4.6 Inflammation and Aortic Stiffness. A Multicentre Longitudinal Study in Patients with Inflammatory Bowel Disease

Abstract

Background

Inflammatory Bowel Disease (IBD) is characterized by a low prevalence of traditional risk factors, an increased aortic pulse-wave velocity (aPWV) [1] and an excess of cardiovascular events. We have previously hypothesized that the difference between expected and observed cardiovascular risk could be explained by chronic inflammation [2]. In this multi-centre longitudinal study, we tested the hypothesis that increased aPWV is reversible with anti-tumor necrosis factor-alpha (anti-TNFα) therapy.

Methods

We enrolled 334 patients (82 patients with ulcerative colitis [UC], 85 patients with Crohn’s disease [CD] and 167 healthy control subjects matched for age, sex and mean blood pressure) from 3 Centres in Europe and followed up them for 4 years (range 2.5–5.7 years).

Results

At baseline, IBD patients had higher aPWV than controls. IBD patients in remission and those treated with anti-TNFα during follow-up experienced an aortic destiffening whereas aPWV increased in those with active disease and those treated with salicylates (Figure 1, P = 0.01). Disease duration (P = 0.02) and, in UC patients, the increase in CRP during follow-up (P = 0.02) were associated with aortic stiffening. All these results were confirmed after adjustment for major confounders. Finally, the duration of anti-TNFα therapy was not associated with the magnitude of the reduction in aPWV at the end of follow-up (P = 0.85). This finding could suggest that anti-TNFα therapy has a beneficial effect on functional arterial stiffening.

Conclusions

Long-term anti-TNFα therapy reduced aPWV, an established surrogate measure of cardiovascular risk, in patients with IBD. This suggests that effective control of inflammation may reduce cardiovascular risk in these patients.