Effects of Atrial Fibrillation Cardioversion after Percutaneous Mitral Balloon Valvuloplasty on Echocardiographic Left and Right Atrial Functions

2014 ◽  
Vol 65 (1-3) ◽  
pp. 69-75
Author(s):  
Aly Ramzy ◽  
Amal Ayoub ◽  
Said Khaled ◽  
Sameh Samir ◽  
Ayman Mortada ◽  
...  
2021 ◽  
Author(s):  
Alexandra S Mighiu ◽  
Alice Recalde ◽  
Klemen Ziberna ◽  
Ricardo Carnicer ◽  
Jakub Tomek ◽  
...  

Abstract Aims Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling in animal models and predicts incident AF in humans; however, a direct causal role for NOX2 in AF has not been demonstrated. Accordingly, we investigated whether myocardial NOX2 overexpression in mice (NOX2-Tg) is sufficient to generate a favourable substrate for AF and further assessed the effects of atorvastatin, an inhibitor of NOX2, on atrial superoxide production and AF susceptibility. Methods and results NOX2-Tg mice showed a 2- to 2.5-fold higher atrial protein content of NOX2 compared with wild-type (WT) controls, which was associated with a significant (twofold) increase in NADPH-stimulated superoxide production (2-hydroxyethidium by HPLC) in left and right atrial tissue homogenates (P = 0.004 and P = 0.019, respectively). AF susceptibility assessed in vivo by transoesophageal atrial burst stimulation was modestly increased in NOX2-Tg compared with WT (probability of AF induction: 88% vs. 69%, respectively; P = 0.037), in the absence of significant alterations in AF duration, surface ECG parameters, and LV mass or function. Mechanistic studies did not support a role for NOX2 in promoting electrical or structural remodelling, as high-resolution optical mapping of atrial tissues showed no differences in action potential duration and conduction velocity between genotypes. In addition, we did not observe any genotype difference in markers of fibrosis and inflammation, including atrial collagen content and Col1a1, Il-1β, Il-6, and Mcp-1 mRNA. Similarly, NOX2 overexpression did not have consistent effects on RyR2 Ca2+ leak nor did it affect PKA or CaMKII-mediated RyR2 phosphorylation. Finally, treatment with atorvastatin significantly inhibited atrial superoxide production in NOX2-Tg but had no effect on AF induction in either genotype. Conclusion Together, these data indicate that while atrial NOX2 overexpression may contribute to atrial arrhythmogenesis, NOX2-derived superoxide production does not affect the electrical and structural properties of the atrial myocardium.


2008 ◽  
Vol 130 (1) ◽  
pp. 69-71 ◽  
Author(s):  
Qiqiong Cui ◽  
Wei Zhang ◽  
Hu Wang ◽  
Xin Sun ◽  
Huanyi Yang ◽  
...  

1993 ◽  
Vol 22 (6) ◽  
pp. 1666-1672 ◽  
Author(s):  
A.T.Marcel Gosselink ◽  
Harry J.G.M. Crijns ◽  
Hans P.M. Hamer ◽  
Hans Hillege ◽  
Kong I. Lie

1993 ◽  
Vol 264 (4) ◽  
pp. H1093-H1097 ◽  
Author(s):  
E. Leistad ◽  
G. Christensen ◽  
A. Ilebekk

The effects of atrial fibrillation on left and right atrial dimensions, pressures, and compliances were examined in two groups of seven barbiturate-anesthetized open-chest pigs. Atrial diameters and pressures were recorded during atrioventricular (AV) pace and thereafter during atrial fibrillation. Both rhythms were studied with constant ventricular rate after complete AV block. Left atrial maximal diameter, which appeared at the end of the atrial filling phase, decreased from 32.4 (28.9-36.7; median and 95% confidence interval) to 31.3 (28.4-35.7) mm after induction of atrial fibrillation. The right atrial maximal diameter also decreased, although not significantly. Atrial pressure at the peak of the v wave rose from 7.0 (5.5-8.5) to 9.6 (8.3-11.2) mmHg in the left atrium and from 5.0 (4.3-5.6) to 7.3 (6.2-8.7) mmHg in the right atrium. Left and right atrial chamber stiffness constants increased from 0.25 (0.19-0.48) to 0.41 (0.28-0.66) mm-1 and from 0.21 (0.11-0.31) to 0.33 (0.30-0.39) mm-1, respectively. Instantaneous diastolic atrial compliance decreased in both atria after induction of atrial fibrillation. Thus, during atrial fibrillation with regular ventricular rate, changes in atrial diameter, pressure, and compliance take place.


