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Journal of Cardiovascular... Mar 2024The mechanism of typical slow-fast atrioventricular nodal re-entrant tachycardia (AVNRT) and its anatomical and electrophysiological circuit inside the right atrium (RA)...
High-density mapping of Koch's triangle during sinus rhythm and typical atrioventricular nodal re-entrant tachycardia, integrated with direct recording of atrio-ventricular node structure potential.
BACKGROUND
The mechanism of typical slow-fast atrioventricular nodal re-entrant tachycardia (AVNRT) and its anatomical and electrophysiological circuit inside the right atrium (RA) and Koch's Triangle (KT) are not well known.
OBJECTIVE
To identify the potentials of the compact AV node and inferior extensions and to perform accurate mapping of the RA and KT in sinus rhythm (SR) and during AVNRT, to define the tachycardia circuit.
METHODS
Consecutive patients with typical AVNRT were enrolled in 12 Italian centers and underwent mapping and ablation by means of a basket catheter with small electrode spacing for ultrahigh-density mapping and a modified signal-filtering toolset to record the potentials of the AV nodal structures.
RESULTS
Forty-five consecutive cases of successful ablation of typical slow-fast AVNRT were included. The mean SR cycle length (CL) was 784.1 ± 6 ms and the mean tachycardia CL was 361.2 ± 54 ms. The AV node potential had a significantly shorter duration and higher amplitude in sinus rhythm than during tachycardia (60 ± 40 ms vs. 160 ± 40 ms, p < .001 and 0.3 ± 0.2 mV vs. 0.09 ± 0.12 mV, p < .001, respectively). The nodal potential duration extension was 169.4 ± 31 ms, resulting in a time-window coverage of 47.6 ± 9%. The recording of AV nodal structure potentials enabled us to obtain 100% coverage of the tachycardia CL during slow-fast AVNRT.
CONCLUSION
Detailed recording of the potentials of nodal structures is possible by means of multipolar catheters for ultrahigh-density mapping, allowing 100% of the AVNRT CL to be covered. These results also have clinical implications for the ablation of right-septal and para-septal arrhythmias.
Topics: Humans; Atrioventricular Node; Tachycardia, Atrioventricular Nodal Reentry; Catheter Ablation; Heart Atria; Electrodes
PubMed: 38185855
DOI: 10.1111/jce.16168 -
Journal of Molecular and Cellular... Aug 2016Background inward sodium current (IB,Na) that influences cardiac pacemaking has been comparatively under-investigated. The aim of this study was to determine for the...
Background inward sodium current (IB,Na) that influences cardiac pacemaking has been comparatively under-investigated. The aim of this study was to determine for the first time the properties and role of IB,Na in cells from the heart's secondary pacemaker, the atrioventricular node (AVN). Myocytes were isolated from the AVN of adult male rabbits and mice using mechanical and enzymatic dispersion. Background current was measured using whole-cell patch clamp and monovalent ion substitution with major voltage- and time-dependent conductances inhibited. In the absence of a selective pharmacological inhibitor of IB,Na, computer modelling was used to assess the physiological contribution of IB,Na. Net background current during voltage ramps was linear, reversing close to 0mV. Switching between Tris- and Na(+)-containing extracellular solution in rabbit and mouse AVN cells revealed an inward IB,Na, with an increase in slope conductance in rabbit cells at -50mV from 0.54±0.03 to 0.91±0.05nS (mean±SEM; n=61 cells). IB,Na magnitude varied in proportion to [Na(+)]o. Other monovalent cations could substitute for Na(+) (Rb(+)>K(+)>Cs(+)>Na(+)>Li(+)). The single-channel conductance with Na(+) as charge carrier estimated from noise-analysis was 3.2±1.2pS (n=6). Ni(2+) (10mM), Gd(3+) (100μM), ruthenium red (100μM), or amiloride (1mM) produced modest reductions in IB,Na. Flufenamic acid was without significant effect, whilst La(3+) (100μM) or extracellular acidosis (pH6.3) inhibited the current by >60%. Under the conditions of our AVN cell simulations, removal of IB,Na arrested spontaneous activity and, in a simulated 1D-strand, reduced conduction velocity by ~20%. IB,Na is carried by distinct low conductance monovalent non-selective cation channels and can influence AVN spontaneous activity and conduction.
