European Heart Journal Advance Access originally published online on June 7, 2006
European Heart Journal 2006 27(14):1712-1718; doi:10.1093/eurheartj/ehl087
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Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation
1 Department of Medical and Surgical Critical Care; Thrombosis Centre, Azienda Ospedaliero-Universitaria Careggi; Center or the Study at Molecular and Clinical Level of Chronic, Degenerative and Neoplastic Diseases to Develop Novel Therapies, University of Florence, Viale Morgagni 85, 50134, Italy
2 Fondazione Don Carlo Gnocchi ONLUS, Centro S. Maria degli Ulivi-IRCCS, Florence, Italy
3 Department of Clinical Pathophysiology, Unit of Medical Genetic, University of Florence Italy
Received 2 November 2005; revised 2 May 2006; accepted 12 May 2006; online publish-ahead-of-print 7 June 2006.
* Corresponding author. Tel: +39 (0) 557949417; fax: +39 (0) 557949418. E-mail address: cinziafatini{at}hotmail.com
See page 1640 for the editorial comment on this article (doi:10.1093/eurheartj/ehl076)
Aim Mink protein, a ß-subunit of Iks potassium channels modulate cardiac cellular electrophysiology, and experimental data demonstrated that NO is involved in cardiac vagal activity and in the inhibition of sympathetic activity. We evaluated the role of eNOS –786T>C, 894G>T, 4a/4b and of minK S38G polymorphisms as predisposing factors to non-valvular atrial fibrillation (NVAF).
Methods and results We studied 331 consecutive patients with documented NVAF and in 441 control subjects, comparable for age and gender. A significant difference in allele frequencies between patients and controls for minK S38G and eNOS –786T>C, but not for eNOS 894G>T and 4a/4b polymorphisms, was observed. The minK 38G allele was significantly associated with susceptibility to NVAF at both univariate and multivariable analysis, according to dominant and recessive genetic model (multivariable analysis, dominant: OR=1.73, P=0.004 and recessive: OR=1.59, P=0.006). The eNOS –786C allele weakly influenced NVAF at univariate analysis, according to the dominant model (OR=1.50, P=0.01). The contemporary presence of minK 38G and eNOS –786C alleles increased the predisposition to NVAF, after adjustment with cardiovascular risk factors (OR minK 38G*eNOS –786C=2.11, P<0.0001; OR=2.58, P=0.003; OR=3.08, P=0.002, according to dominant, recessive, and additive model, respectively).
Conclusion Our findings suggest a role for minK and eNOS genes as predisposing factors to NVAF.
Key Words: eNOS –786T>C • 894G>T • 4a/4b polymorphisms • minK S38G polymorphism • Non-valvular atrial fibrillation
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