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Abstract Background In Italy, the incidence of SARS-CoV-2 infection peaked in April and November 2020, defining two pandemic waves of coronavirus disease 2019 (COVID-19). This study compared the characteristics and outcomes of patients with inflammatory bowel disease (IBD) and SARS-CoV-2 infections between pandemic waves. Methods Observational longitudinal study of IBD patients with SARS-CoV-2 infection. Patients with established diagnoses of IBD and of SARS-CoV-2 infection were consecutively enrolled in two periods: (i) first wave, from 1 March 2020 to 31 May 2020; and (ii) second wave, from 15 September to 15 December 2020. Results We enrolled 937 IBD patients (219 in the first wave, 718 in the second wave). Patients of the first wave were older (mean ± SD: 46.3 ± 16.2 vs. 44.1 ± 15.4 years, p = 0.06), more likely to have ulcerative colitis (58.0% vs. 44.4%, p

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 multicentre 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.

Importance: The finding that aortic pulse wave velocity (aPWV) is increased may explain why patients with inflammatory bowel disease (IBD) have an increased cardiovascular risk despite the low prevalence of classic cardiovascular risk factors. Objective: To determine why these patients have an increased aPWV. Data sources: A systematic literature search for aPWV in IBD was performed using PubMed, Scopus, Web of Science, and Google Scholar databases. Study selection: Inclusion criterion was peer-reviewed publications on clinical studies reporting original data. Data extraction and synthesis: This study followed PRISMA-IPD 2015 guidelines. Data were provided for 4 cohorts in 3 countries (151 participants with ulcerative colitis [UC], 159 with Crohn disease [CD], and 227 controls). Using aPWV, cohort-specific z-scores were calculated after loge-transform and combined in meta-analysis to form pooled effects using a random- effects model. Main outcome and measures: The aPWV, a reference measure of aortic stiffness, after adjusting for age, sex, mean blood pressure, known cardiovascular risk factors, and study of origin. Results: The pooled z-score was 1.2 m/s. The aPWV was dependent on CD (β 0.80 z-score [1.0 m/s], 95% confidence interval 0.61–1.00 z-score, P < 0.001) and UC (β 0.69 z- score [0.8 m/s], 95% confidence interval 0.49–0.88 z-score, P < 0.001). In patients with IBD, the aPWV was dependent on disease duration (square root [years], β 0.15 z- score, 95% confidence interval 0.02–0.29 z-score, P = 0.03) and white blood cell count (Loge [billion cells/L], β 0.48 z-score, 95% confidence interval 0.12–0.84 z-score, P = 0.01) but not on cardiovascular risk factors and therapy. Conclusions: The increased aPWV reported in this patient population is dependent on inflammation.