Inflammatory Bowel Disease and Cardiovascular Disease

Main Article Content

Stephanie Shields
John Paul Seenan
Jonathan Macdonald

Abstract

Inflammatory bowel diseases (IBDs) are immune-mediated inflammatory conditions causing inflammation of the gastrointestinal tract. A range of medical treatment options are used to treat IBD-related inflammation including biologic tumor necrosis factor (TNF) antagonists. IBD prevalence is growing with patients increasingly older and more comorbid. Globally, cardiovascular diseases remain the leading cause of morbidity and mortality. IBD patients are at higher risk of cardiovascular disease, but this does not appear to be conferred by traditional risk factors such as hyperlipidemia and obesity. Appreciation of the relationship between IBD, cardiovascular disease, and inflammation is, therefore, of clinical importance. TNF-α is a key pro-inflammatory cytokine in the development of IBD-related inflammation, hypertension, and cardiovascular disease. Data suggest that commonly prescribed TNF antagonists may mitigate the increased cardiovascular risk in IBD patients. It is unclear if this is a direct effect of TNF antagonism or reflects better control of inflammation. Future research should focus on an improved understanding of the cardiovascular impact of IBD-related inflammation, the risk of adverse outcomes, and the potential effects of IBD treatment on cardiovascular risk profiles. This knowledge should allow better risk stratification when selecting treatment options, contributing to our goal of personalizing the approach to IBD treatment.

Metrics

Metrics Loading ...

Article Details

How to Cite
Shields, S., Seenan, J. P., & Macdonald, J. (2022). Inflammatory Bowel Disease and Cardiovascular Disease. Hypertension Journal, 7(3), 112–115. Retrieved from https://9vom.in/journals/index.php/htnj/article/view/52
Section
Review Articles
Author Biographies

Stephanie Shields, Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom & School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom

&

School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

John Paul Seenan, Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom & School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom

&

School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

Jonathan Macdonald, Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom & School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

Department of Gastroenterology, Queen Elizabeth University Hospital, Glasgow, Scotland, United Kingdom

&

School of Medicine, Dentistry and Nursing, University of Glasgow, Glasgow, Scotland, United Kingdom

References

Yang YZ, Li YY. Inflammatory bowel disease: Pathogenesis. World J Gastroenterol 2014;20:91-9.

Lamb CA, Kennedy NA, Raine T, Hendy PA, Smith PJ, Limdi JK, et al. British society of gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults. Gut 2019;68:s1-106.

Alatab S, Sepanlou SG, Ikuta K, Vahedi H, Bisignano C, Safiri S, et al. The global, regional, and national burden of inflammatory bowel disease in 195 countries and territories, 1990-2017: A systematic analysis for the global burden of disease study 2017. Lancet Gastroenterol Hepatol 2020;5:17-30.

Jones GR, Lyons M, Plevris N, Jenkinson PW, Bisset C, Burgess C, et al. IBD prevalence in Lothian, Scotland, derived by capture-recapture methodology. Gut 2019;68:1953-60.

Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 2021;18:56-66.

World Health Organization. A Global Brief on Hypertension. Geneva: World Health Organization; 2013. Available from: https://www.who.int/publications/i/item/a-global-brief-onhypertension-silent-killer-global-public-health-crisis-worldhealth-day-2013. [Last accessed on 2021 Dec 15].

Zanoli L, Rastelli S, Inserra G, Castellino P. Arterial structure and function in inflammatory bowel disease. World J Gastroenterol 2015;21:11304-11.

Zanoli L, Inserra G, Castellino P. Increased cardiovascular risk in subjects with a low prevalence of classic cardiovascular risk factors: The inflammatory bowel disease paradox. Trends Cardiovasc Med 2015;25:705-6.

Mantaka A, Tsoukali E, Fragaki M, Karmiris K, Viazis N, Mantzaris G, et al. Disease severity in patients with inflammatory bowel disease associated with cardiovascular diseases. J Crohns Colitis 2018;2 Suppl 1:S521.

Anderson AA, Jess T. Risk of cardiovascular disease in inflammatory bowel disease. World J Gastrointest Pathophysiol 2014;5:359-65.

Gareb B, Otten AT, Frijink HW. Review: Local tumor necrosis factor-α inhibition in inflammatory bowel disease. Pharmaceutics 2020;12:539.

Levin AD, Wildenberg ME, Van den Brink GR. Mechanism of action of anti-TNF therapy in inflammatory bowel disease. J Crohns Colitis 2016;10:989-97.

Mazor R, Itzhaki O, Sela S, Yagil Y, Cohen-Mazor M, Yagil C, et al. Tumor necrosis factor-alpha: A possible priming agent for the polymorphonuclear leukocyte-reduced nicotinamideadenine dinucleotide phosphate oxidase in hypertension. Hypertension 2010;55:353-62.

