scholarly journals Altered dystrophin expression in the right atrium of a patient after Fontan procedure with atrial flutter

Heart ◽  
2004 ◽  
Vol 90 (12) ◽  
pp. e65-e65 ◽  
Author(s):  
C J McMahon
Keyword(s):  
Atrial Flutter ◽  
Right Atrium ◽  
Fontan Procedure ◽  
Dystrophin Expression ◽  
The Right

scholarly journals P649 Before and after: sinus venosus atrial septal defect

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
I Marco Clement ◽  
R Eiros ◽  
R Dalmau ◽  
T Lopez ◽  
G Guzman ◽  
...  
Keyword(s):  
Atrial Septal Defect ◽  
Left Atrium ◽  
Atrial Flutter ◽  
Superior Vena Cava ◽  
Right Atrium ◽  
Septal Defect ◽  
Superior Vena ◽  
Pulmonary Veins ◽  
Vena Cava ◽  
The Right

Abstract Introduction The diagnosis of sinus venosus atrial septal defect (SVASD) is complex and requires special imaging. Surgery is the conventional treatment; however, transcatheter repair may become an attractive option. Case report A 60 year-old woman was admitted to the cardiology department with several episodes of paroxysmal atrial flutter, atrial fibrillation and atrioventricular nodal reentrant tachycardia. She reported a 10-year history of occasional palpitations which had not been studied. A transthoracic echocardiography revealed severe right ventricle dilatation and moderate dysfunction. Right volume overload appeared to be secondary to a superior SVASD with partial anomalous pulmonary venous drainage. A transesophageal echocardiography confirmed the diagnosis revealing a large SVASD of 16x12 mm (Figure A) with left-right shunt (Qp/Qs 2,2) and two right pulmonary veins draining into the right superior vena cava. Additionally, it demonstrated coronary sinus dilatation secondary to persistent left superior vena cava. CMR and cardiac CT showed right superior and middle pulmonary veins draining into the right superior vena cava 18 mm above the septal defect (Figures B and C). After discussion in clinical session, a percutaneous approach was planned to correct the septal defect and anomalous pulmonary drainage. For this purpose, anatomical data obtained from CMR and CT was needed to plan the procedure. During the intervention two stents graft were deployed in the right superior vena cava. The distal stent was flared at the septal defect level so as to occlude it while redirecting the anomalous pulmonary venous flow to the left atrium (Figure D). Control CT confirmed the complete occlusion of the SVASD without residual communication from pulmonary veins to the right superior vena cava or the right atrium (Figure E). Anomalous right superior and middle pulmonary veins drained into the left atrium below the stents. Transthoracic echocardiographies showed progressive reduction of right atrium and ventricle dilatation. The patient also underwent successful ablation of atrial flutter and intranodal tachycardia. She is currently asymptomatic, without dyspnea or arrhythmic recurrences. Conclusions In this case, multimodality imaging played a key role in every stage of the clinical process. First, it provided the diagnosis and enabled an accurate understanding of the patient’s anatomy, particularly of the anomalous pulmonary venous connections. Secondly, it allowed a transcatheter approach by supplying essential information to guide the procedure. Finally, it assessed the effectiveness of the intervention and the improvement in cardiac hemodynamics during follow-up. Abstract P649 Figure.

scholarly journals P189 Duplication of the tricuspid valve (DOTV): case report of a rare congenital anomaly

2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
S Moscatelli ◽  
G Trocchio ◽  
N Stagnaro ◽  
A Siboldi ◽  
M Derchi ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Atrial Flutter ◽  
Tricuspid Valve ◽  
Tricuspid Regurgitation ◽  
Right Atrium ◽  
Rare Condition ◽  
Systolic Pulmonary Artery Pressure ◽  
Severe Tricuspid Regurgitation ◽  
One Year ◽  
The Right

