Aldosterone synthase gene polymorphism as a determinant of atrial fibrillation in patients with heart failure

被引:51
作者
Amir, Offer [1 ,2 ,4 ]
Amir, Ruthie E. [3 ]
Paz, Hagar [1 ,2 ]
Mor, Roi [3 ]
Sagiv, Michael [3 ]
Lewis, Basil S. [1 ,2 ,4 ]
机构
[1] Lady Davis Carmel Ctr, Heart Failure Ctr, Dept Cardiovasc Med, Haifa, Israel
[2] Lin Med Ctr, Haifa, Israel
[3] Wingate Inst Phys Educ & Sports, Zinman Coll Phys Educ & Sport Sci, Dept Genet & Mol Biol, Haifa, Israel
[4] Technion Israel Inst Technol, Ruth & Bruce Rappaport Sch Med, Haifa, Israel
关键词
D O I
10.1016/j.amjcard.2008.03.063
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We analyzed the possible association between aldosterone synthase (CYP11B2) T-344C polymorphism, which is associated with increased aldosterone activity, and the prevalence of atrial fibrillation (AF) in 196 consecutive patients who had symptomatic systolic heart failure (HF; left ventricular ejection fraction <40%) for >= 3 months before recruitment. Genomic DNA was extracted from peripheral blood leukocytes using a standard protocol. Subjects were genotyped for the CYP11B2 polymorphism using the polymerase chain reaction/restriction fragment length polymorphism approach. AF was present in 63 patients (33%) with HF. We found the -344 CC genotype to be a strong independent marker for AF. Almost 1/2 (45%) of patients with this genotype had AF compared with 1/4 (27%) with -344 TT and TC genotypes (p = 0.01). A multivariate stepwise logistic regression model that included age, gender, New York Heart Association class, CYP11B2 -344CC genotype, and echocardiographic measurements of left ventricular ejection fraction, left atrial dimension, left ventricular end-diastolic diameter, and mitral regurgitation severity showed that the CYP11B2 CC genotype (adjusted for age and left atrial size) was an independent predictor of AF (adjusted odds ratio 2.35, 95% confidence interval 1.57 to 3.51, p = 0.03). In conclusion, CYP11B2 T-344C promoter polymorphism predisposes to clinical AF in patients with HF. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:326 / 329
页数:4
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