Topics: Action Potentials; Algorithms; Animals; Atrioventricular Node; Computer Simulation; Electrophysiological Phenomena; Male; Mice; Models, Cardiovascular; Myocardium; Patch-Clamp Techniques; Rabbits; Sodium
PubMed: 27132017
DOI: 10.1016/j.yjmcc.2016.04.014 -
Herz Dec 2021Cardiac pacemakers are an extremely effective treatment for bradycardia but can, however, cause desynchronization of ventricular contraction leading to cardiomyopathy.... (Review)
Review
Cardiac pacemakers are an extremely effective treatment for bradycardia but can, however, cause desynchronization of ventricular contraction leading to cardiomyopathy. Pacing of the conduction system can prevent and even reverse desynchronization, which is impressively visible in echocardiography with speckle tracing. His' bundle and left bundle branch pacing requires a specific implantation technique, sheaths and leads which can achieve successful stimulation of the conduction system in up to 98% of cases. Data on conduction system pacing have been acquired in numerous studies but only a few randomized outcome studies. Therefore, in the current European guidelines His' bundle and left bundle branch pacing only have a low level recommendation. The guidelines recommend His' bundle pacing in patients in whom a coronary sinus lead cannot be implanted and in patients with permanent atrial fibrillation and planned atrioventricular (AV) node ablation for heart rate control. Additionally, conduction system pacing appears to be meaningful in patients with an AV block who require pacing of the ventricle for ≥20% of the time or who already show a slightly or moderately reduced left ventricular ejection fraction (36-50%). Even in patients scheduled for generator replacement who have developed a cardiac pacemaker-induced cardiomyopathy, the opportunity should not be missed to upgrade the system by implantation of a His' bundle electrode.
Topics: Atrioventricular Node; Bundle of His; Cardiac Pacing, Artificial; Electrocardiography; Humans; Stroke Volume; Treatment Outcome; Ventricular Function, Left
PubMed: 34766195
DOI: 10.1007/s00059-021-05080-9 -
Pflugers Archiv : European Journal of... Dec 2021The atrioventricular (AV) node is the only conduction pathway where electrical impulse can pass from atria to ventricles and exhibits spontaneous automaticity. This...
The atrioventricular (AV) node is the only conduction pathway where electrical impulse can pass from atria to ventricles and exhibits spontaneous automaticity. This study examined the function of the rapid- and slow-activating delayed rectifier K currents (I and I) in the regulation of AV node automaticity. Isolated AV node cells from guinea pigs were current- and voltage-clamped to record the action potentials and the I and I current. The expression of I or I was confirmed in the AV node cells by immunocytochemistry, and the positive signals of both channels were localized mainly on the cell membrane. The basal spontaneous automaticity was equally reduced by E4031 and HMR-1556, selective blockers of I and I, respectively. The nonselective β-adrenoceptor agonist isoproterenol markedly increased the firing rate of action potentials. In the presence of isoproterenol, the firing rate of action potentials was more effectively reduced by the I inhibitor HMR-1556 than by the I inhibitor E4031. Both E4031 and HMR-1556 prolonged the action potential duration and depolarized the maximum diastolic potential under basal and β-adrenoceptor-stimulated conditions. I was not significantly influenced by β-adrenoceptor stimulation, but I was concentration-dependently enhanced by isoproterenol (EC: 15 nM), with a significant negative voltage shift in the channel activation. These findings suggest that both the I and I channels might exert similar effects on regulating the repolarization process of AV node action potentials under basal conditions; however, when the β-adrenoceptor is activated, I modulation may become more important.
Topics: Action Potentials; Adrenergic beta-Agonists; Animals; Atrioventricular Node; Female; Guinea Pigs; Heart Atria; Heart Ventricles; Isoproterenol; Myocardium; Patch-Clamp Techniques; Potassium Channels
PubMed: 34704178
DOI: 10.1007/s00424-021-02617-z -
Circulation. Cardiovascular Genetics Apr 2015Several transcription factors regulate cardiac conduction system (CCS) development and function but the role of each in specifying distinct CCS components remains...
BACKGROUND
Several transcription factors regulate cardiac conduction system (CCS) development and function but the role of each in specifying distinct CCS components remains unclear. GATA-binding factor 6 (GATA6) is a zinc-finger transcription factor that is critical for patterning the cardiovascular system. However, the role of GATA6 in the embryonic heart and CCS has never been shown.
