A unified functional/anatomic substrate for circus movement atrial flutter: Activation and refractory patterns in the canine right atrial enlargement model

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (> 1 min duration, monomorphic; regular cycle length, 127 ± 12 ms, mean ± SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, <1 min; cycle length, 129 ± 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 ± 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6–25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.Key words: atrial flutter, atrial fibrillation, atrial mapping, antiarrhythmic drugs, vagal stimulation.

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Activation sequence during atrial flutter in dogs with surgically induced right atrial enlargement: I. Observations during sustained rhythms.

Circulation Research ◽

10.1161/01.res.62.3.596 ◽

1988 ◽

Vol 62 (3) ◽

pp. 596-608 ◽

Cited By ~ 50

Author(s):

P A Boyden

Keyword(s):

Atrial Flutter ◽

Right Atrial ◽

Atrial Enlargement ◽

Surgically Induced ◽

Activation Sequence

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Characterization of Low Right Atrial Isthmus as the Slow Conduction Zone and Pharmacological Target in Typical Atrial Flutter

Circulation ◽

10.1161/01.cir.96.8.2601 ◽

1997 ◽

Vol 96 (8) ◽

pp. 2601-2611 ◽

Cited By ~ 54

Author(s):

Ching-Tai Tai ◽

Shih-Ann Chen ◽

Chern-En Chiang ◽

Shih-Huang Lee ◽

Kwo-Chang Ueng ◽

...

Keyword(s):

Atrial Flutter ◽

Right Atrial ◽

Slow Conduction ◽

Typical Atrial Flutter ◽

Pharmacological Target ◽

Conduction Zone

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Atrial dilation as a substrate for atrial fibrillation in the canine complete chronic atrioventricular block model

European Heart Journal ◽

10.1093/ehjci/ehaa946.0471 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

A Smoczynska ◽

H.D.M Beekman ◽

R.W Chui ◽

S Rajamani ◽

M.A Vos

Keyword(s):

Atrial Fibrillation ◽

Atrioventricular Block ◽

Volume Overload ◽

Right Atrial ◽

Funding Source ◽

Private Company ◽

Structural Remodeling ◽

2D Echocardiography ◽

Atrial Enlargement ◽

The Right

Abstract Background Atrial fibrillation (AF) is the most common cardiac arrhythmia treated in clinical practice. Structural remodeling is characterized by atrial enlargement and contributes to the therapeutic resistance in patients with long-standing AF. Purpose To study the atrial arrhythmogenic and echocardiographic consequences induced by volume overload in the complete chronic atrioventricular block (CAVB) dog. Methods Echocardiographic and electrophysiological data was obtained in 14 anaesthetized Mongrel dogs, in acute AV-block (AAVB), after 6 weeks of CAVB (CAVB6) and CAVB10. Left atrial (LA) volume was determined with 2D echocardiography by using the biplane method. An electrocardiogram and monophasic action potentials (MAP) at the right atrial (RA) free wall were recorded. Atrial effective refractory period (AERP) was determined by continuous programmed electrical stimulation (PES) of 20 beats with a cycle length of 400 ms and an extrastimulus with decremental design until refractoriness was reached. A continuous PES protocol of 20 beats with an extrastimulus 5 ms longer than the AERP was applied for 150 seconds to trigger AF. After 5 min without arrhythmias, autonomic neuromodulation was performed by intravenous infusion (IV) of acetylcholine (1,5μg/kg/min to 6,0μg/kg/min) for 20 min followed by prompt IV infusion of isoprenaline (3μg/min) until the atrial heart rate increased by 20 bpm. PES with an extrastimulus was repeated for 150 seconds to induce AF. Results LA volume increased from 13.7±3.2 ml at AAVB to 20.5±5.9 ml* at CAVB6, and 22.7±6.0 ml* at CAVB10 (Fig. 1A). AERP was similar at AAVB, CAVB6, and CAVB10 (115.8±11.9, 117.3±11.7, and 106.8±12.1 ms respectively). Repetitive AF paroxysms of >10 seconds were induced in 1/14 (7%) dogs at AAVB, 1/11 (9%) at CAVB6, and 5/10 (50%)* at CAVB10 (*p<0.05) upon PES (Fig. 1B). Combined neuromodulation and PES did not increase the AF inducibility rate, but prolonged the longest episode of AF in the inducible dogs from 55±49 seconds to 236±202 seconds* at CAVB10 (Fig. 1C). LA volume was higher in inducible dogs 25.0±4.9 ml compared to 18.4±4.2 ml in non-inducible dogs at CAVB10. Conclusion Sustained atrial dilation forms a substrate for repetitive paroxysms of AF. Neuro-modulation prolongs AF episode duration in susceptible dogs. This animal model can be used to study structural remodeling of the atria and possible therapeutic advances in the management of AF. Figure 1 Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Amgen Research

