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. 2006 Apr 19;7:39. doi: 10.1186/1471-2350-7-39

Table 2.

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

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%

* 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.