INTRODUCTION: Atrial fibrillation (AF) is the most common type of complex arrhythmia found in everyday clinical practice. Lone AF is a particular form occurring in 2% to 31% of patients with confirmed AF. Genetic factors may underline this arrhythmia. AIM: To determine the relationship between G38S polymorphism in the MinK gene and the incidence of lone AF, and to evaluate this polymorphism as a genetic marker of susceptibility to AF. METHODS: The study involved 69 patients with lone AF and 60 control healthy subjects. Both groups included patients aged up to 65 years without cardiovascular or thyroid disease. MinK genotype was determined with PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism). The MinK gene was present in two allelic forms: G and S. RESULTS: The MinK G allele was found significantly more often in patients with AF (62.32%) compared to control subjects (41.80%) (p=0.009). In the AF group GS occurred more frequently (55.07%) than GG (34.78%) and SS genotypes (10.14%). In a logistic regression model the presence of G variant was associated with increase of AF risk in the study population (OR 2.39; 95% CI 0.88-6.54; p=0.084). Presence of GG genotype was associated with significant, over 10-fold, increase of AF risk. Presence of S allele of the MinK gene met criteria of protective factor against AF in the study population. CONCLUSIONS: 1. G38S polymorphism in the MinK gene seems to be associated with incidence of lone AF in the study population. 2. GG genotype carrier state may significantly relate to increased risk of AF in the study group. 3. G38S polymorphism in the MinK gene could be used as a genetic marker of risk of lone AF.
INTRODUCTION:Atrial fibrillation (AF) is the most common type of complex arrhythmia found in everyday clinical practice. Lone AF is a particular form occurring in 2% to 31% of patients with confirmed AF. Genetic factors may underline this arrhythmia. AIM: To determine the relationship between G38S polymorphism in the MinK gene and the incidence of lone AF, and to evaluate this polymorphism as a genetic marker of susceptibility to AF. METHODS: The study involved 69 patients with lone AF and 60 control healthy subjects. Both groups included patients aged up to 65 years without cardiovascular or thyroid disease. MinK genotype was determined with PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism). The MinK gene was present in two allelic forms: G and S. RESULTS: The MinK G allele was found significantly more often in patients with AF (62.32%) compared to control subjects (41.80%) (p=0.009). In the AF group GS occurred more frequently (55.07%) than GG (34.78%) and SS genotypes (10.14%). In a logistic regression model the presence of G variant was associated with increase of AF risk in the study population (OR 2.39; 95% CI 0.88-6.54; p=0.084). Presence of GG genotype was associated with significant, over 10-fold, increase of AF risk. Presence of S allele of the MinK gene met criteria of protective factor against AF in the study population. CONCLUSIONS: 1. G38S polymorphism in the MinK gene seems to be associated with incidence of lone AF in the study population. 2. GG genotype carrier state may significantly relate to increased risk of AF in the study group. 3. G38S polymorphism in the MinK gene could be used as a genetic marker of risk of lone AF.
Authors: Paul M Heerdt; Ritu Kant; Zhaoyang Hu; Vikram A Kanda; David J Christini; Jaideep K Malhotra; Geoffrey W Abbott Journal: J Mol Cell Cardiol Date: 2012-05-25 Impact factor: 5.000
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
Authors: Steven A Lubitz; Cevher Ozcan; Jared W Magnani; Stefan Kääb; Emelia J Benjamin; Patrick T Ellinor Journal: Circ Arrhythm Electrophysiol Date: 2010-06