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The Journal of Clinical Investigation May 1983Amiodarone was selectively perfused into the sinus node artery and atrioventricular node artery of 51 dogs. Amiodarone had an immediate negative chronotropic and...
Amiodarone was selectively perfused into the sinus node artery and atrioventricular node artery of 51 dogs. Amiodarone had an immediate negative chronotropic and dromotropic effect. Threshold concentration was 2.5 micrograms/ml. 25 and 50 micrograms/ml of amiodarone injected into the sinus node artery slowed the heart by 25.6 +/- 3.1 and 33.7 +/- 2.6 beats/min (mean +/- 1 SEM), respectively. Amiodarone 25 and 50 micrograms/ml injected into the AV node artery during AV junctional rhythm slowed the AV junctional pacemaker by 12.2 +/- 1.8 and 17.4 +/- 1.7 beats/min, respectively. Injections of amiodarone into the AV node artery during sinus rhythm regularly increased AV conduction time sometimes causing 2 degrees AV block at the highest concentration used. Impaired conduction was exclusively measured at the level of the A-H interval in the His electrogram. Neither atropine nor propranolol prevented the negative chronotropic effects of amiodarone. Amiodarone had no significant effect on sinus node response to either stellate stimulation or intranodal administration of norepinephrine. The negative chronotropic action of amiodarone was significantly enhanced when amiodarone was administered in a perfusate containing low (0.6 mM) instead of normal calcium. Taken collectively these observations indicate that amiodarone has immediate depressant electrophysiologic effects on both the sinus node and the AV junction and that these early effects might involve the blockade of the slow channel.
Topics: Amiodarone; Animals; Atrioventricular Node; Autonomic Nerve Block; Benzofurans; Calcium; Depression, Chemical; Dogs; Dose-Response Relationship, Drug; Electric Conductivity; Female; Heart Conduction System; Heart Rate; Male; Norepinephrine; Sinoatrial Node
PubMed: 6853721
DOI: 10.1172/jci110899 -
Revista Portuguesa de Cardiologia Feb 2021In patients with supraventricular arrhythmias and high ventricular rate, unresponsive to rate and rhythm control therapy or catheter ablation, atrioventricular (AV) node...
INTRODUCTION
In patients with supraventricular arrhythmias and high ventricular rate, unresponsive to rate and rhythm control therapy or catheter ablation, atrioventricular (AV) node ablation may be performed.
OBJECTIVES
To assess long-term outcomes after AV node ablation and to analyze predictors of adverse events.
METHODS
We performed a detailed retrospective analysis of all patients who underwent AV node ablation between February 1997 and February 2019, in a single Portuguese tertiary center.
RESULTS
A total of 123 patients, mean age 69±9 years and 52% male, underwent AV node ablation. Most of them presented atrial fibrillation at baseline (65%). During a median follow-up of 8.5 years (interquartile range 3.8-11.8), patients improved heart failure (HF) functional class (NYHA class III-IV 46% versus 13%, p=0.001), and there were reductions in hospitalizations due to HF (0.98±1.3 versus 0.28±0.8, p=0.001) and emergency department (ED) visits (1.1±1 versus 0.17±0.7, p=0.0001). There were no device-related complications. Despite permanent pacemaker stimulation, left ventricular ejection fraction did not worsen (47±13% vs. 47%±12, p=0.63). Twenty-eight patients died (23%). The number of ED visits due to HF before AV node ablation was an independent predictor of the composite adverse outcome (OR 1.8, 95% CI 1.24-2.61, p=0.002).
CONCLUSIONS
Despite pacemaker dependency, the clinical benefit of AV node ablation persisted at long-term follow-up. The number of ED visits due to HF before AV node ablation was an independent predictor of the composite adverse outcome. AV node ablation should probably be considered earlier in the treatment of patients with supraventricular arrhythmias and HF, especially in cases that are unsuitable for selective ablation of the specific arrhythmia.
Topics: Aged; Atrial Fibrillation; Atrioventricular Node; Catheter Ablation; Female; Humans; Male; Middle Aged; Portugal; Retrospective Studies; Stroke Volume; Ventricular Function, Left
PubMed: 33422375
DOI: 10.1016/j.repc.2020.05.016 -
Journal of the American College of... Mar 1991The "corridor" operation is designed to restore sinus rhythm to patients with atrial fibrillation by electrically isolating the sinus node, a band of atrial tissue and...
