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.

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.

Abstract 009: Cardiac Human Mesenchymal Stromal Cells from Patients with Ischemic Heart Disease are Proinflammatory and Impair Recovery after Myocardial Infarction in Rat

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Nili Naftali-Shani ◽  
Ayelet Itzhaki-Alfia ◽  
Natalie Landa-Rouben ◽  
David Kain ◽  
Radka Holbova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Stromal Cells ◽  
Right Atrium ◽  
Subcutaneous Fat ◽  
Epicardial Fat ◽  
Human Mesenchymal Stromal Cells ◽  
The Right ◽  
Different Sources

Introduction: Human mesenchymal stromal cells (hMSCs) from adipose cardiac tissue have attracted considerable interest for cell-based therapies. However, the best source of hMSCs for infarct repair is still unknown. Hypothesis: We aimed to test the hypothesis that, because of their proximity to the heart, hMSCs from the heart and epicardial fat would be better cells for infarct repair. Methods and Results: We isolated and grew hMSCs from patients with ischemic heart disease (IHD) from four different sources: 1) epicardial fat 2) pericardial fat 3) subcutaneous fat and 4) the right atrium. hMSCs from the right atrium and epicardial fat secreted the highest amounts of trophic and inflammatory cytokines, while hMSCs from pericardial and subcutaneous fat secreted the lowest (p<0.05, n=5-6 per source). Subsequently, the greatest angiogenic effect was induced with conditioned medium from atrium and epicardial fat hMSCs, by tube formation assay. To determine the effect of hMSCs in vivo , we allocated rats to hMSC transplantation 7 days after myocardial infarction (MI) (n=8-10 per group). Atrial hMSCs induced the highest number of vessels in the infarct, together with the highest inflammation score and macrophage accumulation 27 days after their injection. However, left ventricular (LV) dysfunction was worst after therapy with atrium and epicardial fat hMSCs, and minimal after subcutaneous fat hMSC therapy. Notably, there was a correlation between levels of tumor necrosis factor-α and hepatocyte growth factor, in vitro , and post-transplantation LV systolic dilatation. These surprising findings were supported by gene expression analysis in hMSCs from different sources of a patient with IHD. We found that the relative expression of inflammation and fibrosis-related genes was considerably higher in hMSCs from the right atrium and epicardial fat than in subcutaneous fat hMSCs. Conclusions: The origin of hMSCs affects their reparative and immunomodulatory properties. Because of their pro-inflammatory properties, hMSCs from the right atrium and epicardial fat of IHD patients could impair heart function after MI. Our findings might be relevant to autologous MSC therapy and pathogenesis and progression of IHD.

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.

Acetylcholine release by a stimulus train lowers atrial fibrillation threshold

1987 ◽  
Vol 253 (4) ◽  
pp. H863-H868 ◽  
Author(s):  
D. E. Euler ◽  
P. J. Scanlon
Keyword(s):  
Atrial Fibrillation ◽  
Action Potential ◽  
Right Atrium ◽  
Single Pulse ◽  
Monophasic Action Potential ◽  
Adrenergic Blockade ◽  
The Right ◽  
Alpha Chloralose ◽  
Electrical Stimuli ◽  
Local Release

This study was designed to evaluate the importance of local release of autonomic neuromediators when electrical stimuli are applied to the right atrium to measure the atrial fibrillation threshold (AFT). Experiments were performed in 16 open-chest dogs anesthetized with alpha-chloralose. The dogs were denervated by bilateral transection of the stellates and cervical vagi. The AFT was determined in 11 dogs by delivering either a train of stimuli (14 pulses, 4 ms, 100 Hz) or a single stimulus (10 ms) to the right atrium during its vulnerable period. In eight dogs, beta-adrenergic blockade with timolol (0.1 mg/kg) had no effect on the AFT determined with either method. Atropine (0.2 mg/kg), given after timolol, significantly increased the train-of-pulses AFT from 4.7 +/- 0.4 to 32.3 +/- 4.6 mA (P less than 0.001). The single-pulse AFT increased from 16.5 +/- 1.5 to 17.8 +/- 1.5 mA (P less than 0.05). Atropine had a similar effect on the AFT when it was given in the absence of timolol (n = 3). In five additional dogs, a monophasic action potential was recorded while a 10-mA train was delivered to the atrium during its absolute refractory period. There was marked shortening of the monophasic action potential duration (55 +/- 6 ms) in the first beat after the train. The shortening was totally abolished by atropine (0.2 mg/kg). The results suggest that a train of stimuli liberates local stores of acetylcholine, which cause a shortening of atrial repolarization time and a profound decrease in the current necessary to evoke fibrillation.

The thyroid hormone analog DITPA restoresI to in rats after myocardial infarction

2000 ◽  
Vol 278 (4) ◽  
pp. H1105-H1116 ◽  
Author(s):  
Alan D. Wickenden ◽  
Roger Kaprielian ◽  
Xiao-Mang You ◽  
Peter H. Backx
Keyword(s):  
Myocardial Infarction ◽  
Thyroid Hormone ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Monophasic Action Potential ◽  
Mrna Levels ◽  
Hormone Analog ◽  
Life Threatening ◽  
The Right

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current ( I to) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that I to density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored I to density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in I toexpression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores I to density in the setting of MI, which may be useful in preventing complications associated with I to downregulation.

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.

The Monophasic Action Potential of the Right Atrium

Cardiology ◽  
1972 ◽  
Vol 57 (4) ◽  
pp. 200-207 ◽  
Author(s):  
S. Gavrilescu ◽  
S. Cotoi ◽  
T. Pop
Keyword(s):  
Action Potential ◽  
Right Atrium ◽  
Monophasic Action Potential ◽  
The Right
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