Gene Expression Of ATP Sensitive Potassium Channel And Delayed Rectifier Potassium Channels In Atria Of Patients With Atrial Fibrillation

Objective To investigate the gene expression of ATP sensitive potassium channel (Kir6.2) and delayed rectifier potassium channels(Kv1.5,HERG and KvLQT1)in atria of patients with rheumatic heart disease (RHD) accompanied by atrial fibrillation(AF).Methods The samples of right atrial appendages were obtained from 7 patients with paroxymal AF, 15 patients with chronic AF and 13 patients considered as controls in sinus rhythm. All patients were undergoing valve replacement surgery. The mRNA amount of Kir6.2,Kv1.5,HERG and KvLQT1 genes was measured by reverse transcription-polymerse chain reaction(RT-PCR) and normalized to the mRNA content of glyceraldehydes-3phosphate dehydrogenase (GAPDH).Result The mRNA concentrations of Kir6.2 and Kv1.5 were decreased significantly in patients with CAF(P<0.05) and correlated positively with duration of AF(Kir6.2:r=0.43,P=0.004;Kv1.5:r=0.42,P=0.005), and remained stable in patients with PAF(P>0.05), compared with those in patients with SR; there were no significant changes in mRNA concentrations of HERG and KvLQT1 in all groups(P>0.05).Conclusions The down-regulation of the gene expression of atrial Kir6.2 and Kv1.5 may serve as the molecular basis of ATP sensitive potassium current(IKATP) and ultra rapid delayed rectifier current(IKur) remodeling in patients with CAF. Atrial myocytes adapt to AF by downregulating mRNA contents of Kir6.2 and Kv1.5 to counteract the shortening of the atrial effective refractory period due to electrical remodrling. The mRNA expression of HERG and KvLQT1,keep stable in patients with AF,which accords with the electrophysiological study of the fast delayed rectifier potassium current(IKr) and the slow delayed rectifier potassium current(IKs)in animal models with AF.