Background-Congestive heart failure (CHF) is frequently associated with atrial fibrillation (AF), but little is known about the effects of CHF on atrial cellular electrophysiology. Methods and Results-We studied action potential (AP) properties and ionic currents in atrial myocytes from dogs with CHF induced by ventricular pacing at 220 to 240 bpm for 5 weeks. Atrial myocytes from CHF dogs were hypertrophied (meanϮSEM capacitance, 89Ϯ2 pF versus 71Ϯ2 pF in control, nϭ160 cells per group,

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... ). CHF significantly reduced the density of L-type Ca 2ϩ current (I Ca ) by Ϸ30%, of transient outward K ϩ current (I to ) by Ϸ50%, and of slow delayed rectifier current (I Ks ) by Ϸ30% without altering their voltage dependencies or kinetics. The inward rectifier, ultrarapid and rapid delayed rectifier, and T-type Ca 2ϩ currents were not altered by CHF. CHF increased transient inward Na ϩ /Ca 2ϩ exchanger (NCX) current by Ϸ45%. The AP duration of atrial myocytes was not altered by CHF at slow rates but was increased at faster rates, paralleling in vivo refractory changes. CHF created a substrate for AF, prolonging mean AF duration from 8Ϯ4 to 535Ϯ82 seconds (PϽ0.01). Conclusions-Experimental CHF selectively decreases atrial I to , I Ca , and I Ks , increases NCX current, and leaves other currents unchanged. The cellular electrophysiological remodeling caused by CHF is quite distinct from that caused by atrial tachycardia, highlighting important differences in the cellular milieu characterizing different clinically relevant AF substrates. (Circulation. 2000;101:2631-2638.) Key Words: ion channels Ⅲ biophysics Ⅲ electrophysiology Cellular Electrophysiology Cells were isolated from 28 control and 28 CHF dogs. Cells in a 1-mL bath were superfused (3 mL/min, 35°C, or for the ultrarapid