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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.
J Am Coll Cardiol. 2010 May 25; 55(21):2346-54.JACC

Abstract

OBJECTIVES

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.

Authors+Show Affiliations

Department of Pharmacology, School of Medicine, Universidad Complutense de Madrid, Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20488306

Citation

Caballero, Ricardo, et al. "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." Journal of the American College of Cardiology, vol. 55, no. 21, 2010, pp. 2346-54.
Caballero R, de la Fuente MG, Gómez R, et al. 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. J Am Coll Cardiol. 2010;55(21):2346-54.
Caballero, R., de la Fuente, M. G., Gómez, R., Barana, A., Amorós, I., Dolz-Gaitón, P., Osuna, L., Almendral, J., Atienza, F., Fernández-Avilés, F., Pita, A., Rodríguez-Roda, J., Pinto, A., Tamargo, J., & Delpón, E. (2010). 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. Journal of the American College of Cardiology, 55(21), 2346-54. https://doi.org/10.1016/j.jacc.2010.02.028
Caballero R, et al. 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. J Am Coll Cardiol. 2010 May 25;55(21):2346-54. PubMed PMID: 20488306.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - 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. AU - Caballero,Ricardo, AU - de la Fuente,Marta González, AU - Gómez,Ricardo, AU - Barana,Adriana, AU - Amorós,Irene, AU - Dolz-Gaitón,Pablo, AU - Osuna,Lourdes, AU - Almendral,Jesús, AU - Atienza,Felipe, AU - Fernández-Avilés,Francisco, AU - Pita,Ana, AU - Rodríguez-Roda,Jorge, AU - Pinto,Angel, AU - Tamargo,Juan, AU - Delpón,Eva, PY - 2009/12/04/received PY - 2010/01/28/revised PY - 2010/02/15/accepted PY - 2010/5/22/entrez PY - 2010/5/22/pubmed PY - 2010/6/17/medline SP - 2346 EP - 54 JF - Journal of the American College of Cardiology JO - J Am Coll Cardiol VL - 55 IS - 21 N2 - OBJECTIVES: 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. SN - 1558-3597 UR - https://www.unboundmedicine.com/medline/citation/20488306/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_ DB - PRIME DP - Unbound Medicine ER -