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ASSA13-03-9 Decreased Expression of Small-Conductance Ca2+-Activated K+ Channels SK1, SK2, and SK3 in Patients with Persistent Atrial Fibrillation
  1. Lan Huan1,
  2. Li Miaoling1,
  3. Xu Qiang2,
  4. Chen Tangting1,
  5. Zeng Xiaorong1
  1. 1The Institute of Cardiovascular Research, Luzhou Medical College
  2. 2Department of Histology and Embryology, Luzhou Medical College


Background Small-conductance Ca2+-activated K+ channels (SK channels) have been reported involved in atrial fibrillation (AF) as a new ion channel candidates, as they aid in integrating changes in intracellular Ca2+ with membrane potential and their high expression level in atrial myocytes.

Objective We recently reported that the current density of apamin-sensitive SK channels was significantly increased in AF group with persistent atrial fibrillation than SR group. The purpose of this study was to investigate whether the current density increase of SK channels in patients with persistent atrial fibrillation was because of its differential expression between the sinus rhythm (SR) and persistent atrial fibrillation patients and whether SK channels are involved in electrical remodelling of human persistent atrial fibrillation.

Methods The right atrial appendage myocytes were obtained from 8 sinus rhythm (SR) and 24 persistent atrial fibrillation patients underwent surgical valve replacement. Three SK channel subtypes (SK1–3) expressions were assayed by real-time quantitative PCR analysis.

Results The mRNA expression levels of SK1, SK2 and SK3 were decreased in persistent atrial fibrillation patients compared with SR patients. The expression of SK1, SK2 and SK3 in persistent atrial fibrillation patients were 23% (p < 0.05), 37% (p < 0.01) and 18% (p < 0.05) of SR patients, respectively.

Conclusions Our results demonstrated that SK1, SK2 and SK3 are involved in electrical remodelling of persistent atrial fibrillation. The SK1, SK2 and SK3 showed decreased expression in persistent atrial fibrillation. These findings provide a new insight into mechanisms of electrical remodelling of human persistent atrial fibrillation.

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