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Table 2 Distribution of genotypes in controls without atrial fibrillation (AF) and subjects with AF.

From: A role for CETP TaqIB polymorphism in determining susceptibility to atrial fibrillation: a nested case control study

Locus

AF Controls (n = 97)

AF Cases (n = 97)

P value (Chi-square) OR (95%CI)*

ACE gene I/D

  

0.44

II

22.7%

31.1%

0.65 (0.33–1.27)

ID

50.0%

43.3%

0.92 (0.47–1.78)

DD

27.3%

25.6%

 

AGT gene G-6A

  

0.96

AA

16.1%

17.6%

1.07 (0.59–1.97)

AG

46.0%

46.2%

1.11 (0.51–2.44)

GG

37.9%

36.3%

 

AT1R gene A1166C

  

0.28

CC

8.0%

11.6%

0.73 (0.41–1.32)

AC

46.0%

34.7%

1.50 (0.55–4.05)

AA

46.0%

53.7%

 

Bradykinin 2 C58T CC

34.1%

36.8%

0.92 0.89 (0.48–1.63)

TT

18.2%

16.8%

0.91 (0.43–1.96)

CT

47.7%

46.3%

 

Bradykinin 2 C181T

  

0.54

CC

72.7%

76.3%

0.83 (0.42–1.62)

TT

1.1%

 

n.a. (empty cells)

CT

26.1%

23.7%

 

Bradykinin 2 exon1

  

0.35

-9/-9

38.2%

29.3%

1.08 (0.60–1.94)

-9/+9

43.8%

45.7%

1.49 (0.80–2.77)

+9/+9

18.0%

25.0%

1.52 (0.74–3.12)

CETP I405V

  

0.02

AA

44.3%

46.8%

0.90 (0.50–1.62)

AG

52.3%

38.3%

4.96 (1.37–17.90)

GG

3.4%

14.9%

 

CETP TaqIB

  

0.02

B1B1

24.1%

44.1%

0.40 (0.21–0.77)

B1B2

62.1%

43.0%

0.93 (0.39–2.19)

B2B2

13.8%

12.9%

 
  1. * Odds ratios (95% Confidence Intervals) for the presence of AF on the electrocardiogram were obtained by logistic regression; the top OR is for autosomal dominant model and the bottom for autosomal recessive model.