SNP | Gene name | Discovery cohort (n=763) | Replication cohort (n=836) | ||||||||
HWE p | Risk allele frequency | OR | P value | HWE p | Risk allele frequency | OR | P value | ||||
MI+ | MI- | MI+ | MI- | ||||||||
rs17849502 | NCF2 | 0.013 | 0.12 | 0.08 | 2.00 (1.08 to 3.68) | 0.027 | 8.80×10-7 | 0.18 | 0.11 | 1.94 (0.94 to 4.04) | 0.075 |
rs11889341 | STAT4 | 0.81 | 0.44 | 0.34 | 1.76 (1.18 to 2.63) | 0.0054 | 0.53 | 0.40 | 0.31 | 1.81 (0.94 to 3.47) | 0.075 |
rs564799 | IL12A | 0.29 | 0.68 | 0.59 | 1.53 (1.01 to 2.31) | 0.042 | 1.00 | 0.74 | 0.61 | 2.15 (1.08 to 4.26) | 0.029 |
Using a forward conditional multiple logistic regression model, 60 genetic variants with previously established association with SLE (p<5×10−8, online supplemental table 2) were analysed for associations with myocardial infarction in the discovery cohort. The table shows SNPs included in the final model. These SNPs were subsequently analysed in the replication cohort. Age at follow-up and disease duration were included as covariates. P<0.05 (unadjusted for multiple comparisons) in bold. HWE was tested on all patients in the discovery and replication cohorts, respectively.
HWE, Hardy-Weinberg equilibrium; IL12a, Interleukin12A; ; MI, myocardial infarction; NCF2, neutrophil cytosolic factor 2; ; SLE, systemic lupus erythematosus; SNPs, single-nucleotide polymorphisms; STAT4, signal transducer and activator of transcription 4.