Abstract Introduction Tricuspid valve duplication is an extremely rare condition and in most of the cases it is associated with other congenital cardiac malformations. Because of its rarity, the clinical presentation and the management are not defined yet. Clinical Case We report the case of an 18 y/o caucasian male, who was admitted to our Hospital in February 2018 for rapid atrial flutter not responsive to medical therapy (propanolol and digossin). He had a pre-natal diagnose of ventricular septum defect (VSD) and tricuspid straddling. At 1 year of age he underwent pulmonary artery bandage and one year later VSD closure was performed. Blood test showed sub-clinic hypothyroidism, probably related to previous amiodaron therapy. A transthoracic echocardiogram was obtained. The right atrium (RA) was severely dilated and the atrial septum dislocated towards left ventricle (LV); two right atrioventricular valves (tricuspid valves) were detected: the ‘true’ tricuspid opening was inside the right ventricle, and an ‘accessory‘ opening was located inside the LV and severely regurgitant into the RA; the mitral valve was morphologically and functionally normal; both ventricles were dilated with preserved systolic function; systolic pulmonary artery pressure was not detectable. A Cardiac Magnetic Resonance clearly delineated the anomaly. Atrial flutter radio frequency transcatheter ablation was succesfully performed before corrective surgery. The regurgitant accessory tricuspid orifice was closed with an heterologous pericardial patch and a right reduction atrioplasty was also done. The post-operative course was uneventful and only a mild paraseptal tricuspid jet with LV to RA shunt was present at post op echocardiography. After one year follow-up the patient remained asymptomatic, without arrhythmia recurrence. Conclusion DOTV is an extremely rare condition that could be responsible of severe tricuspid regurgitation. At the moment, there are not sufficient data to establish the correct timing for surgical intervention. In our case, the presence of severe tricuspid regurgitation, right atrium dilatation, biventricular overload and atrial flutter guided the clinical management and suggested surgical correction. Abstract P189 Figure.

scholarly journals Changes of electrophysiological parameters in patients with atrial flutter

Medicina ◽  
2007 ◽  
Vol 43 (8) ◽  
pp. 614 ◽  
Author(s):  
Diana Žaliaduonytė-Pekšienė ◽  
Tomas Kazakevičius ◽  
Vytautas Zabiela ◽  
Vytautas Šileikis ◽  
Remigijus Vaičiulis ◽  
...  
Keyword(s):  
Response Time ◽  
Atrial Flutter ◽  
Right Atrium ◽  
Propagation Speed ◽  
Control Group ◽  
Type I ◽  
Stimulus Response ◽  
Refractory Periods ◽  
Impulse Propagation ◽  
The Right

Objectives. The aim of the study was to study some anatomic and electrophysiological features of the right atrium, related to the presence of atrial flutter. Materials and methods. A total 23 patients with type I atrial flutter and 22 patients without atrial flutter were studied. Right atrium size was assessed using echocardiography before intracardiac examination and radiofrequency ablation. Results. Effective refractory periods of coronary sinus, high right atrium, low right atrium were different comparing with the control group (P<0.05). A stimulus–response time between high right atrium and low right atrium positions in anterograde and retrograde ways, an impulse propagation speed along the lateral wall of the right atrium were statistically different comparing both groups (P<0.05). There was a significant correlation among effective refractory periods measured in different sites of the right atrium (r²=0.64, 0.44, 0.44, respectively). All measured effective refractory periods also correlated with stimulus–response time in anterograde way (P<0.05) and impulse propagation speed (P<0.05). Right atrium dimensions were significantly larger in atrial flutter group. There was no correlation between the right atrium dimensions and measured electrophysiological parameters in both groups.Conclusions. The presence of atrial flutter associates with diffuse alterations of the right atrium, but not the focal or single changes of refractoriness.

Electrophysiologic Characteristics and Ablation of an Atypical Atrial Flutter in the Right Atrium

2000 ◽  
Vol 11 (3) ◽  
pp. 334-338 ◽  
Author(s):  
KUAN-CHENG CHANG ◽  
YU-CHIN LIN ◽  
HSIANG-TAI CHOU ◽  
JUI-SUNG HUNG
Keyword(s):  
Atrial Flutter ◽  
Right Atrium ◽  
The Right

scholarly journals Electrophysiological Response of the Right Atrium to Ibutilide During Typical Atrial Flutter