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Lipomatous Hypertrophy of the Intraatrial Septum Resulting in Right Atrial Inflow Obstruction and Atrial Flutter

The Annals of Thoracic Surgery ◽

10.1016/j.athoracsur.2009.10.001 ◽

2010 ◽

Vol 89 (5) ◽

pp. 1647-1649 ◽

Cited By ~ 5

Author(s):

Jennifer A. Dickerson ◽

Macy Smith ◽

Steven Kalbfleisch ◽

Michael S. Firstenberg

Keyword(s):

Atrial Flutter ◽

Right Atrial ◽

Lipomatous Hypertrophy

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Localized reentry in the superior vena cava giving rise to an atypical right atrial flutter: Insights from an analysis of two cases

Journal of Electrocardiology ◽

10.1016/j.jelectrocard.2020.12.007 ◽

2021 ◽

Vol 64 ◽

pp. 91-94

Author(s):

Valentino Ducceschi ◽

Francesco Maddaluno

Keyword(s):

Atrial Flutter ◽

Superior Vena Cava ◽

Superior Vena ◽

Vena Cava ◽

Right Atrial

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Abstract 3265: A Comparison of Echocardiographic and Electrocardiographic Characteristics of Patients with Apical Hypertrophic Cardiomyopathy

Circulation ◽

10.1161/circ.116.suppl_16.ii_734-c ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Josepha Binder ◽

Brandon R Grossardt ◽

Christine Attenhofer Jost ◽

Kyle W Klarich ◽

Michael J Ackerman ◽

...

Keyword(s):

Hypertrophic Cardiomyopathy ◽

Ejection Fraction ◽

Left Ventricular ◽

Right Atrial ◽

Apical Hypertrophic Cardiomyopathy ◽

T Wave ◽

Atrial Enlargement ◽

Lv Ejection Fraction ◽

The Relationship ◽

T Waves

Background: Apical hypertrophic cardiomyopathy (apical HCM) is a less common subtype of HCM characterized by a focal thickening in the left ventricular apex. “Classic” ECG features have been described, however, apical HCM can persist for many years without detection. We investigated the relationship between ECG findings and echocardiographic morphometry in a large referral series of patients with apical HCM. Methods: We enumerated all patients diagnosed with apical HCM prior to Sept. 30, 2006 using the Mayo Clinic HCM database. We compared echocardiographic measures separately for patients with positive status for two ECG indices of left ventricular hypertrophy (LVH); the Sokolow-Lyon index and the Romhilt-Estes (RE) point-score. We also compared echocardiographic measurements in patients with and without negative T-waves in the precordial leads. Results: Apical HCM was detected in 177 patients (111 men and 68 women). Only 51% had positive Sokolow criteria and 51% had positive RE criteria. The agreement between Sokolow and RE status was high (agreement = 75.0%; kappa = 0.50; 95% CI = 0.38 – 0.62). In particular, Sokolow positive patients had increased LV ejection fraction (P = 0.02), and decreased LV end-systolic diameter (P = 0.03) compared with Sokolow negative patients. The prevalence of right atrial enlargement (47 vs. 28%; P = 0.02) and intracavity obstruction (22 vs. 8%; P = 0.01) were more common in Sokolow positive patients. Positive RE criteria was associated with a greater thickness of the basal septal and basal posterior walls (P = 0.001 and 0.02, respectively), and with a higher frequency of intracavity obstruction (21 vs. 9%; P = 0.04). Most patients (89%) exhibited at least one negative T-wave in the precordial leads; however, only 10% of patients had a negative T-wave of greater than 1.0 mV. We found that patients with an inverted T-wave larger than 0.4 mV (median) had a significantly increased LV ejection fraction (P = 0.03) compared with patients who had smaller or no negative T-waves. Conclusions: Among patients with apical HCM, nearly half do not have ECG evidence of LVH based on classic criteria and most do not have marked T-wave inversions. However, the majority did have at least a mild expression of negative T-waves.

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