Carvalho-Galvão A, Guimarães DD, De Brito Alves J, Braga VA. Central inhibition of tumor necrosis factor alpha reduces hypertension by attenuating oxidative stress in the rostral ventrolateral medulla in renovascular hypertensive rats. Front Physiol 2019;10:491.

Gonzalez-Juanatey C, Vazquez-Rodriguez TR, MirandaFilloy JA. Anti-TNF-alpha-adalimumab therapy is associated withpersistent improvement of endothelial function withoutprogression of carotid intima-media wall thickness in patientswith rheumatoid arthritis refractory to conventional therapy. Mediators Inflamm 2012;2012:674265.

Végh E, Kerekes G, Pusztai A, Hamar A, Szamosi S, Váncsa A, et al. Efects of 1-year anti-TNF-α therapy on vascular function in rheumatoid arthritis and ankylosing spondylitis. Rheumatol Int 2020;40:427-36.

Kirchgesner J, Andersen NN, Carrat F, Jess T, Beaugerie L, BERENICE Study Group. Exposure to combination therapy with thiopurines and anti-TNF agents is associated with reduced incidence of acute arterial events in patients with inflammatory bowel disease (IBD): A nationwide French cohort study. United Eur Gastroenterol J. 2017;5 Suppl 1:A148.

Sultan KS, Berkowitz JC, Khan S. Combination therapy for inflammatory bowel disease. World J Gastrointest Pharmacol Ther 2017;8:103-13.

Bhattacharya A, Rao BB, Koutroubakis I, Rivers CR, Regueiro M, Swoger J, et al. Investigating the changes in atherosclerotic cardiovascular risk profile of IBD patients over 6 years. Gastroenterol 2016;150 Suppl 1:S226.

Mantaka A, Tsoukali E, Fragaki M, Karmiris K, Viazis N, Mantzaris G, et al. Association between the use of antihypertensive agents and disease severity in patients with inflammatory bowel disease. J Crohns Colitis 2019;13 Suppl 1:S497.

Shi Y, Liu T, He L, Dougherty U, Chen L, Adhikari S, et al. Activation of the renin-angiotensin system promotes colitis development. Sci Rep 2016;6:27552.

Garg M, Royce SG, Tikellis C, Shallue C, Batu D, Velkoska E, et al. Imbalance of the renin-angiotensin system may contribute to inflammation and fibrosis in IBD: A novel therapeutic target? Gut 2020;69:841-51.

Yoshida S, Takeuchi T, Kotani T, Yamamoto N, Hata K, Nagai K, et al. Infliximab, a TNF-ainhibitor, reduces 24-h ambulatory bloodpressure in rheumatoid arthritis patients. J HumHypertens 2014;28:165-9.

Sandoo A, Panoulas VF, Toms TE, Smith JP, StavropoulosKalinoglou A, Metsios GS, et al. Anti-TNFa therapy may lead to blood pressure reductions through improved endotheliumdependent microvascular function in patients with rheumatoid arthritis. J Human Hypertens 2011;25:699-702.

De Faria AP, Ritter AM, Santa-Catharina A, Souza DP, Naseri EP, Bertolo MB, et al. Effects of anti-TNF alpha therapy on blood pressure in resistant hypertensive subjects: A randomized, double-blind, placebo-controlled pilot study. Arq Bras Cardiol 2021;116:443-51.

Roubille C, Richer V, Starnino T, McCourt C, McFarlane A, Fleming P, et al. The effects of tumour necrosis factor inhibitors, methotrexate, non-steroidal anti-inflammatory drugs and corticosteroids on cardiovascular events in rheumatoid arthritis, psoriasis and psoriatic arthritis: A systematic review and metaanalysis. Ann Rheum Dis 2015;74:480-9.

Low AS, Lunt M, Mercer LK. Association between anti-tumour necrosis factor therapy and risk of ischaemic stroke in patients with rheumatoid arthritis: Results from the British society for rheumatology biologics registers-rheumatoid arthritis (BSRBR-RA). Lancet 2013;381:s66.

Chan SC, Teo CK, Li PH, Lau KK, Lau CS, Chung HY. Cardiovascular risk in patients with spondyloarthritis and association with anti-TNF drugs. Ther Adv Musculoskelet Dis 2021;13:1759720X211032444.

Schumacher SM, Prasad SV. Tumor necrosis factor-α in heart failure: An updated review. Curr Cardiol Rep 2018;20:117.

Chung ES, Packer M, Lo KH, Fasanmade AA, Willerson JT, AntiTNF Therapy Against Congestive Heart Failure Investigators. Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-α, in patients with moderate-to-severe heart failure. Circulation 2003;107:3133-40.

Rutgeerts P, Sandborn WJ, Feagan BG, Reinisch W, Olson A, Johanns J, et al. Infliximab for induction and maintenance therapy for ulcerative colitis. N Engl J Med 2005;353:2462-76.