کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5945329 | 1172350 | 2014 | 6 صفحه PDF | دانلود رایگان |
- We performed a case-control study consisted of 1146 CHD patients and 1146 controls.
- Ten SNPs were significantly associated with CHD after adjustment for confounders.
- A genetic risk score was used to assess the combined effects of the loci on CHD risk.
- Genetic risk score significantly improved the net reclassification of CHD.
Objective: Genome-wide association studies have identified multiple genetic loci associated with coronary heart disease (CHD) risk. However, whether these loci could improve the CHD risk prediction is unclear. Methods and results: The present case-control study (1146 CHD cases and 1146 controls) genotyped 19 recently discovered SNPs that associated with CHD risk. As a result, 10 SNPs were successfully replicated with odds ratios (ORs) ranging from 1.16 to 1.78 (PÂ =Â 4.6Â ÃÂ 10â2 to 5.99Â ÃÂ 10â6). A genetic risk score was constructed to assess the combined effects of the susceptibility loci on CHD risk. Subject in the second tertile (ORÂ =Â 1.32, 95% CI, 1.02-1.73, PÂ =Â 3.84Â ÃÂ 10â2) and the third tertile (ORÂ =Â 2.62, 95% CI, 2.00-3.43, PÂ =Â 3.18Â ÃÂ 10â12) had an increased risk of CHD comparing with those in the first genetic risk score tertile after adjustment for traditional risk factors including family history of CHD. Addition of the genetic risk score to the traditional model significantly improved the net reclassification as measured by the net reclassification index (NRI) (4.82%, PÂ =Â 0.0001), however, no significant improvement was observed in discrimination of CHD, the area under the receiver operating characteristic curve (AUC) increased from 0.811 to 0.822 (PÂ =Â 0.18). Conclusions: A multilocus genetic risk score was associated with CHD risk in a Chinese Han population. This genetic risk score improved the net reclassification but not improved the CHD discrimination. The potential clinical use of this variations remains to be defined.
Journal: Atherosclerosis - Volume 237, Issue 2, December 2014, Pages 480-485