Author(s):  
Óscar Salvador‐Montañés ◽  
Rafael J. Ramirez ◽  
Yoshio Takemoto ◽  
Steven R. Ennis ◽  
Daniel Garcia‐Iglesias ◽  
...  

Background Activation during onset of atrial fibrillation is poorly understood. We aimed at developing a panoramic optical mapping system for the atria and test the hypothesis that sequential rotors underlie acceleration of atrial fibrillation during onset. Methods and Results Five sheep hearts were Langendorff perfused in the presence of 0.25 µmol/L carbachol. Novel optical system recorded activations simultaneously from the entire left and right atrial endocardial surfaces. Twenty sustained (>40 s) atrial fibrillation episodes were induced by a train and premature stimuli protocol. Movies obtained immediately (Initiation stage) and 30 s (Early Stabilization stage) after premature stimulus were analyzed. Serial rotor formation was observed in all sustained inductions and none in nonsustained inductions. In sustained episodes maximal dominant frequency increased from (mean±SD) 11.5±1.74 Hz during Initiation to 14.79±1.30 Hz at Early Stabilization ( P <0.0001) and stabilized thereafter. At rotor sites, mean cycle length (CL) during 10 prerotor activations increased every cycle by 0.53% ( P =0.0303) during Initiation and 0.34% ( P =0.0003) during Early Stabilization. In contrast, CLs at rotor sites showed abrupt decreases after the rotors appearances by a mean of 9.65% ( P <0.0001) during both stages. At Initiation, atria‐wide accelerations and decelerations during rotors showed a net acceleration result whereby post‐rotors atria‐wide minimal CL (CLmin) were 95.5±6.8% of the prerotor CLmin ( P =0.0042). In contrast, during Early Stabilization, there was no net acceleration in CLmin during accelerating rotors (prerotor=84.9±11.0% versus postrotor=85.8±10.8% of Initiation, P =0.4029). Levels of rotor drift distance and velocity correlated with atria‐wide acceleration. Nonrotor phase singularity points did not accelerate atria‐wide activation but multiplied during Initiation until Early Stabilization. Increasing number of singularity points, indicating increased complexity, correlated with atria‐wide CLmin reduction ( P <0.0001). Conclusions Novel panoramic optical mapping of the atria demonstrates shortening CL at rotor sites during cholinergic atrial fibrillation onset. Atrial fibrillation acceleration toward Early Stabilization correlates with the net result of atria‐wide accelerations during drifting rotors activity.


2016 ◽  
Vol 32 (5) ◽  
pp. 807-815 ◽  
Author(s):  
Michael Markl ◽  
Maria Carr ◽  
Jason Ng ◽  
Daniel C. Lee ◽  
Kelly Jarvis ◽  
...  

PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0129124 ◽  
Author(s):  
Natalia Smorodinova ◽  
Lucie Lantová ◽  
Martin Bláha ◽  
Vojtěch Melenovský ◽  
Jan Hanzelka ◽  
...  

Heart Rhythm ◽  
2014 ◽  
Vol 11 (9) ◽  
pp. 1584-1591 ◽  
Author(s):  
Miguel Rodrigo ◽  
María S. Guillem ◽  
Andreu M. Climent ◽  
Jorge Pedrón-Torrecilla ◽  
Alejandro Liberos ◽  
...  

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