METHODS AND RESULTS
We report that Gata6 is expressed abundantly in the proximal CCS during midgestation in mice. Myocardial-specific deletion of the carboxyl zinc-finger of Gata6 induces loss of hyperpolarizing cyclic nucleotide-gated channel, subtype 4 staining in the compact atrioventricular node with some retention of hyperpolarizing cyclic nucleotide-gated channel, subtype 4 staining in the atrioventricular bundle, but has no significant effect on the connexin-40-positive bundle branches. Furthermore, myocardial-specific deletion of the carboxyl zinc-finger of Gata6 alters atrioventricular conduction in postnatal life as assessed by surface and invasive electrophysiological evaluation, as well as decreasing the number of ventricular myocytes and inducing compensatory myocyte hypertrophy. Myocardial-specific deletion of the carboxyl zinc-finger of Gata6 is also associated with downregulation of the transcriptional repressor ID2 and the cardiac sodium-calcium exchanger NCX1 in the proximal CCS, where GATA6 transactivates both of these factors. Finally, carboxyl zinc-finger deletion of Gata6 reduces cell-cycle exit of TBX3+ myocytes in the developing atrioventricular bundle during the period of atrioventricular node specification, which results in fewer TBX3+ cells in the proximal CCS of mature mutant mice.
CONCLUSIONS
GATA6 contributes to the development and postnatal function of the murine atrioventricular node by promoting cell-cycle exit of specified cardiomyocytes toward a conduction system lineage.
Topics: Animals; Atrioventricular Node; GATA6 Transcription Factor; Gene Expression Regulation, Developmental; Mice; Mice, Mutant Strains; Myocardium; Myocytes, Cardiac
PubMed: 25613430
DOI: 10.1161/CIRCGENETICS.113.000587 -
Herzschrittmachertherapie &... Jun 2022The atrioventricular (AV) valve plane and the central septum are of particular importance for electrophysiological diagnosis and interventional therapy of... (Review)
Review
The atrioventricular (AV) valve plane and the central septum are of particular importance for electrophysiological diagnosis and interventional therapy of supraventricular tachycardias because accessory electrical connections of various types may be present in addition to the specific conduction system. Although modern 3D electroanatomic reconstruction systems including high-density mapping can be of great assistance, detailed knowledge of the anatomic structures involved, their complex three-dimensional arrangement, and their electrical properties in conjunction with electrophysiological features of supraventricular arrhythmias is essential for safe and efficient electrophysiological treatment. The aim of this article is to present current anatomical, topographical, and electrophysiological findings against the background of historical, seminal, and still indispensable literature.
Topics: Accessory Atrioventricular Bundle; Atrioventricular Node; Catheter Ablation; Electrocardiography; Heart Conduction System; Humans; Tachycardia, Atrioventricular Nodal Reentry; Tachycardia, Supraventricular
PubMed: 35608665
DOI: 10.1007/s00399-022-00860-0 -
Heart, Lung & Circulation Sep 2017Atrioventricular node ablation (AVNA) is generally reserved for patients whose atrial fibrillation (AF) is refractory all other therapeutic options, since the recipients... (Review)
Review
Atrioventricular node ablation (AVNA) is generally reserved for patients whose atrial fibrillation (AF) is refractory all other therapeutic options, since the recipients will often become pacemaker dependent. In such patients, this approach may prove particularly useful, especially if a tachycardia-induced cardiomyopathy is suspected. Historically, an "ablate and pace" approach has involved AVNA and right ventricular pacing, with or without an atrial lead. There is also an evolving role for atrioventricular node ablation in patients with AF who require cardiac resynchronisation therapy for treatment of systolic heart failure. A mortality benefit over pharmacotherapy has been demonstrated in observational studies and this concept is being further investigated in multi-centre randomised control trials.
Topics: Atrial Fibrillation; Atrioventricular Node; Cardiac Pacing, Artificial; Cardiac Resynchronization Therapy; Catheter Ablation; Heart Rate; Humans
PubMed: 28687248
DOI: 10.1016/j.hlc.2017.05.124 -
Journal of the American Heart... Nov 2021
Topics: Arrhythmias, Cardiac; Atrioventricular Node; Catheter Ablation; Electrocardiography; Humans; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 34719243
DOI: 10.1161/JAHA.121.022811 -
Circulation. Arrhythmia and... May 2023Confirming the presence and participation of concealed nodo-ventricular (cNV) or concealed His-ventricular (cHV) pathways in tachyarrhythmias is challenging. We describe...
