Clinical Study Of Kir2.1 And Kir3.4 Potassium Channel Gene Expression In Atria Of Patients With Atrial Fibrillation

Objective To investigate whether patients with rheumatic heart disease accompanied by atrial fibrillation show alterations in kir2.1 and kir3.4 potassium channel gene expression.Methods Right atrial appendages were obtained from 7 patients with paroxysmal AF, 21 patients with chronic AF and 18 patients matched controls in sinus rhythm. All were patients undergoing valve replacement surgery. Total RNA was isolated and reversely transcribed into cDNA . In a semi-quantitative polymerase chain reaction the cDNA of interest and of glyceraldehydes-3-phosphate dehydrogenase were coamplified and separated by ethidium bromide stained gel-electrophoresis.Results Compared with SR, mRNA levels of Kir2.1 were increased in patients with CAF [(0.38 0.24), (0.62 0.23), P <0.01] , and were positive correlation with duration of AF (r=0. 42, P =0. 004) ; mRNA levels of Kir3.4 were reduced in patients with PAF and CAF[(0.56 0.25),(0.35 0.18),P<0.05; (0.56 0.25),(0.32 0.11), P <0.01,respectively] , also were negative correlation with duration of AF(r=-0. 44, P =0. 003).Conclusions The gene expression of kir2.1 and kir3.4 potassium channel in atria of patients with atrial fibrillation were increased and decreased respectively. Human atrial fibrillation induces transcriptionally mediated upregulation of IK1 and downregulation of IKACH- Atrial myocytes adapt to AF by downregulating mRNA levels of Kir3.4 to counteract the shortening of the atrial effective refractory period due to electrical remodeling.