Mechanisms of Atrial Tachyarrhythmias Associated With Coronary Artery Occlusion in a Chronic Canine Model

Coronary artery disease predisposes to atrial fibrillation (AF), but the effects of chronic atrial ischemia/infarction on AF-related substrates are unknown. Regional right atrial myocardial infarction (MI) was created in 40 dogs by ligating an artery that supplies the right atrial free wall and not...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 2011-01, Vol.123 (2), p.137-146
Hauptverfasser: NISHIDA, Kunihiro, XIAO YAN QI, MICHAEL, Georghia, TALAJIC, Mario, NATTEL, Stanley, WAKILI, Reza, COMTOIS, Philippe, CHARTIER, Denis, HARADA, Masahide, IWASAKI, Yu-Ki, ROMEO, Philippe, MAGUY, Ange, DOBREV, Dobromir
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Sprache:eng
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Zusammenfassung:Coronary artery disease predisposes to atrial fibrillation (AF), but the effects of chronic atrial ischemia/infarction on AF-related substrates are unknown. Regional right atrial myocardial infarction (MI) was created in 40 dogs by ligating an artery that supplies the right atrial free wall and not the ventricles; 35 sham dogs with the same artery isolated but not ligated were controls. Dogs were observed 8 days after MI and subjected to open-chest study, in vitro optical mapping, and/or cell isolation for patch-clamp and Ca(2+) imaging on day 8. Holter ECGs showed more spontaneous atrial ectopy in MI dogs (eg, 662±281 on day 7 versus 34±25 ectopic complexes per day at baseline; 52±21 versus 1±1 atrial tachycardia episodes per day). Triggered activity was increased in MI border zone cells, which had faster decay of caffeine-evoked Ca(2+) transients and enhanced (by ≈73%) Na(+)-Ca(2+) exchange current. Spontaneous Ca(2+) sparks (confocal microscopy) occurred under β-adrenergic stimulation in more MI dog cells (66±9%) than in control cells (29±4%; P
ISSN:0009-7322
1524-4539
DOI:10.1161/CIRCULATIONAHA.110.972778