BACKGROUND
Confirming the presence and participation of concealed nodo-ventricular (cNV) or concealed His-ventricular (cHV) pathways in tachyarrhythmias is challenging. We describe novel observations to aid in diagnosing cNV or cHV pathways.
METHODS
We present 7 cases of cNV and cHV pathway-mediated arrhythmias and focus on several laboratory observations: (1) differential ventricular overdrive pacing (VOD) from the base versus apex, (2) response to His refractory premature ventricular complexes, (3) paradoxical atriohisian response (shorter atriohisian interval during tachycardia than that during sinus rhythm) in long RP tachycardia, and (4) the role of adenosine to aid in the diagnosis.
RESULTS
Three cases underwent differential VOD during tachycardia. All demonstrated a shorter postpacing interval minus tachycardia cycle length during basal pacing than apical pacing with one case exhibiting apical VOD results compatible with atrioventricular nodal reentrant tachycardia. Basal VOD was useful for localizing the ventricular connection in a case with cHV pathway. In 3 cases, His refractory premature ventricular complexes reset the tachycardia without conduction to the atrium, which excluded the involvement of an atrioventricular pathway or atrial tachycardia, or atrioventricular nodal reentrant tachycardia alone. One case had His refractory premature ventricular complexes followed by subsequent constant AA interval and then tachycardia termination, suggesting a bystander cNV pathway involvement. Two cNV pathway cases presented with long RP tachycardia had paradoxical atriohisian shortening of >15 ms, suggesting parallel activation of the atrium and the atrioventricular node. Adenosine terminated the tachycardia with retrograde block in 2 cases with cNV pathways but had no response on a cHV pathway.
CONCLUSIONS
cNV and cHV pathways mediated tachyarrhythmias can present with variable clinical presentations. We emphasize the important role of differential VOD sites, His refractory premature ventricular complexes that reset or terminate the tachycardia without conduction to the atrium, paradoxical atriohisian response in long RP tachycardia, and the use of adenosine for diagnosing cNV and cHV pathways.
Topics: Humans; Tachycardia, Atrioventricular Nodal Reentry; Atrioventricular Node; Tachycardia; Tachycardia, Supraventricular; Adenosine; Electrocardiography; Ventricular Premature Complexes; Cardiac Pacing, Artificial
PubMed: 37082968
DOI: 10.1161/CIRCEP.122.011771 -
Heart (British Cardiac Society) Aug 2022Knowledge of the anatomy of the 'conduction tissues' of the heart is a 20th century phenomenon. Although controversies still continue on the topic, most could have been... (Review)
Review
Knowledge of the anatomy of the 'conduction tissues' of the heart is a 20th century phenomenon. Although controversies still continue on the topic, most could have been avoided had greater attention been paid to the original descriptions. All cardiomyocytes, of course, have the capacity to conduct the cardiac impulse. The tissues specifically described as 'conducting' first generate the cardiac impulse, and then deliver it in such a fashion that the ventricles contract in orderly fashion. The tissues cannot readily be distinguished by gross inspection. Robust definitions for their recognition had been provided by the end of the first decade of the 20th century. These definitions retain their currency. The sinus node lies as a cigar-shaped structure subepicardially within the terminal groove. There is evidence that it is associated with a paranodal area that may have functional significance. Suggestions of dual nodes, however, are without histological confirmation. The atrioventricular node is located within the triangle of Koch, with significant inferior extensions occupying the atrial vestibules and with septal connections. The conduction axis penetrates the insulating plane of the atrioventricular junctions to continue as the ventricular pathways. Remnants of a ring of cardiomyocytes observed during development are also to be found within the atrial vestibules, particularly a prominent retroaortic remnant, although that their role has still to be determined. Application of the initial criteria for nodes and tracts shows that there are no special 'conducting tissues' in the pulmonary venous sleeves that might underscore the abnormal rhythm of atrial fibrillation.
Topics: Atrial Fibrillation; Atrioventricular Node; Heart Conduction System; Heart Rate; Humans; Sinoatrial Node
PubMed: 34969873
DOI: 10.1136/heartjnl-2021-320304