Chronic atrial fibrillation does not further decrease outward currents. It increases them.

2003 ◽  
Vol 285 (4) ◽  
pp. H1378-H1384 ◽  
Author(s):  
Wen Dun ◽  
Parag Chandra ◽  
Peter Danilo ◽  
Michael R. Rosen ◽  
Penelope A. Boyden
Keyword(s):  
Atrial Fibrillation ◽  
Voltage Dependence ◽  
Cell Voltage ◽  
Chronic Atrial Fibrillation ◽  
Right Atrial ◽  
Electrical Remodeling ◽  
Atrial Pacing ◽  
Decay Kinetics ◽  
Atrial Electrophysiology ◽  
Recovery From Inactivation

Rapid atrial pacing causes electrical remodeling that leads to atrial fibrillation (AF). AF can further remodel atrial electrophysiology to maintain AF. Our previous studies showed that there was a marked difference in the duration of AF in dogs that have been atrial paced at 400 beats/min for 6 wk. We hypothesized that this difference is based on the changes in the degree of electrical remodeling caused by rapid atrial pacing versus that by AF. Right atrial cells were isolated from control dogs (Con, N = 28), from dogs with chronic AF (cAF dogs, N = 13, episodes lasting at least 6 days), or from dogs with nonsustained or brief episodes of AF (nAF dogs, N = 10, episodes lasting minutes to hours). Both transient outward ( Ito) and sustained outward K+ current ( Isus) densities/functions were determined using whole cell voltage-clamp techniques. In nAF cells, Ito density was reduced by 69% at +40 mV: from 7.1 ± 0.5 pA/pF (Con, n = 59) to 2.2 ± 0.2 pA/pF (nAF, n = 24) ( P < 0.05). The voltage dependence of inactivation of Ito was shifted positively and decay kinetics were changed; however, recovery from inactivation was not altered in nAF cells. In contrast, Ito density in cAF cells was both significantly different from Con cells and larger than that in nAF cells [at +40 mV, 3.5 ± 0.3 pA/pF (cAF, n = 29), P < 0.05]. In cAF cells, recovery from inactivation and decay of Ito were both slow; yet, voltage dependence inactivation of Ito approached that of Con cells. Furthermore, “recovered” Ito of cAF cells was more sensitive to tetraethylammonium than currents of Con and nAF cells. Isus densities of nAF and cAF cells did not differ. Both nAF and cAF cells have reduced Ito versus Con cells, but Ito remodeling of nAF cells differed from that of cAF cells. Ito in cAF dogs was likely remodeled by AF per se, whereas that in nAF dogs was likely the consequence of the rapid rate in the absence of sustained AF.

Slow conduction zone as an early electrical remodeling change in patients with atrial fibrillation

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Kishima ◽  
T Mine ◽  
E Fukuhara ◽  
M Ishihara
Keyword(s):  
Atrial Fibrillation ◽  
Low Voltage ◽  
Ascending Aorta ◽  
Right Atrial ◽  
Electrical Remodeling ◽  
Atrial Pacing ◽  
Descending Aorta ◽  
Contact Areas ◽  
Slow Conduction ◽  
Conduction Zone

Abstract Background The slow conduction zone (SCZ) in the left atrium (LA) detected using 3-D mapping and high-resolution imaging system has attracted attention as an arrhythmia substrate of atrial fibrillation (AF). However, the occurrence mechanism of SCZ remains unclear. Purpose This aim of this study is to clarify whether SCZ is related to the low voltage zone (LVZ) or the LA anatomical contact areas with other organs such as aorta or thoracic spine in patients with AF. Methods We studied 36 patients (21 males, 68±10 years, 14 paroxysmal AF; PAF, 17 persistent AF; PeAF, 5 long-standing persistent AF; LS-PeAF) who received catheter ablation for AF. High-density LA mapping during sinus rhythm or right atrial pacing after pulmonary vein isolation were constructed by acquiring more than 2000 endocardial points in each patient. Isochronal activation maps were created at 5-ms interval setting, and the SCZ was identified on the activation map by finding a site with isochronal crowding of ≥3 isochrones, which are calculated as ≤27 cm/s (figure). The LVZ was defined as the following; mild (&lt;1.5 mV), moderate (&lt;1.0 mV), and severe LA-LVZ (&lt;0.5 mV). The LA contact areas (CoAs; ascending aorta-anterior LA, descending aorta-posterior LA, and vertebrae-posterior LA) were assessed using computed tomography. Results The SCZ was distributed linearly (figure), and observed in 35 of 36 patients (97.2%). The SCZ was often found in the anterior (89%), roof (64%), and septal wall (47%) of LA, and longest in patients with LS-PeAF (PAF: 56±34 mm, PeAF; 79±41 mm, LS-PeAF; 107±34mm, P=0.0351). The prevalence rate of SCZ (97.2%) was higher than LVZ (figure, mild LA-LVZ; 91.7%, moderate LA-LVZ: 66.7%, severe LA-LVZ; 25%). The 55.8% of SCZ overlapped with mild LA-LVZ, 37.6% of SCZ with moderate LA-LVZ, and 19.1% of SCZ with severe LA-LVZ. The LA CoAs were found in all patients. A total of 72 CoAs (average surface area, 7.0±4.0 cm2) were identified. A CoA was found in each of the three representative regions, ascending aorta-anterior LA (4.1±2.0 cm2, 36 of 36 patients, 100%), descending aorta-posterior LA (2.3±1.2 cm2, 12 of 36 patients, 33%), and vertebrae-posterior LA (3.4±2.1 cm2, 24 of 36 patients, 67%). However, only 22% of SCZ matched with the LA anatomical contact areas. Conclusion The slow conduction zone reflects LA electrical remodeling and may be a precursor finding of the low voltage zone, not LA contact areas in patients with atrial fibrillation. Funding Acknowledgement Type of funding source: None

