Introduction: Many observational studies have identified aortic aneurysm (AA) as a cardiovascular complication of immune-mediated inflammatory diseases (IMIDs). However, due to the effects of various confounders, it is still uncertainty whether this association holds or whether reverse causality is involved. Here we conducted a two-sample bidirectional MR study to infer the causal relationships between the two diseases. Method: We obtained genetic association datasets from public GWAS databases in populations of European ancestry. Abiding by the assumptions of Mendelian randomization (MR), we selected valid instrumental variables from genetic variants. Different statistic methods were performed for MR analysis and sensitivity analysis, and the inverse variance weighted (IVW) method was regarded as the most efficient estimate of the causal effect in this study. Results: The IVW method found evidence that genetically predicted AA had a causal effect on rheumatoid arthritis (RA) (OR = 1.06, 95%CI = 1.01-1.12, p = 0.029), but not of RA or other IMIDs on AA. Besides, no evidence showed that AA may increase the risk of inflammatory bowel disease (IBD), Crohn’s disease (CD), ulcerative colitis (UC), systemic lupus erythematosus (SLE) and psoriasis (PSO). The sensitivity analysis confirmed the absence of heterogeneity or horizontal pleiotropy effect. Conclusion: In summary, our study discovered that genetically predicted AA may increase the risk of RA, while no evidence was found that patients with RA had an increased risk of AA. Furthermore, we confirmed no evidence of association between IBD, CD, UC, SLE, PSO and AA. This is in accordance with other reports that demonstrated the human leukocyte antigen molecule in inflammatory aortic aneurysm was a genetic risk loci. Our study provides directions for future research on genetic susceptibility to inflammatory aortic aneurysm.