The "corridor" operation is designed to restore sinus rhythm to patients with atrial fibrillation by electrically isolating the sinus node, a band of atrial tissue and the atrioventricular (AV) node from the remaining atrial tissue. Nine patients with drug-refractory atrial fibrillation underwent this operation; four patients had chronic atrial fibrillation and five had paroxysmal atrial fibrillation; the mean duration of symptoms was 12 +/- 8 years. Patient ages ranged from 25 to 68 years (mean 48 +/- 12). At preoperative electrophysiologic study, no patient had evidence of an accessory AV pathway or AV node reentry. Sinus node recovery time could not be determined in five patients because of recurrent atrial fibrillation during or before programmed stimulation. At operation the corridor of atrial tissue connecting the sinus and AV nodes was successfully isolated from the remaining left and right atrial tissue in all patients. One patient required early reoperation for recurrent atrial fibrillation before hospital discharge. At the predischarge electrophysiologic study, the corridor remained isolated in all patients except for one patient who had intermittent conduction between the corridor and excluded right atrium. One patient had nonsustained atrial fibrillation and one had atrial tachycardia evident in the corridor. Atypical AV node reentry of uncertain significance was induced in one other patient. Over a total follow-up of 191 patient months (mean 21 +/- 20), seven patients remained free of atrial fibrillation. Two patients had recurrent atrial fibrillation, which in one patient was effectively controlled by a single antiarrhythmic agent. A permanent pacemaker was implanted in four patients for sinus node dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
Topics: Arrhythmia, Sinus; Atrial Fibrillation; Atrioventricular Node; Cardiac Pacing, Artificial; Cryosurgery; Electrophysiology; Female; Humans; Male; Middle Aged; Postoperative Complications; Sinoatrial Node
PubMed: 1999635
DOI: 10.1016/0735-1097(91)90881-9 -
JACC. Clinical Electrophysiology Mar 2023
Topics: Humans; Bundle of His; Heart Conduction System; Atrioventricular Node
PubMed: 36752481
DOI: 10.1016/j.jacep.2022.11.011 -
Channels (Austin, Tex.) Jan 2017
Topics: Action Potentials; Anions; Atrioventricular Node; Ions; Sinoatrial Node; Sodium
PubMed: 27367468
DOI: 10.1080/19336950.2016.1207476 -
Revista Espanola de Cardiologia Nov 2003Concomitant with the development of catheter ablation techniques for the treatment of atrial arrhythmias, there has been renewed interest in the morphologic arrangement... (Review)
Review
Concomitant with the development of catheter ablation techniques for the treatment of atrial arrhythmias, there has been renewed interest in the morphologic arrangement of the cardiac conduction system. The first descriptions of the anatomy of the nodes and atrioventricular conduction system appeared nearly 100 years ago. Since then the subject has been controversial, possibly because of the early researchers' imprecise knowledge of histology. The components and structure of the specific conduction system in humans are similar to those found in commonly used laboratory animals. The conduction system is composed of specialized myocytes. Its atrial components, the sinus node and the atrioventricular node, are in contact with atrial myocardium. The His bundle penetrates the right fibrous trigone, then divides into two specialized ventricular bundle branches (right and left), which also are surrounded by a fibrous sheath that separates the specialized myocytes from the ordinary myocardium. Only at the distal ramifications of the bundle branches do the fibrous sheaths disappear, allowing continuity with the ventricular myocardium. Knowledge of the specialized myocardium can help in the development of potentially useful therapies for some forms of cardiac arrhythmia.
Topics: Atrioventricular Node; Heart; Heart Conduction System; Humans; Sinoatrial Node
PubMed: 14622540
DOI: 10.1016/s0300-8932(03)77019-5 -
Clinical Cardiology Apr 1993Normal anatomic and histologic features of the atrioventricular junction (transitional cell zone, atrioventricular node, penetrating portion of bundle) and the... (Review)
Review
Normal anatomic and histologic features of the atrioventricular junction (transitional cell zone, atrioventricular node, penetrating portion of bundle) and the bifurcation of the penetrating portion into bundle branches are reviewed. Terminal ventricular Purkinje fibers are also discussed.
Topics: Atrioventricular Node; Bundle of His; Heart Conduction System; Humans; Purkinje Fibers
PubMed: 8458115
DOI: 10.1002/clc.4960160410 -
Journal of the American College of... Dec 1997This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node...