Circulation ◽  
2002 ◽  
Vol 106 (7) ◽  
pp. 814-819 ◽  
Author(s):  
Jie Cheng ◽  
Kathryn Glatter ◽  
Yanfei Yang ◽  
Shulong Zhang ◽  
Randall Lee ◽  
...  
Keyword(s):  
Atrial Flutter ◽  
Right Atrium ◽  
Electrophysiological Response ◽  
Typical Atrial Flutter ◽  
The Right

scholarly journals Right Atrial Fibroelastoma Presenting as Typical Atrial Flutter: Rare Disease in Unusual Location

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Ahmad Abuarqoub ◽  
Ghada Elshimy ◽  
Muhammed Shittu ◽  
Aiman Hamdan ◽  
Fayez Shamoon
Keyword(s):  
Inferior Vena Cava ◽  
Atrial Flutter ◽  
Right Atrium ◽  
Inferior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Unusual Location ◽  
Typical Atrial Flutter ◽  
The Right ◽  
Right Atria

Typical atrial flutter as initial presentation of papillary fibroelastoma involving the cavotricuspid isthmus is not described before in literature. To our knowledge only 14 cases have been reported in literature involving the right atrium. Very unusual location is at the junction between inferior vena cava (IVC) and right atria as only 1 case has been reported.

Chronic nicotine in hearts with healed ventricular myocardial infarction promotes atrial flutter that resembles typical human atrial flutter

2005 ◽  
Vol 288 (6) ◽  
pp. H2878-H2886 ◽  
Author(s):  
Mizuho Miyauchi ◽  
Zhilin Qu ◽  
Yasushi Miyauchi ◽  
Sheng-Mei Zhou ◽  
Hui Pak ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Atrial Flutter ◽  
Right Atrium ◽  
Interstitial Fibrosis ◽  
Fold Increase ◽  
Monophasic Action Potential ◽  
Crista Terminalis ◽  
Bipolar Electrodes ◽  
Chronic Nicotine ◽  
The Right

The potential of chronic nicotine exposure for atrial fibrillation (AF) and atrial flutter (AFL) in hearts with and without chronic myocardial infarction (MI) remains poorly explored. MI was created in dogs by permanent occlusion of the left anterior descending coronary artery, and dogs were administered nicotine (5 mg·kg−1·day−1 sc) for 1 mo using osmotic minipumps. High-resolution epicardial (1,792 bipolar electrodes) and endocardial Halo catheters were used to map activation during induced atrial rhythms. Nicotine promoted inducible sustained AFL at a mean cycle length of 134 ± 10 ms in all MI dogs ( n = 6) requiring pacing and electrical shocks for termination. No AFL could be induced in MI dogs ( n = 6), control (non-MI) dogs ( n = 3) not exposed to nicotine, and dogs with no MI and exposed to nicotine ( n = 3). Activation maps during AFL showed a single reentrant wavefront in the right atrium that rotated either clockwise (60%) or counterclockwise (40%) around the crista terminalis and through the isthmus. Ablation of the isthmus prevented the induction of AFL. Nicotine caused a significant ( P < 0.01) but highly heterogeneous increase in atrial interstitial fibrosis (2- to 10-fold increase in left and right atria, respectively) in the MI group but only a 2-fold increase in the right atrium in the non-MI group. Nicotine also flattened ( P < 0.05) the slope of the epicardial monophasic action potential duration (electrical restitution) curve of both atria in the MI but not in non-MI dogs. Two-dimensional simulation in an excitable matrix containing an isthmus and nicotine's restitutional and reduced gap junctional coupling (fibrosis) parameters replicated the experiments. Chronic nicotine in hearts with MI promotes AFL that closely resembles typical human AFL. Increased atrial interstitial fibrosis and flattened electrical restitution are important substrates for the AFL.

Transitions among atrial fibrillation, atrial flutter, and sinus rhythm during procainamide infusion and vagal stimulation in dogs with sterile pericarditis

1991 ◽  
Vol 69 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Pierre L. Pagé ◽  
Hamid Hassanalizadeh ◽  
René Cardinal
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Atrial Flutter ◽  
Right Atrium ◽  
Cycle Length ◽  
Vagal Stimulation ◽  
Right Atrial ◽  
Free Wall ◽  
Circus Movement ◽  
The Right

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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