Introduction: We measured mRNA levels of delayed rectifier potassium channe
ls in human atrial tissue to investigate the mechanism of the shortening of
the atrial effective refractory period and the loss of rate-adaptive short
ening of the atrial effective refractory period in human atrial fibrillatio
n. Methods and Results: A total of 34 patients undergoing open heart surger
y were included. Atrial tissue was obtained from the right atrial free wall
, right atrial appendage, left atrial free wall and left atrial appendage,
respectively. The mRNA amounts of K-VLQT1 (I-Ks), minK (beta-subunit of I-K
s), HERG (I-Kr), and K-V1.5 (I-Kur) were measured by reverse transcription-
polymerase chain reaction and normalized to the mRNA amount of GAPDH. We fo
und that the mRNA levels of K-V1.5, HERG and K-VLQT1 were all significantly
decreased in patients with persistent atrial fibrillation for more than 3
months. In contrast, the mRNA level of minK was significantly increased in
patients with persistent atrial fibrillation for more than 3 months. We fur
ther showed that these changes were independent of the underlying cardiac d
isease, atrial filling pressure, gender and age. We also found that there w
as no spatial dispersion of mRNA levels among the four atrial sampling site
s. Conclusions: Because the decrease in potassium currents results in a pro
longed action potential, the shortening of the atrial effective refractory
period in a trial fibrillation should be attributed to other factors. Howev
er, the decrease in IK, might contribute, at least in part, to the loss of
rate-adaptive shortening of the atrial refractory period. Copyright (C) 200
0 S. Karger AG, Basel.