OBJECTIVES
This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node reentrant tachycardia.
BACKGROUND
Although adenosine is known to depress conduction through the AV node, the relative sensitivity to adenosine of the anterograde fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been studied.
METHODS
Sixteen patients with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients were given incremental doses of adenosine during atrial pacing.
RESULTS
In 14 of 16 patients with dual-AV node physiology, administration of small doses of adenosine during atrial pacing led consistently to transient block of impulse conduction in the fast pathway before block in the slow pathway, resulting in abrupt prolongation of the AH interval with continued 1:1 AV conduction. The mean (+/- SD) doses of adenosine required to cause conduction block in the fast and slow pathways were 2.7 +/- 3.0 and 7.2 +/- 4.7 mg, respectively (p = 0.004). In 9 of 16 patients, administration of low dose adenosine led to initiation of AV node reentrant tachycardia. The control patients showed no abrupt increases in AH interval with administration of adenosine during atrial pacing.
CONCLUSIONS
In most patients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more sensitive than the slow pathway to the effects of adenosine.
Topics: Adenosine; Atrioventricular Node; Cardiac Catheterization; Cardiac Pacing, Artificial; Case-Control Studies; Catheter Ablation; Female; Humans; Male; Middle Aged; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 9385907
DOI: 10.1016/s0735-1097(97)00386-0 -
Heart (British Cardiac Society) Jul 1997
Topics: Animals; Atrioventricular Node; Catheter Ablation; Electrophysiology; Humans; Tachycardia, Atrioventricular Nodal Reentry
PubMed: 9290387
DOI: 10.1136/hrt.78.1.1 -
Cardiovascular Research Feb 2014A recent genome-wide association study identified a susceptibility locus for atrial fibrillation at the KCNN3 gene. Since the KCNN3 gene encodes for a small conductance...
BACKGROUND
A recent genome-wide association study identified a susceptibility locus for atrial fibrillation at the KCNN3 gene. Since the KCNN3 gene encodes for a small conductance calcium-activated potassium channel, we hypothesized that overexpression of the SK3 channel increases susceptibility to cardiac arrhythmias.
METHODS AND RESULTS
We characterized the cardiac electrophysiological phenotype of a mouse line with overexpression of the SK3 channel. We generated homozygote (SK3(T/T)) and heterozygote (SK3(+/T)) mice with overexpression of the channel and compared them with wild-type (WT) controls. We observed a high incidence of sudden death among SK3(T/T) mice (7 of 19 SK3(T/T) mice). Ambulatory monitoring demonstrated that sudden death was due to heart block and bradyarrhythmias. SK3(T/T) mice displayed normal body weight, temperature, and cardiac function on echocardiography; however, histological analysis demonstrated that these mice have abnormal atrioventricular node morphology. Optical mapping demonstrated that SK3(T/T) mice have slower ventricular conduction compared with WT controls (SK3(T/T) vs. WT; 0.45 ± 0.04 vs. 0.60 ± 0.09 mm/ms, P = 0.001). Programmed stimulation in 1-month-old SK3(T/T) mice demonstrated inducible atrial arrhythmias (50% of SK3(T/T) vs. 0% of WT mice) and also a shorter atrioventricular nodal refractory period (SK3(T/T) vs. WT; 43 ± 6 vs. 52 ± 9 ms, P = 0.02). Three-month-old SK3(T/T) mice on the other hand displayed a trend towards a more prolonged atrioventricular nodal refractory period (SK3(T/T) vs. WT; 61 ± 1 vs. 52 ± 6 ms, P = 0.06).
CONCLUSION
Overexpression of the SK3 channel causes an increased risk of sudden death associated with bradyarrhythmias and heart block, possibly due to atrioventricular nodal dysfunction.
Topics: Action Potentials; Animals; Atrioventricular Node; Bradycardia; Cardiac Pacing, Artificial; Connexin 43; Death, Sudden, Cardiac; Electrocardiography, Ambulatory; Genetic Predisposition to Disease; Heart Block; Heterozygote; Homozygote; Mice; Mice, Transgenic; Phenotype; Small-Conductance Calcium-Activated Potassium Channels; Time Factors; Up-Regulation; Voltage-Sensitive Dye Imaging
PubMed: 24296650
DOI: 10.1093/cvr/cvt269