BACKGROUND: Human minK protein is the beta-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 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.
BACKGROUND:HumanminK protein is the beta-subunit of I(Ks) potassium channel and plays an important role in cardiac cellular electrophysiology. We investigated the association between humanatrial 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.
Authors: Rabia Faridi; Risa Tona; Alessandra Brofferio; Michael Hoa; Rafal Olszewski; Isabelle Schrauwen; Muhammad Z K Assir; Akhtar A Bandesha; Asma A Khan; Atteeq U Rehman; Carmen Brewer; Wasim Ahmed; Suzanne M Leal; Sheikh Riazuddin; Steven E Boyden; Thomas B Friedman Journal: Hum Mutat Date: 2018-12-12 Impact factor: 4.878
Authors: Moritz F Sinner; Steven A Lubitz; Arne Pfeufer; Seiko Makino; Britt-Maria Beckmann; Kathryn L Lunetta; Gerhard Steinbeck; Siegfried Perz; Rosanna Rahman; Akshata Sonni; Steven M Greenberg; Karen L Furie; H-Erich Wichmann; Thomas Meitinger; Annette Peters; Emelia J Benjamin; Jonathan Rosand; Patrick T Ellinor; Stefan Kääb Journal: Heart Rhythm Date: 2010-11-04 Impact factor: 6.343