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. 2019 May 10;9:7229. doi: 10.1038/s41598-019-43745-y

Table 2.

Relationships of TREML4 polymorphisms with coronary artery lesion extension in CAD patients.

Polymorphism All Extension of coronary artery lesion p
Without Low Intermediate Major
rs2803495 A/G N = 136 N = 33 N = 39 N = 40 N = 22
Genotypes, % AA 77.9 (106) 78.8 (26) 82.1 (32) 75.6 (31) 73.9 (17) 0.813
(Codominant) AG 20.6 (28) 21.2 (7) 17.9 (7) 22.0 (9) 21.7 (5)
GG 1.5 (2) 0 0 2.4 (1) 4.3 (1)
(Dominant) AA 77.9 (106) 78.8 (26) 82.1 (32) 75.6 (31) 73.9 (17) 0.863
AG + GG 22.1 (30) 21.2 (7) 17.9 (7) 24.4 (10) 26.1 (6)
Alleles, % A 88.2 (134) 89.4 91.0 86.6 84.8 0.702
G 11.8 (2) 10.6 9.0 13.4 15.2
rs2803496 C/T N = 134 N = 31 N = 39 N = 40 N = 23
Genotypes, % TT 76.9 (103) 83.9 (26) 71.8 (28) 80.5 (33) 69.6 (16) 0.526
(Codominant) CT 22.4 (30) 16.1 (5) 28.2 (11) 17.1 (7) 30.4 (7)
CC 0.7 (1) 0 0 2.4 (1) 0
(Dominant) TT 76.9 (103) 83.9 (26) 71.8 (28) 80.5 (33) 69.6 (16) 0.492
CT + CC 23.1 (31) 16.1 (5) 28.2 (11) 19.5 (8) 30.4 (7)
Alleles, % T 88.1 (133) 91.9 85.9 89.0 84.8 0.620
C 11.9 (1) 8.1 14.1 11.0 15.2

Numbers of subjects are indicated in parentheses. Frequencies were compared by the Chi-Square test. p-Values refer to comparisons among genotype frequencies of the different models and among allelic frequencies. For less than 10% of all samples, the genotype could not be determined. ‘Without’, Friesinger index 0; ‘Low’, Friesinger index 1–5; ‘Intermediate’, Friesinger index 6–10; ‘Major’, Friesinger index 11–15.