node; Bundle of His; Heart Atria; Rabbits; Rats
PubMed: 34053145
DOI: 10.1111/jce.15117 -
The American Journal of Cardiology Jun 2020In a 27-year-old man the electrocardiogram suggests increased vagal tone, and not intrinsic atrioventricular nodal disease, as the cause of transient atrioventricular...
In a 27-year-old man the electrocardiogram suggests increased vagal tone, and not intrinsic atrioventricular nodal disease, as the cause of transient atrioventricular block.
Topics: Adult; Atrioventricular Block; Atrioventricular Node; Electrocardiography; Electrocardiography, Ambulatory; Humans; Male; Physical Exertion; Syncope; Vagus Nerve
PubMed: 32279837
DOI: 10.1016/j.amjcard.2020.02.009 -
Journal of Cardiovascular... Sep 2019
Topics: Arrhythmias, Cardiac; Atrioventricular Node; Humans; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 31231872
DOI: 10.1111/jce.14044 -
Circulation. Arrhythmia and... Jan 2020Current maneuvers for differentiation of atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reentry tachycardia (AVRT) lack sensitivity and... (Comparative Study)
Comparative Study
BACKGROUND
Current maneuvers for differentiation of atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reentry tachycardia (AVRT) lack sensitivity and specificity for AVRT circuits located away from the site of pacing. We hypothesized that a premature His complex (PHC) will always perturb AVRT because the His bundle is obligatory to the circuit. Further, AVNRT could not be perturbed by a late PHC (≤20 ms ahead of the His) due to the retrograde His conduction time. Earlier PHCs can advance the AVNRT circuit but only by a quantity less than the prematurity of the PHC.
METHODS
High-output pacing at the distal His location delivered PHCs. AVRT was predicted when late PHCs perturbed tachycardia or when earlier PHCs led to atrial advancement by an amount equal or greater than the degree of PHC prematurity.
RESULTS
Among the 73 supraventricular tachycardias, the test accurately predicted AVRT (n=29) and AVNRT (n=44) in all cases. Late PHC advanced the circuit in all 29 AVRTs and none of the AVNRTs (sensitivity and specificity, 100%). With earlier PHCs, the degree of atrial advancement was equal or greater than the PHC prematurity in 26/29 AVRTs and none of the AVNRTs (90% sensitivity and 100% specificity). The mean prematurity of the PHC required to perturb AVNRT was 48 ms (range, 28-70 ms) and the advancement less than the prematurity of the PHC (mean, 32 ms; range, 18-54 ms).
CONCLUSIONS
The responses to PHCs distinguished AVRT and AVNRT with 100% specificity and sensitivity.
Topics: Adult; Atrioventricular Node; Bundle of His; Cohort Studies; Diagnosis, Differential; Electrocardiography; Female; Heart Conduction System; Humans; Male; Middle Aged; Retrospective Studies; Sensitivity and Specificity; Tachycardia, Atrioventricular Nodal Reentry; Tachycardia, Supraventricular; Ventricular Premature Complexes
PubMed: 31934781
DOI: 10.1161/CIRCEP.119.007796 -
Journal of Interventional Cardiac... Aug 2015The sinoatrial node (SAN) and the atrioventricular node (AVN) are the anatomical and functional regions of the heart which play critical roles in the generation and... (Review)
Review
The sinoatrial node (SAN) and the atrioventricular node (AVN) are the anatomical and functional regions of the heart which play critical roles in the generation and conduction of the electrical impulse. Their functions are ensured by peculiar structural cytological properties and specific collections of ion channels. Impairment of SAN and AVN activity is generally acquired,but in some cases familial inheritance has been established and therefore a genetic cause is involved. In recent years, combined efforts of clinical practice and experimental basic science studies have identified and characterized several causative gene mutations associated with the nodal syndromes. Channelopathies, i.e., diseases associated with defective ion channels, remain the major cause of genetically determined nodal arrhythmias; however, it is becoming increasingly evident that mutations in other classes of regulatory and structural proteins also have profound pathophysiological roles. In this review, we will present some aspects of the genetic identification of the molecular mechanism underlying both SAN and AVN dysfunctions with a particular focus on mutations of the Na, pacemaker (HCN), and Ca channels. Genetic defects in regulatory proteins and calcium-handling proteins will be also considered. In conclusion, the identification of the genetic defects associated with familial nodal dysfunction is an essential step for implementing an appropriate therapeutic treatment.
Topics: Arrhythmias, Cardiac; Atrioventricular Node; Channelopathies; Genetic Predisposition to Disease; Humans; Ion Channels; Mutation; Sinoatrial Node
PubMed: 25863800
DOI: 10.1007/s10840-015-9998-z -
Heart Rhythm Nov 2017
Topics: Arrhythmias, Cardiac; Atrioventricular Node; Catheter Ablation; Cicatrix; Electrocardiography; Humans; Inflammation; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 28843421
DOI: 10.1016/j.hrthm.2017.08.020 -
Journal of the American Heart... Dec 2021Background Left atrial (LA) and right ventricular (RV) performance play an integral role in the pathophysiology and prognosis of heart failure. We hypothesized that...
Background Left atrial (LA) and right ventricular (RV) performance play an integral role in the pathophysiology and prognosis of heart failure. We hypothesized that subclinical left ventricular dysfunction adversely affects LA/RV geometry and function even in a preclinical setting. This study aimed to investigate the atrioventricular and ventricular functional interdependence in a community-based cohort without overt cardiovascular disease. Methods and Results Left ventricular global longitudinal strain (LVGLS), RV free-wall longitudinal strain and LA phasic strain were assessed by speckle-tracking echocardiography in 1080 participants (600 men; 62±12 years) between 2014 and 2018. One hundred and forty-three participants (13.2%) had an abnormal LVGLS (>-18.6%). LA reservoir strain, conduit strain, and RV free-wall longitudinal strain were significantly decreased in abnormal LVGLS group compared with normal LVGLS group (all <0.001). LA and RV dysfunction (LA reservoir strain<31.4% and RVLS>-19.2%) were present in 18.9% and 19.6% of participants with abnormal LVGLS. Decreased LVGLS was associated with worse LA reservoir strain, conduit strain and RV free-wall longitudinal strain (standardized β=-0.20, -0.19 and 0.11 respectively, all <0.01) independent of cardiovascular risk factors. LA and/or RV dysfunction concomitant with abnormal LVGLS carried significantly increased risk of elevated B-type natriuretic peptide levels (>28.6 pg/mL for men and >44.4 pg/mL for women) compared with normal LVGLS (odds ratio, 2.01; =0.030). Conclusions LA/RV dysfunction was present in 20% individuals with abnormal LVGLS and multi-chamber impairment was associated with elevated B-type natriuretic peptide level, which may provide valuable insights for a better understanding of atrioventricular and ventricular interdependence and possibly heart failure preventive strategies.
Topics: Aged; Atrioventricular Node; Heart Diseases; Humans; Middle Aged; Ventricular Function
PubMed: 34775816
DOI: 10.1161/JAHA.121.021624