Association of the human minK gene 38G allele with atrial fibrillation: Evidence of possible genetic control on the pathogenesis of atrial fibrillation

Ling Ping Lai, Ming Jai Su, Huei Ming Yeh, Jiunn Lee Lin, Fu Tien Chiang, Juey Jen Hwang, Kwan Li Hsu, Chuen Den Tseng, Wen Pin Lien, Yung Zu Tseng, Shoei K.Stephen Huang

Research output: Contribution to journalArticlepeer-review

162 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)485-490
Number of pages6
JournalAmerican Heart Journal
Volume144
Issue number3
DOIs
Publication statusPublished - Jan 1 2002
Externally publishedYes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Fingerprint

Dive into the research topics of 'Association of the human minK gene 38G allele with atrial fibrillation: Evidence of possible genetic control on the pathogenesis of atrial fibrillation'. Together they form a unique fingerprint.

Cite this