The ultrarapid and the transient outward K+ current in human atrial fibrillation.: Their possible role in postoperative atrial fibrillation

M. C. BRANDT, L. PRIEBE, T. BOHLE. M. SUDKAMP AND D. J. BEUCKELMANN. The Ultrarapid and the Transient Outward K+ Current in Human Atrial Fibrillation. Their Possible Role in Postoperative Atrial Fibrillation. Journal of Molecular and Cellular Cardiology (2000) 32, 1885-1896. Atrial fibrillation (AF) causes distinct changes in atrial conduction, characterized as electrical remodeling. Experimental data on the possible significance of alterations of specific K+ outward currents in this process are still limited in human AF. The ultra-rapid delayed rectifier current (I-Kur) has not been studied in AF with respect to its sensitivity to 4-Aminopyridine (4-AP). To clarify the role of (1) the 4-AP sensitive I-Kur current, compared to recordings without using 4-AP (I-Kur*), and (2) the transient outward current (I-to) in changes of atrial repolarizarion associated with AF, whole cell voltage-clamp recordings were obtained from atrial myocytes of patients undergoing elective cardiac surgery, with and without a history of atrial fibrillation (AF/non-AF). Further, a possible relation between experimental data and postoperative AF was studied. In AF patients, I-Kur*. was reduced by 40% [5.00 +/- 0.32 pA/pF (non-AF) and 2.91 +/- 0.45 pA/pF (AF) at + 50 mV, P<0.0001, n = 22/11], I-Kur by 55% [3.81 +/- 0.30 pA/pF (non-AF) and 1.71 +/- 0.20 pA/pF (AF) at + 50 mV, P<0.0001, n = 22/11]. The mean amplitude of I-Kur was significantly smaller than I-Kur* Consistently, I-to was reduced by 44% [11.57 +/- 0.77 pA/pF (non-AF) and 6.51 +/- 1.31 pA/pF (AF), P < 0.01, n = 25/11]. In 48% of non-AF patients, postoperative AF was detected. The corresponding voltage-clamp recordings showed a trend to reduced I-Kur*. and I-Kur currents, although it did not reach statistical significance. The consistent reduction of all three K+ currents investigated due to the presence of AF indicates an important association of abnormalities in cellular repolarization with the onset and the self-sustaining nature of human AF. (C) 2000 Academic Press.