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Atrial Refractoriness (atrial + refractoriness)

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Medical Sciences	100%

Selected Abstracts

Identification and Characterization of Atrioventricular Parasympathetic Innervation in Humans

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2002
KARA J. QUAN M.D.
AV Parasympathetic Innervation.Introduction: We hypothesized that in humans there is an epicardial fat pad from which parasympathetic ganglia supply the AV node. We also hypothesized that the parasympathetic nerves innervating the AV node also innervate the right atrium, and the greatest density of innervation is near the AV nodal fat pad. Methods and Results: An epicardial fat pad near the junction of the left atrium and right inferior pulmonary vein was identified during cardiac surgery in seven patients. A ring electrode was used to stimulate this fat pad intraoperatively during sinus rhythm to produce transient complete heart block. Subsequently, temporary epicardial wire electrodes were sutured in pairs on this epicardial fat pad, the high right atrium, and the right ventricle by direct visualization during coronary artery bypass surgery in seven patients. Experiments were performed in the electrophysiology laboratory 1 to 5 days after surgery. Programmed atrial stimulation was performed via an endocardial electrode catheter advanced to the right atrium. The catheter tip electrode was moved in 1-cm concentric zones around the epicardial wires by fluoroscopic guidance. Atrial refractoriness at each catheter site was determined in the presence and absence of parasympathetic nerve stimulation (via the epicardial wires). In all seven patients, an AV nodal fat pad was identified. Fat pad stimulation during and after surgery caused complete heart block but no change in sinus rate. Fat pad stimulation decreased the right atrial effective refractory period at 1 cm (280 ± 42 msec to 242 ± 39 msec) and 2 cm (235 ± 21 msec to 201 ± 11 msec) from the fat pad (P = 0.04, compared with baseline). No significant change in atrial refractoriness occurred at distances > 2 cm. The response to stimulation decreased as the distance from the fat pad increased. Conclusion: For the first time in humans, an epicardial fat pad was identified from which parasympathetic nerve fibers selectively innervate the AV node but not the sinoatrial node. Nerves in this fat pad also innervate the surrounding right atrium. [source]

Mechanism of Propensity to Atrial Fibrillation in Patients Undergoing Isthmus Ablation for Typical Atrial Flutter

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2005
HEMANTH RAMANNA M.D.
Background: Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. Methods: Consecutive patients (n = 42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. Results: Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P < 0.001). Conclusion: Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation. [source]

On the Atrial Response to Focal Discharges in Man

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2004
HEMANTH RAMANNA M.D.
Introduction: Triggers and vulnerability are key factors for the occurrence of atrial fibrillation (AF). The aim of this study was to assess spatial dispersion of atrial refractoriness and vulnerability in response to both focal discharges as well as programmed electrical stimulation in patients undergoing ablation of atrial arrhythmogenic foci. Methods and Results: Twenty-nine patients were studied, and 12 right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol that started with one extrastimulus, followed by more aggressive pacing until AF was obtained. Mean fibrillatory intervals were used to assess the local refractoriness of each recording site. Spatial dispersion of refractoriness was calculated as the coefficient of dispersion (CD value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). Based on our previous study, a CD value , 3.0 was defined as normal, whereas a CD value >3.0 was considered enhanced spatial dispersion of refractoriness. Fifteen of 29 patients had normal dispersion of refractoriness (mean CD value 1.65 ± 0.43), and AF was inducible with burst pacing only. These patients had focal discharges causing rapid atrial tachycardia with a focal activation pattern. Activation mapping of focal activity was possible in 14 of 15 patients. Focal triggering of AF occurred in only 1 of 15 patients. Fourteen of 29 patients had enhanced dispersion (mean CD value 4.2 ± 0.72). AF was inducible with a single extrastimulus in 11 of 14 patients (P < 0.001). Focal triggering of AF occurred in all 14 patients. Conclusion: Spatial dispersion of atrial refractoriness determines whether focal atrial discharges trigger AF with disorganized activity or, alternatively, only rapid atrial tachycardia. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-8, June 2004) [source]

