In a work published in a recent issue of the European Journal of Internal Medicine
[
[1]
], Cappello et al. found that, despite the lower prevalence of dyslipidemia, carotid-femoral
pulse wave velocity, a measure of arterial stiffness, and augmentation index, a measure
of wave reflection, were significantly increased in patients with inflammatory bowel
disease (IBD), a disease characterized by chronic inflammation. This finding confirms
the results of our previous works [
2
,
3
] and is of clinical interest because it helps explain why IBD patients have an increased
cardiovascular risk despite the low prevalence of traditional cardiovascular risk
factors [
[4]
]. In this regard, the significantly higher augmentation index reported by Cappello
et al. in IBD patients treated with salicylates are consistent with current evidences
showing that chronic inflammation could play a role in the arterial stiffening of
patients with IBD [
2
,
3
,
4
,
5
,
6
]. This finding is also in accordance with the results of two recent meta-regression
analyses that has suggested a lack of efficacy of salicylates in protecting IBD patients
from arterial stiffening [
[7]
] and the destiffening effect of anti-tumor necrosis factor α (anti-TNFα) therapy [
Zanoli L, Boutouyrie P, Lentini P, et al. Maintenance therapy with salicylates is associated with aortic stiffening in patients with inflammatory bowel disease. J Hypertens [in press]. http://dx.doi.org/10.1097/HJH.0000000000001235.
[5]
].Keywords
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References
- Increased expression of markers of early atherosclerosis in patients with inflammatory bowel disease.Eur J Intern Med. 2017; 37: 83-89
- Arterial stiffness is increased in patients with inflammatory bowel disease.J Hypertens. 2012; 30: 1775-1781https://doi.org/10.1097/HJH.0b013e3283568abd
- Increased arterial stiffness in inflammatory bowel diseases is dependent upon inflammation and reduced by immunomodulatory drugs.Atherosclerosis. 2014; 234: 346-351https://doi.org/10.1016/j.atherosclerosis.2014.03.023
- Increased cardiovascular risk in subjects with a low prevalence of classic cardiovascular risk factors: the inflammatory bowel disease paradox.Trends Cardiovasc Med. 2015 Nov; 25: 705-706https://doi.org/10.1016/j.tcm.2015.04.001
- Arterial stiffness in inflammatory bowel disease: a systematic review and meta-analysis.J Hypertens. 2016; 34: 822-829https://doi.org/10.1097/HJH.0000000000000867
- Arterial structure and function in inflammatory bowel disease.World J Gastroenterol. 2015; 21: 11304-11311https://doi.org/10.3748/wjg.v21.i40.11304
Zanoli L, Boutouyrie P, Lentini P, et al. Maintenance therapy with salicylates is associated with aortic stiffening in patients with inflammatory bowel disease. J Hypertens [in press]. http://dx.doi.org/10.1097/HJH.0000000000001235.
- Aortic stiffness in patients with inflammatory bowel diseases.Hellenic Journal of Atherosclerosis. 2013; 4: 200-207
- Lipoprotein-associated phospholipase A2 and arterial stiffness evaluation in patients with inflammatory bowel diseases.J Crohns Colitis. 2014; 8: 936-944https://doi.org/10.1016/j.crohns.2014.01.016
- Increased pulse wave velocity and relationship with inflammation, insulin, and insulin resistance in inflammatory bowel disease.Eur J Gastroenterol Hepatol. 2014; 26: 725-732https://doi.org/10.1097/MEG.0000000000000104
Article info
Publication history
Published online: December 22, 2016
Accepted:
December 14,
2016
Received:
December 9,
2016
Identification
Copyright
© 2016 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
