Endothelial and cardiac dysfunction in inflammatory bowel diseases: Does treatment modify the inflammatory load on arterial and cardiac structure and function?

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3021119 14 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Endothelial and cardiac dysfunction in inflammatory bowel diseases: Does treatment modify the inflammatory load on arterial and cardiac structure and function?
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Inflammatory bowel diseases (IBD), largely represented by Crohn’s disease (CD) and ulcerative colitis (UC), alter gastrointestinal physiology and mucosal immunity through a complex inflammatory process. These diseases can lead to significant arterial endothelial dysfunction. There is also evidence linking IBD with a modification of cardiac structure and function. A growing body of research has associated IBD with an acceleration of arterial stiffness and atherosclerosis and an increased risk of cardiovascular (CV) morbidity and mortality. The focus of this review is two-fold. Firstly, the literature on IBD in relation to CV dysfunction was evaluated (mainly based on 25 relevant surveys carried out between 2005 and 2018). The vast majority of these studies support a significant association of IBD with a deterioration in CV function. Secondly, the literature available regarding the effect of IBD treatment on CV dysfunction was considered based on studies published between 2007 and 2018. This literature search suggests that IBD treatment may have the potential to ameliorate CV dysfunction resulting in CV benefits. This review will analyse the literature as well as consider emerging research perspectives regarding how IBD treatment could improve CV dysfunction. © 2020 Bentham Science Publishers.
Έτος δημοσίευσης:
2020
Συγγραφείς:
Triantafyllou, C.
Nikolaou, M.
Ikonomidis, I.
Bamias, G.
Papaconstantinou, I.
Περιοδικό:
Current Vascular Pharmacology
Εκδότης:
Bentham Science Publishers
Τόμος:
18
Αριθμός / τεύχος:
1
Σελίδες:
27-37
Λέξεις-κλειδιά:
amino terminal pro brain natriuretic peptide; angiopoietin 1; atrial natriuretic factor; C reactive protein; CD146 antigen; cell adhesion molecule; cyclic GMP; endothelial nitric oxide synthase; endothelin 1; hemoglobin A1c; high density lipoprotein cholesterol; intercellular adhesion molecule 1; interleukin 6; interleukin 8; interstitial collagenase; low density lipoprotein cholesterol; placental growth factor; platelet derived growth factor; probiotic agent; prostacyclin; reactive oxygen metabolite; scatter factor; triacylglycerol; trimethylamine oxide; tumor necrosis factor; unindexed drug; vascular cell adhesion molecule 1; vasculotropin receptor 2; very low density lipoprotein cholesterol; von Willebrand factor, angiogenesis; arterial stiffness; arterial thromboembolism; arterial wall thickness; atherosclerosis; augmentation index; cardiovascular disease; cardiovascular mortality; cardiovascular risk; coronary artery disease; coronary artery ectasia; coronary flow reserve; Crohn disease; endothelial dysfunction; fibrinolysis; graft rejection; heart disease; heart failure; heart function; heart infarction; hospitalization; human; hyperemia; inflammation; inflammatory bowel disease; left ventricular diastolic dysfunction; New York Heart Association class; nonhuman; prognosis; psoriasis; pulse wave; Review; risk factor; sarcoidosis; shear stress; tissue Doppler imaging; tonometry; transthoracic echocardiography; ulcerative colitis; ultrasound; vasodilatation; artery; cardiovascular disease; complication; Crohn disease; heart; pathophysiology; risk assessment; ulcerative colitis; vascular endothelium, Arteries; Cardiovascular Diseases; Colitis, Ulcerative; Crohn Disease; Endothelium, Vascular; Heart; Humans; Prognosis; Risk Assessment; Risk Factors
Επίσημο URL (Εκδότης):
DOI:
10.2174/1570161117666181129095941
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