Inhibitors of the Na+/H+ Exchanger Cannot Prevent Atrial Electrical Remodeling in the Goat

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2004
YURI BLAAUW M.D.
Introduction: It has been suggested that blockade of the Na+/H+ exchanger (NHE1) can prevent atrial fibrillation (AF)-induced electrical remodeling and the development of AF. Methods and Results: AF was maintained by burst pacing in 10 chronically instrumented conscious goats. Intravenous and oral dosages of two NHE1 blockers (EMD87580 and EMD125021) resulted in plasma levels several magnitudes higher than required for effective NHE1 blockade. Shortening of atrial refractoriness immediately after 5 minutes of AF was not prevented by NHE1 blockade. In remodeled atria, increasing dosages of EMD87580 and EMD125021 did not reverse shortening of the atrial refractory period or reduce the duration of AF episodes. The cycle length during persistent AF also was not affected. Oral pretreatment with EMD87580 (8 mg/kg bid) starting 3 days before AF could not prevent electrical remodeling. After 24 and 48 hours of remodeling, the duration of AF paroxysms was 47 ± 32 seconds and 135 ± 63 seconds compared to 56 ± 17 seconds and 136 ± 52 seconds in placebo-treated animals (P > 0.8), respectively. Conclusion: In the goat model of AF, the Na+/H+ exchanger inhibitors EMD87580 and EMD125021 did not prevent or revert AF-induced electrical remodeling. This indicates that activation of the Na+/H+ exchanger is not involved in the intracellular pathways of electrical remodeling. This does not support the suggestion that blockers of the Na+/H+ exchanger may be beneficial for prevention and treatment of AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 440-446, April 2004) [source]

Identification and Characterization of Atrioventricular Parasympathetic Innervation in Humans

Focal Atrial Fibrillation: Experimental Evidence for a Pathophysiologic Role of the Autonomic Nervous System

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001
PATRICK SCHAUERTE M.D.
Focal AF and Autonomic Nerves.Introduction: Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high-frequency electrical stimulation produces focal atrial activation and AF/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports. Methods and Results: In 21 mongrel dogs, local high-frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing highfrequency electrical stimulation voltage. APD/AT/AF originated adjacent to the site of high-frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7/8, right superior PV: 6/8; right inferior PV: 4/8). In the PVs, APDs occurred at 13 ± 8 V and AT/AF at 15 ± 9 V (P < 0.01; n = 25). In the SVC, APDs were elicited at 19 ± 6 V and AT/AF at 26 ± 6 V (P < 0.01; n = 12). High-frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high-frequency electrical stimulation was blunted or prevented after beta-receptor blockade and abolished by atropine. In vitro, high-frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from 89 ± 35 msec to 60 ± 22 msec; P < 0.001; n = 7) but lengthening of the action potential and development of early afterdepolarizations that triggered APD/AT in other cells. Action potential shortening was abolished by atropine. Conclusion: High-frequency electrical stimulation evokes rapid ectopic beats from the PV/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high-frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high-frequency electrical stimulation were caused by autonomic nerve stimulation. [source]

Ectopic Atrial Rhythm with Exit Block Following Catheter Ablation for Focal Atrial Tachycardias in a Patient with Prior Surgery for Atrial Septal Defect

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2002
KIMIE OHKUBO
OHKUBO, K., et al.: Ectopic Atrial Rhythm with Exit Block Following Catheter Ablation for Focal Atrial Tachycardias in a Patient with Prior Surgery for Atrial Septal Defect. The patient was a 40-year-old woman with a history of surgery for atrial septal defect and catheter ablation for typical atrial flutter. An electrophysiological study was performed because she had palpitation and syncope. She had ectopic atrial rhythm originating from low lateral RA. Two focal atrial tachycardias ([1] superior vena cava-RA junction and [2] a low posteroseptal RA) were successfully ablated. Following catheter ablation for the second atrial tachycardia, she developed junctional rhythm because ectopic atrial rhythm showed exit block. However, atrial activation of junctional rhythm could conduct into the ectopic atrial rhythm focus and reset the rhythm when atrial activation of junctional rhythm reached the blocked line after atrial refractoriness by preceding ectopic atrial rhythm. [source]

Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001
RIK WILLEMS
WILLEMS, R. et al.: Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model. In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 ± 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., >1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 ± 5 ms in the continuously paced group and 107 ± 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 ± 4 ms in this group versus 116 ± 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 ± 0.1 cm2 at baseline to 4.2 ± 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 ± 0.1 to 2.8 ± 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions. [source]

Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fihriliation

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2000
ANTONIO DE SISTI
DE SISTI, A., ET AL.: Electrophysiologicai Characteristics of the Atrium in Sinus Node Dysfunction With and Without Postpacing Atrial Fibrillation . In patients with sinus node dysfunction (SND) with or without associated paroxysmal atrial fibrillation (AF), the effectiveness of atrial pacing in reducing the incidence of AF is not definitive. In addition, despite several studies involving large populations of implanted patients, little attention has been paid to the electrophysioiogicai (EP) atrial substrate and the effect of permanent atrial pacing. The aim of this study is to correlate EP data and the risk of AF after DDD device implantation. We reviewed FP data of 38 consecutive patients with SND. mean age 70 ± 8 years, who were investigated free of antiarrhythmic treatment, for the evaluation of the atrial substrate. We also considered as control group 25 subjects, mean age 63 ± 14 years, referred to our EP laboratory for unexplained syncope or various atrioventricular disturbances. Following pharmacological washout and at a drive cycle length of 600 ms. effective and functional refractory periods (ERP, FRP), Sl-Al and S2-A2 latency, Al and A2 conduction duration, and latent vulnerability index (EHP/A2) were measured. AF induction was tested with up to three extrastimuli at paced cycle lengths of 600 and 400 ms in 20 patients. Induction of sustained AF (> 30 seconds) was considered as the endpoint. P wave duration on the surface ECG in lead II/Vl was also measured. DDD pacing mode was chosen in all patients with the minimal atrial rate programmed between 60 and 75 beats/min (mean 64 ± 4 beats/min). After implantation, the patients were followed-up for 29 ± 17 months and clinically documented occurrence of AF was determined. When comparing patients with SND and subjects of the control group, we did not find any significant statistical differences in terms of ERP (237 ± 33 vs 250 ± 29 ms), FRP (276 ± 30 vs 280 ± 32 ms) and Sl-Al (39 ± 16 vs 33 ± 11 ms) and S2-A2 latency (69 ± 24 vs 63 ± 25 ms). In contrast, we observed significant differences regarding Al (55 ± 19 vs 39 ± 13 ms; P < 0.001), A2 (95 ± 34 vs 57 ± 18 ms; P < 0.001) and P wave duration (104 ± 18 vs 94 ± 15 ms; P < 0.05), and ERP/A2 (2.8 ± 1.2 vs 4.8 ± 1.6; P < 0.001). When comparing patients with (n = 11) or without (n =27) postpacing AF occurrence, we did not find any difference with reference to ERP, FRP. Sl-Al, S2-A2, Al duration, or follow-up duration. In patients with postpacing AF occurrence, A2 was longer (116 ± 41 vs 87 ± 27 ms; P < 0.01), FRP/A2 lower (2.1 ± 0.4 vs 3.1 ± 1.4; P < 0.05), P wave more prolonged (116 ± 22 vs 99 ± 14 ms; P < 0.01), and preexisting AF history predominant (6/11 vs 5/27 patients; P < 0.05). No difference was observed between patients with (n = 8) and without (n = 12) AF induction during the EP study. In patients with SND, the atrial refractoriness appears normal and the most important abnormality concerns conduction slowing disturbances. Persistence of AF despite pacing stresses the importance of mechanisms responsible for AF not entirely brady-dependent. In this setting, more prolonged atrial conduction disturbances, responsible for a low vulnerability index, and a preexisting history of AF enable us to identify a high risk patient group for AF in the follow-up. sinus node dysfunction, atrial fibrillation, electrophysiologicai study, atrial pacing [source]