European Heart Journal Advance Access published online on June 7, 2006
European Heart Journal, doi:10.1093/eurheartj/ehl087
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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
* To whom correspondence should be addressed. Aim Mink protein, a 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.
Received November 2, 2005
Revised May 2, 2006
Accepted May 12, 2006
Clinical research
Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation
Cinzia Fatini 1 *,
Elena Sticchi 2,
Maurizio Genuardi 3,
Francesco Sofi 1,
Francesca Gensini 3,
Anna Maria Gori 1,
Meri Lenti 1,
Antonio Michelucci 1,
Rosanna Abbate 1,
and
Gian Franco Gensini 2
2 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; 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
Cinzia Fatini, E-mail: cinziafatini{at}hotmail.com
Abstract 
-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).
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