Current guidelines state that systemic inflammation, together with endothelial dysfunction, calcification, and hypercoagulability, predispose to premature atherosclerosis in patients with inflammatory bowel disease (IBD). We assessed whether IBD can affect aortic stiffness, a well-recognized vascular biomarker and an independent risk factor for cardiovascular (CV) disease (CVD) in several populations. Recent studies reported that aortic stiffness is increased in adults with IBD compared with matched controls. This association is dependent on inflammatory burden and disease duration, and is reduced by antitumor necrosis factor therapy. Considered together, current findings suggest that increased aortic stiffness is an extraintestinal manifestation of IBD. This is clinically relevant since measuring aortic stiffness in patients with IBD could improve risk assessment, especially in those without established CVD. Moreover, effective control of inflammation could lower CV risk in patients with IBD by reducing aortic stiffness. Further longitudinal studies are needed to better clarify (i) the relationship between disease duration and irreversible changes of the arterial wall, (ii) the clinical characteristics of patients with IBD that have an increased arterial stiffness at least in part reversible, and (iii) whether arterial stiffness is useful to evaluate the efficacy of immunosuppressive therapy.

Aortic Stiffening Is an Extraintestinal Manifestation of Inflammatory Bowel Disease: Review of the Literature and Expert Panel Statement / Zanoli, Luca; Mikhailidis, Dimitri P; Bruno, Rosa Maria; Abreu, Maria T; Danese, Silvio; Eliakim, Rami; Gionchetti, Paolo; Katsanos, Konstantinos H; Kirchgesner, Julien; Koutroubakis, Ioannis E; Kucharzik, Torsten; Lakatos, Peter L; Nguyen, Geoffrey C; Papa, Alfredo; Vavricka, Stephan R; Wilkinson, Ian B; Boutouyrie, Pierre. - In: ANGIOLOGY. - ISSN 0003-3197. - 71:8(2020), pp. 689-697-697. [10.1177/0003319720918509]

Aortic Stiffening Is an Extraintestinal Manifestation of Inflammatory Bowel Disease: Review of the Literature and Expert Panel Statement

Danese, Silvio;
2020-01-01

Abstract

Current guidelines state that systemic inflammation, together with endothelial dysfunction, calcification, and hypercoagulability, predispose to premature atherosclerosis in patients with inflammatory bowel disease (IBD). We assessed whether IBD can affect aortic stiffness, a well-recognized vascular biomarker and an independent risk factor for cardiovascular (CV) disease (CVD) in several populations. Recent studies reported that aortic stiffness is increased in adults with IBD compared with matched controls. This association is dependent on inflammatory burden and disease duration, and is reduced by antitumor necrosis factor therapy. Considered together, current findings suggest that increased aortic stiffness is an extraintestinal manifestation of IBD. This is clinically relevant since measuring aortic stiffness in patients with IBD could improve risk assessment, especially in those without established CVD. Moreover, effective control of inflammation could lower CV risk in patients with IBD by reducing aortic stiffness. Further longitudinal studies are needed to better clarify (i) the relationship between disease duration and irreversible changes of the arterial wall, (ii) the clinical characteristics of patients with IBD that have an increased arterial stiffness at least in part reversible, and (iii) whether arterial stiffness is useful to evaluate the efficacy of immunosuppressive therapy.
2020
arterial stiffness
biomarkers
extraintestinal manifestation
inflammation
inflammatory bowel disease
pulse wave velocity
Animals
Anti-Inflammatory Agents
Cardiovascular Diseases
Humans
Immunosuppressive Agents
Inflammatory Bowel Diseases
Risk Factors
Treatment Outcome
Tumor Necrosis Factor Inhibitors
Vascular Stiffness
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11768/119564
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 18
  • ???jsp.display-item.citation.isi??? 20
social impact