Abstract 5347: Alpha-Adrenergic-Regulation of I K1 and Acetylcholine-gated I K,ACh is Impaired in Patients with Atrial Fibrillation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Niels Voigt ◽  
Birgit Bollmann ◽  
Erich Wettwer ◽  
Klaus Matschke ◽  
Ursula Ravens ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Cell Voltage ◽  
Chronic Atrial Fibrillation ◽  
Right Atrial ◽  
Constitutive Activity ◽  
Atrial Myocytes ◽  
Channel Activation ◽  
Adrenergic Regulation ◽  
Sympathetic Nervous ◽  
Stimulation Of

In chronic atrial fibrillation (cAF) the major effector of vagal excitation I K,ACh develops arrhythmogenic ACh-independent constitutive activity with limited additional activation via muscarinic receptors. Since the sympathetic nervous system prevents excessive vagal nerve activation we tested whether modulation of I K,ACh by adrenoceptors (ARs) is affected in cAF. I K,ACh was measured with whole-cell voltage-clamp in isolated right atrial myocytes from 29 sinus rhythm (SR) and 17 cAF patients. Compared to SR basal current was higher in cAF whereas carbachol (CCh, 2 μM)-activated I K,ACh was smaller (Figure ). Activation of beta-ARs with isoproterenol (ISO, 1 μM) increased CCh-activated I K,ACh by ~25% and ~20% in SR and cAF, respectively, whereas activation of adenylyl cyclase with forskolin (FSK, 1 μM) was without effect suggesting channel activation by G-beta/gamma-binding rather than PKA. Stimulation of alpha-1-ARs with phenylephrine (PE, 100 μM) reduced CCh-activated I K,ACh in SR by ~80%, but was ineffective in cAF. Neomycin (NEO, 500 μM), a blocker of phospholipase-C (PLC), prevented the PE effect suggesting that PE blunts I K,ACh activation via PLC-induced depletion of membrane PIP2 content required for I K,ACh stimulation. PE, but not ISO or FSK, reduced basal current in SR by ~50%, suggesting inhibition of I K1 , but was ineffective on basal current in cAF which consists of I K1 and constitutively active I K,ACh . Inhibition of CCh-activated I K,ACh and suppression of I K1 by alpha-1-ARs are impaired in cAF. These changes may shift the balance to stronger beta-AR-mediated I K,ACh activation promoting the maintenance of AF.

Local Capture by Atrial Pacing in Spontaneous Chronic Atrial Fibrillation

Circulation ◽  
1997 ◽  
Vol 95 (10) ◽  
pp. 2416-2422 ◽  
Author(s):  
Claudio Pandozi ◽  
Leopoldo Bianconi ◽  
Mauro Villani ◽  
Antonio Castro ◽  
Giuliano Altamura ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Chronic Atrial Fibrillation ◽  
Atrial Pacing ◽  
Local Capture

Thoracic vein ablation terminates chronic atrial fibrillation in dogs

2004 ◽  
Vol 286 (6) ◽  
pp. H2072-H2077 ◽  
Author(s):  
Angela M. Park ◽  
Chung-Chuan Chou ◽  
Paul C. Drury ◽  
Yuji Okuyama ◽  
Anish Peter ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Sinus Rhythm ◽  
Superior Vena Cava ◽  
Superior Vena ◽  
Vena Cava ◽  
Chronic Atrial Fibrillation ◽  
Atrial Pacing ◽  
Bipolar Electrodes ◽  
Cycle Lengths ◽  
Activation Cycle

The thoracic vein hypothesis of chronic atrial fibrillation (AF) posits that rapid, repetitive activations from muscle sleeves within thoracic veins underlie the mechanism of sustained AF. If this is so, thoracic vein ablation should terminate sustained AF and prevent its reinduction. Six female mongrel dogs underwent chronic pulmonary vein (PV) pacing at 20 Hz to induce sustained (>48 h) AF. Bipolar electrodes were used to record from the atria and thoracic veins, including the vein of Marshall, four PVs, and the superior vena cava. Radio frequency (RF) application was applied around the PVs and superior vena cava and along the vein of Marshall until electrical activity was eliminated. Computerized mapping (1,792 electrodes, 1 mm resolution) was also performed. Sustained AF was induced in 30.6 ± 6.5 days, and ablation was done 17.3 ± 8.5 days afterward. Before ablation, the PVs had shorter activation cycle lengths than the atria, and rapid, repetitive activations were observed in the PVs. All dogs converted to sinus rhythm during ( n = 4 dogs) or within 90 min of completion of RF ablation. Rapid atrial pacing afterward induced only nonsustained (<60 s) AF in all dogs. Average AF cycle lengths after reinduction were significantly ( P = 0.01) longer (183 ± 31.5 ms) than baseline (106 ± 16.2 ms). There were no activation cycle length gradients after RF application. We conclude that thoracic vein ablation converts canine sustained AF into sinus rhythm and prevents the reinduction of sustained AF. These findings suggest that thoracic veins are important in the maintenance of AF in dogs.

Interventional Therapeutic Procedures in Patients With a Preexisting Dual Site Right Atrial Pacing System for Refractory Atrial Fibrillation

1998 ◽  
Vol 81 (10) ◽  
pp. 1274-1277 ◽  
Author(s):  
Atul Prakash ◽  
Philippe Delfaut ◽  
Irakli Giorgberidze ◽  
Ryszard B Krol ◽  
Philip Mathew ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Therapeutic Procedures ◽  
Dual Site
Sign in / Sign up

Export Citation Format

Share Document