In humans, chronic atrial fibrillation decreases the transient outward current and ultrarapid component of the delayed rectifier current differentially on each atria and increases the slow component of the delayed rectifier current in both.
OBJECTIVE
The purpose of this study was to compare the voltage-dependent K(+) currents of human cells of the right and left atria and determine whether electrical remodeling produced by chronic atrial fibrillation (CAF) is chamber-specific.


BACKGROUND
Several data point to the existence of interatrial differences in the repolarizing currents. Therefore, it could be possible that CAF-induced electrical remodeling differentially affects voltage-dependent K(+) currents in each atrium.


METHODS
Currents were recorded using the whole-cell patch-clamp in myocytes from left (LAA) and right atrial appendages (RAA) obtained from sinus rhythm (SR) and CAF patients.


RESULTS
In SR, LAA and RAA myocytes were divided in 3 types, according to their main voltage-dependent repolarizing K(+) current. CAF differentially modified the proportion of these 3 types of cells on each atrium. CAF reduced the Ca(2+)-independent 4-aminopyridine-sensitive component of the transient outward current (I(to1)) more markedly in the LAA than in the RAA. Therefore, an atrial right-to-left I(to1) gradient was created by CAF. In contrast, the ultrarapid component of the delayed rectifier current (I(Kur)) was more markedly reduced in the RAA than in the LAA, thus abolishing the atrial right-to-left I(Kur) gradient observed in SR. Importantly, in both atria, CAF increased the slow component of the delayed rectifier current (I(Ks)).


CONCLUSIONS
Our results demonstrated that in SR there are intra-atrial heterogeneities in the repolarizing currents. CAF decreases I(to1) and I(Kur) differentially in each atrium and increases I(Ks) in both atria, an effect that further promotes re-entry.
Caballero
Ricardo
R
Department of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.
de la Fuente
Marta González
MG
Gómez
Ricardo
R
Barana
Adriana
A
Amorós
Irene
I
Dolz-Gaitón
Pablo
P
Osuna
Lourdes
L
Almendral
Jesús
J
Atienza
Felipe
F
Fernández-Avilés
Francisco
F
Pita
Ana
A
Rodríguez-Roda
Jorge
J
Pinto
Angel
A
Tamargo
Juan
J
Delpón
Eva
E
D001281:Atrial Fibrillation / Q000175:diagnosis* / Q000188:drug therapy / Q000503:physiopathology; D002908:Chronic Disease; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D006325:Heart Atria / Q000166:cytology / Q000378:metabolism; D006801:Humans; D015640:Ion Channel Gating / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D012494:Sampling Studies
D026902:Potassium Channel Blockers; D015221:Potassium Channels