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Multicenter Study
. 2019 Feb 5;8(3):e010942.
doi: 10.1161/JAHA.118.010942.

Inflammation and Aortic Pulse Wave Velocity: A Multicenter Longitudinal Study in Patients With Inflammatory Bowel Disease

Luca Zanoli  1 , Kadir Ozturk  2 , Maria Cappello  3 , Gaetano Inserra  4 , Giulio Geraci  5 , Antonio Tuttolomondo  3 , Daniele Torres  3 , Antonio Pinto  3 , Andrea Duminuco  4 , Gaia Riguccio  4 , Musa B Aykan  6 , Giuseppe Mulé  5 , Santina Cottone  5 , Alessandra F Perna  7 , Stephane Laurent  8 , Pasquale Fatuzzo  1 , Pietro Castellino  4 , Pierre Boutouyrie  8
Affiliations
Multicenter Study

Inflammation and Aortic Pulse Wave Velocity: A Multicenter Longitudinal Study in Patients With Inflammatory Bowel Disease

Luca Zanoli et al. J Am Heart Assoc. .

Abstract

Background Inflammatory bowel disease ( IBD ) is characterized by a low prevalence of traditional risk factors, an increased aortic pulse-wave velocity ( aPWV ), and an excess of cardiovascular events. We have previously hypothesized that the cardiovascular risk excess reported in these patients could be explained by chronic inflammation. Here, we tested the hypothesis that chronic inflammation is responsible for the increased aPWV previously reported in IBD patients and that anti-TNFa (anti-tumor necrosis factor-alpha) therapy reduce aPWV in these patients. Methods and Results This was a multicenter longitudinal study. We enrolled 334 patients: 82 patients with ulcerative colitis, 85 patients with Crohn disease, and 167 healthy control subjects matched for age, sex, and mean blood pressure, from 3 centers in Europe, and followed them for 4 years (range, 2.5-5.7 years). At baseline, IBD patients had higher aPWV than controls. IBD patients in remission and those treated with anti-TNFa during follow-up experienced an aortic destiffening, whereas aPWV increased in those with active disease and those treated with salicylates ( P=0.01). Disease duration ( P=0.02) was associated with aortic stiffening as was, in patients with ulcerative colitis, high-sensitivity C-reactive protein during follow-up ( P=0.02). All these results were confirmed after adjustment for major confounders. Finally, the duration of anti-TNFa therapy was not associated with the magnitude of the reduction in aPWV at the end of follow-up ( P=0.85). Conclusions Long-term anti-TNFa therapy reduces 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.

Keywords: Crohn disease; arterial stiffness; inflammation; pulse wave velocity; tumor necrosis factor‐alpha; ulcerative colitis.

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Figures

Figure 1
Figure 1
Changes in aortic pulse‐wave velocity (ΔaPWV) during follow‐up in patients with Crohn disease (CD) and in those with ulcerative colitis (UC) sorted for disease activity during follow‐up (A), anti–tumor necrosis factor‐alpha (anti‐TNFα) therapy during follow‐up (B), immunosuppressive therapy at baseline (C), and disease duration at baseline (D). Patients with inflammatory bowel disease (IBD) in remission during follow‐up and those treated with anti‐TNFα experienced an aortic destiffening during follow‐up, whereas aPWV increased in patients with active disease during follow‐up, in patients never treated with anti‐TNFα during follow‐up, and in those treated with salicylates. Bars represent means and SEMs. *Data of patients with CD and UC were analyzed as a whole group using repeated measures ANOVA. †Bonferroni Test of within‐subject contrasts.
Figure 2
Figure 2
A, Changes in high‐sensitivity C‐reactive protein (ΔhsCRP) were correlated with aortic pulse‐wave velocity (ΔaPWV) during follow‐up in patients with ulcerative colitis (UC) but not in patients with Crohn disease (CD). B, Effect of therapy on aPWV in patients with inflammatory bowel disease (IBD; data of patients with CD and UC were analyzed as a whole group); aPWV was higher in patients never treated with anti‐TNFα during follow‐up than in control subjects at both baseline (Bonferroni test: A≠G) and follow‐up examination (Bonferroni test: B≠H), whereas in patients always treated with anti‐TNFα during follow‐up, aPWV was higher at baseline examination (Bonferroni test: E≠G) and reduced to a level comparable to that of control subjects at the end of follow‐up. C, Effect of disease activity on aPWV in patients with IBD (data of patients with CD and UC were analyzed as a whole group). At the end of follow‐up aPWV was higher in patients with active disease than in control subjects (Bonferroni test: F≠H). *Data were analyzed using repeated‐measures ANOVA). †Bonferroni test of within‐subject contrasts.
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