Clinical Research Papers:
Combination of susceptibility gene and traditional risk factors might enhance the performance of coronary heart disease screening strategy
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Shiyan Nian1,*, Lei Feng2,*, Yang Zhao3, Feng Luo3, Shu Zhang3, Dan Li2, Wenbo Xu2, Xingfeng Zhang2, Dan Ye2 and Xuejing Bai3
1 Intensive Care Unit, People’s Hospital of Yuxi City, Yuxi, Yunnan, P.R. China
2 Department of Laboratory, People’s Hospital of Yuxi City, Yuxi, Yunnan, P.R. China
3 Department of Laboratory, The Sixth Affiliated Hospital of Kunming Medical University, Yuxi, Yunnan, P.R. China
* These authors have contributed equally to this study
Shiyan Nian, email:
Lei Feng, email:
Keywords: coronary heart disease; serum biochemical indices; susceptibility gene; screening strategy; performance
Received: January 23, 2017 Accepted: March 19, 2017 Published: March 29, 2017
Coronary heart disease (CHD) associated risk factors and susceptibility genes were studied in parallel for decades, however, the combination of the classic CHD risk factors and genetic risk factors has been rarely studied. Previously; we reported that a single nucleotide polymorphism (SNP) in the stromal cell-derived factor 1 (SDF-1) gene was associated with CHD risk; in addition, we also established a CHD screening strategy using traditional CHD risk factors as independent variables. To explore how to combine genetic factors and traditional risk factors in CHD screening strategy, the CHD probabilities were tested in 218 males and 121 females according to their stromal cell-derived factor 1 (SDF-1) genotypes using CHD screening equations we reported previously. The genotypes had not altered the distribution characteristics of age, high-density lipoprotein cholesterol (HDL-C), triglyceride (TG), lipoprotein(a) (LP(a)), homocysteine (HCY) and total bilirubin (TBil) in males and age, HDL-C, HCY and γ-glutamyl transpeptidase (GGT) in females among genotypes. However, the mean CHD probability of subjects with G/G genotype was significantly higher than that of subjects with A/A genotype (0.51 ± 0.35 vs. 0.31 ± 0.31, P = 0.035). The mean CHD probability of subjects with G homozygous and G heterozygote was 0.48 ± 0.34 which displayed a difference trend to that of subjects with A homozygous (0.31 ± 0.31, P = 0.059). Our data suggested that genetic risk factors might be used as a classification standard to improve current CHD screening strategies.
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