|Title:||Association of the Human Mink Gene 38g Allele with Atrial Fibrillation: Evidence of Possible Genetic Control on the Pathogenesis of Atrial Fibrillation
|Keywords:||LONG-QT SYNDROME;POTASSIUM CHANNEL GENE;CARDIAC-ARRHYTHMIA;EPIDEMIOLOGIC FEATURES;BRUGADA-SYNDROME;LANGENIELSEN||Issue Date:||2002||Journal Volume:||v.144||Journal Issue:||n.3||Start page/Pages:||485-490||Source:||THE AMERICAN HEART JOURNAL||Abstract:||
Background Human minK protein is the p-subunit Of I-Ks. 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 I and 2 minK 38G alleles were 2.16 (95% Cl 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% Cl 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.
|Appears in Collections:||醫學系|
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