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Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 28, 2015; 21(40): 11304-11311
Published online Oct 28, 2015. doi: 10.3748/wjg.v21.i40.11304
Arterial structure and function in inflammatory bowel disease
Luca Zanoli, Stefania Rastelli, Gaetano Inserra, Pietro Castellino
Luca Zanoli, Stefania Rastelli, Gaetano Inserra, Pietro Castellino, Department of Internal Medicine, Policlinico Universitario, University of Catania, 95123 Catania, Italy
Author contributions: Zanoli L, Rastelli S, Inserra G and Castellino P contributed equally to this work and wrote the paper.
Conflict-of-interest statement: None of the authors have any conflicts of interest to report.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Luca Zanoli, MD, PhD, Department of Internal Medicine, Policlinico Universitario, University of Catania, Via Santa Sofia 78, 95123 Catania, Italy. zanoli.rastelli@gmail.com
Telephone: +39-95-3782736 Fax: +39-95-3782376
Received: March 30, 2015
Peer-review started: March 31, 2015
First decision: May 18, 2015
Revised: May 30, 2015
Accepted: September 2, 2015
Article in press: September 2, 2015
Published online: October 28, 2015
Processing time: 207 Days and 10.2 Hours
Abstract

Inflammatory bowel disease (IBD) is the result of a combination of environmental, genetic and immunologic factors that trigger an uncontrolled immune response within the intestine, which results in inflammation among genetically predisposed individuals. Several studies have reported that the prevalence of classic cardiovascular risk factors is lower among subjects with IBD than in the general population, including obesity, dyslipidaemia, diabetes and hypertension. Therefore, given the risk profile of IBD subjects, the expected cardiovascular morbidity and mortality should be lower in these patients than in the general population. However, this is not the case because the standardized mortality ratio is not reduced and the risk of coronary heart disease is increased in patients with IBD. It is reasonable to hypothesize that other factors not considered in the classical stratification of cardiovascular risk may be involved in these subjects. Therefore, IBD may be a useful model with which to evaluate the effects of chronic low-grade inflammation in the development of cardiovascular diseases. Arterial stiffness is both a marker of subclinical target organ damage and a cardiovascular risk factor. In diseases characterized by chronic systemic inflammation, there is evidence that the inflammation affects arterial properties and induces both endothelial dysfunction and arterial stiffening. It has been reported that decreasing inflammation via anti tumor necrosis factor alpha therapy decreases arterial stiffness and restores endothelial function in patients with chronic inflammatory disorders. Consistent with these results, several recent studies have been conducted to determine whether arterial properties are altered among patients with IBD. In this review, we discuss the evidence pertaining to arterial structure and function and present the available data regarding arterial stiffness and endothelial function in patients with IBD.

Keywords: Arterial stiffness; Ulcerative colitis; Pulse wave velocity; Crohn’s disease; Inflammation; Tumour necrosis factor alpha

Core tip: The prevalence of classic cardiovascular risk factors, including obesity, dyslipidaemia, diabetes and hypertension, is lower among patients with inflammatory bowel disease (IBD) than in the general population. However, the risk of coronary heart disease is increased in IBD patients. Chronic inflammation may explain the difference between expected and observed cardiovascular risk. Arterial stiffness, a marker of subclinical target organ damage and a cardiovascular risk factor, is increased in chronic inflammatory disorders. In this review, we discuss the evidence pertaining to arterial structure and function and present the available data regarding arterial stiffness and endothelial function in patients with IBD.