Increased arterial stiffness in inflammatory bowel diseases is dependent upon inflammation and reduced by immunomodulatory drugs

Background. Inflammatory bowel diseases (IBD) are associated with an increased cardiovascular risk that is not fully explained by traditional cardiovascular risk factors but may be due to inflammation and mediated by an increased arterial stiffness. Aims: Study 1, to investigate the relationship between inflammation and arterial stiffening; Study 2, to look whether aortic stiffening is reduced by immunomodulatory therapy in IBD.Methods. Study 1 (Cross-sectional study): pulse wave velocity (PWV) was measured in 74 IBD subjects (40 ulcerative colitis and 34 Crohn’s disease) and 80 matched controls. Study 2 (Longitudinal study): the effect of therapy on PWV was measured at baseline and 3.4±0.5 years later in 14 IBD subjects treated only with salicylates, 11 subjects treated with steroids and azathioprine, 7 subjects treated with anti TNF-alpha and 30 matched controls.Results. Study 1: All parameters were comparable between subjects with ulcerative colitis and Crohn’s disease. Compared to controls, subjects with ulcerative colitis and those with Crohn’s disease have both higher carotid-femoral PWV (7.0±1.1, 7.8±1.7 and 8.0±1.6 m/s, respectively; P<0.001) and carotid-radial PWV (7.2±0.9, 8.8±1.4 and 8.8±1.3 m/s, respectively; P<0.001). In fully adjusted models carotid-femoral PWV was positively associated with disease duration whereas carotid-radial PWV was associated with C-reactive protein and history of relapse. Study 2: in fully adjusted model carotid-femoral PWV increased significantly at follow-up in IBD subjects treated with salicylates but not in those treated with steroids and azathioprine or anti TNF-alpha.Conclusion. Increased arterial stiffness in IBD is dependent upon inflammation and reduced by immunomodulatory drugs.