TY - JOUR
T1 - Association of the human minK gene 38G allele with atrial fibrillation
T2 - Evidence of possible genetic control on the pathogenesis of atrial fibrillation
AU - Lai, Ling Ping
AU - Su, Ming Jai
AU - Yeh, Huei Ming
AU - Lin, Jiunn Lee
AU - Chiang, Fu Tien
AU - Hwang, Juey Jen
AU - Hsu, Kwan Li
AU - Tseng, Chuen Den
AU - Lien, Wen Pin
AU - Tseng, Yung Zu
AU - Huang, Shoei K.Stephen
PY - 2002/1/1
Y1 - 2002/1/1
N2 - Background: Human mink protein is the β-subunit of IKs potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between human atrial fibrillation and the polymorphism of mink gene (38G or 38S) with a case-control study. Methods: We included 108 patients with atrial fibrillation and 108 control subjects. The case patients and control subjects were matched regarding age, sex, presence of valvular heart disease, and presence of left ventricular dysfunction. The genotype of mink was determined with polymerase chain reaction and restriction fragment analysis. Results: The results showed an association between the mink 38G allele and atrial fibrillation. The odds ratios for atrial fibrillation in patients with 1 and 2 mink 38G alleles were 2.16 (95% CI 0.81-5.74) and 3.58 (95% CI 1.38-9.27), respectively, when compared with patients without mink 38G allele. In a logistic regression model, the odds ratio for atrial fibrillation was 1.80 (95% CI 1.20-2.71, P < .0046) for patients with 1 more mink 38G allele. Conclusion: We report the association between the mink 38G allele and clinical atrial fibrillation. Our findings suggest possible genetic control on the pathogenesis of atrial fibrillation.
AB - Background: Human mink protein is the β-subunit of IKs potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between human atrial fibrillation and the polymorphism of mink gene (38G or 38S) with a case-control study. Methods: We included 108 patients with atrial fibrillation and 108 control subjects. The case patients and control subjects were matched regarding age, sex, presence of valvular heart disease, and presence of left ventricular dysfunction. The genotype of mink was determined with polymerase chain reaction and restriction fragment analysis. Results: The results showed an association between the mink 38G allele and atrial fibrillation. The odds ratios for atrial fibrillation in patients with 1 and 2 mink 38G alleles were 2.16 (95% CI 0.81-5.74) and 3.58 (95% CI 1.38-9.27), respectively, when compared with patients without mink 38G allele. In a logistic regression model, the odds ratio for atrial fibrillation was 1.80 (95% CI 1.20-2.71, P < .0046) for patients with 1 more mink 38G allele. Conclusion: We report the association between the mink 38G allele and clinical atrial fibrillation. Our findings suggest possible genetic control on the pathogenesis of atrial fibrillation.
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U2 - 10.1067/mhj.2002.123573
DO - 10.1067/mhj.2002.123573
M3 - Article
C2 - 12228786
AN - SCOPUS:0036735143
SN - 0002-8703
VL - 144
SP - 485
EP - 490
JO - American Heart Journal
JF - American Heart Journal
IS - 3
ER -