Pulse wave velocity differs between ulcerative colitis and chronic kidney disease

Zanoli, Luca; Lentini, Paolo; Boutouyrie, Pierre; Fatuzzo, Pasquale; Granata, Antonio; Corrao, Salvatore; Gaudio, Agostino; Inserra, G.; Rapisarda, Francesco; Rastelli, Stefania; Laurent, Stéphane; Malatino, Lorenzo; Castellino, Pietro

doi:10.1016/j.ejim.2017.08.020

Cited by 30 publications

(21 citation statements)

References 38 publications

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“…6 Interestingly, arterial remodeling during CKD seems to be different in elastic arteries (i.e., aorta and carotid artery) and muscular arteries (i.e., brachial, femoral, and renal artery), because aortic and carotid stiffness increases in patients with CKD whereas brachial and femoral stiffness does not increase and can be even reduced during CKD. 48,49 Loss of elastic fibers in the wall of the aorta has been reported in forms of aortic disease and can account for the circumstance of having aortic dilation yet reduced compliance in the same patient. 50 Finally, an inward remodeling (reduction of diameter) of the renal arteries has been reported in patients with CKD with a low prevalence of renal artery stenosis and a high CV risk.…”

Section: Uremic Toxins Are Also Vascular Toxinsmentioning

confidence: 99%

Arterial Stiffness in the Heart Disease of CKD

Zanoli

Lentini

Briet

et al. 2019

JASN

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155

130

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CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (i.e., uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD.

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Section: Uremic Toxins Are Also Vascular Toxinsmentioning

confidence: 99%

Arterial Stiffness in the Heart Disease of CKD

Zanoli

Lentini

Briet

et al. 2019

JASN

Self Cite

155

130

View full text Add to dashboard Cite

show abstract

“…Starting from 2010, it was repeatedly reported that aortic stiffness is increased in adults patients with IBD compared with matched controls. 32 –50,51 To date, at least 13 single-center cross-sectional studies 33 –45 and 2 multicenter longitudinal studies 37,50,51 suggest that aortic stiffness and reflected waves are increased in adult patients with CD and UC, even after adjustment for known CV risk factors (Table 1) and that the severity and duration of inflammation over time has a key role in the arterial stiffening process. These results have been confirmed in 4 aggregated data 32,46,47,48 and 1 individual participant data meta-analysis 49 performed in patients with IBD, which are in agreement with similar findings reported in patients with rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and periodontitis 16 –18,53 and could suggest that arterial stiffness is a vascular biomarker of chronic inflammation.…”

Section: Aortic Stiffness Is Increased In Ibd and In Patients With Chmentioning

confidence: 99%

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

et al. 2020

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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.

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“…The non-invasive study of haemodynamic variables was performed as previously reported [15] in a centralized vascular laboratory. Briefly, brachial BP measurements were performed using an oscillometric device (Dinamap ProCare 100; GE Healthcare, Milwaukee, WI, USA).…”

Section: Haemodynamic Datamentioning

confidence: 99%

Inflammation and ventricular-vascular coupling in hypertensive patients with metabolic syndrome

Zanoli

Pino

Terranova

et al. 2018

Nutrition, Metabolism and Cardiovascular Diseases

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Background and aims: Metabolic syndrome (MetS) is currently considered to raise the risk for type 2 diabetes and cardiovascular events. It has been suggested that part of this risk excess may be due to a cluster of additional factors associated with MetS. We aimed to investigate the role of inflammation on the ventricular-vascular coupling in patients with MetS. Methods and results: We enrolled a total of 227 hypertensive patients (106 with MetS and 121 without MetS) matched for age and gender. Aortic pulse wave velocity (aPWV), intima-media thickness (IMT) and high sensitivity C-reactive protein (CRP) increased according to the number of MetS components. Patients with MetS showed increased aPWV (11.5 AE 3.7 vs. 10.3 AE 2.5 m/s, P Z 0.03) compared with controls. In a model adjusted for age, sex, heart rate and mean blood pressure, aPWV resulted increased in patients with CKD (beta 1.29 m/s, 95%CI 0.61e1.96 m/s, P < 0.001) and MetS (beta 0.89 m/s, 95%CI 0.28e1.51 m/s, P Z 0.005). After additional adjustment for CRP and IMT, the slope of aPWV was respectively reduced by 16% and 62%, suggesting that inflammation and intima-media thickening could contribute to aortic stiffening in patients with MetS. In these patients, aPWV was also associated with left-ventricular mass index (beta 0.79 g/m 2.7 , 95%CI 0.05e1.52 g/m 2.7 , P Z 0.05). Conclusion: MetS is characterized by an inflammation-dependent acceleration in cardiovascular ageing. This pattern of pathophysiological abnormalities may contribute to amplify the burden of cardiovascular risk in patients with MetS.

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Pulse wave velocity differs between ulcerative colitis and chronic kidney disease

Cited by 30 publications

References 38 publications

Arterial Stiffness in the Heart Disease of CKD

Arterial Stiffness in the Heart Disease of CKD

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

Inflammation and ventricular-vascular coupling in hypertensive patients with metabolic syndrome

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