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The article offers information on the relationship between inflammation, arterial physiology alterations, and increased cardiovascular risk in the context of COVID-19. Topics include the study by Can et al, which measured the cardio-ankle vascular index (CAVI) in 70 subjects 1 and 7 months after the acute phase of COVID-19, revealing a worsening of vascular function 7 months after recovery.

(1) Background: Systemic sclerosis (SSc) is an autoimmune disease characterized by endothelial dysfunction and fibrosis of skin and visceral organs. In the last decade, attention has been focused on the macrovascular involvement of the disease. In particular, the observation of increased arterial stiffness represented an interesting aspect of the disease, as predictor of cardiovascular risk. (2) Methods: We recruited 60 SSc patients (52 ± 12 years old, 90% females) and 150 age/sex-matched healthy controls in order to evaluate both intima-media thickness of the right common carotid artery and arterial stiffness using the B-mode echography and the SphygmoCor system® tonometer. (3) Results: The carotid-femoral pulse wave velocity (PWV) was higher in SSc patients than in controls (8.6 ± 1.7 vs. 7.8 ± 1.5 m/s; p < 0.001), as was the carotid-radial PWV (7.8 ± 1.1 vs. 6.7 ± 1.4 m/s; p < 0.001). The intima-media thickness was higher in SSc than in controls (654 ± 108 vs. 602 ± 118 µm; p = 0.004). The other parameters measured at carotid (radial strain, Young's modulus, compliance and distensibility) all indicated that arterial stiffness in tension was more pronounced in SSc. Of interest, the direct correlation between PWV and age corresponded closely in SSc. Moreover, a significant difference between SSc and controls as regards the carotid parameters was evident in younger subjects. (4) Conclusions: SSc patients showed an increased arterial stiffness compared to healthy controls. In particular, an SSc-related pathologic effect was suggested by the more pronounced increase in PWV with age and lower values of carotid elasticity in younger SSc patients than in age-matched controls. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

An editorial is presented on the pathophysiology of cardiovascular disease in healthy subjects and a number of different populations including patients with an evidence of chronic inflammation. It expresses view that physiological pulmonary and arterial function is the result of an equilibrium between production and degradation of elastin and collagen. An overview of the association between lung dysfunction and increased arterial stiffness is presented.

Arterial stiffening is associated with increased cardiovascular risk. Whether exposure to relatively high levels of air pollution is associated with arterial stiffening is unclear. We aimed to assess the association between exposure to major air pollutants and arterial stiffening. PubMed, SCOPUS and Web of Science databases (through 31 January 2017) were searched using a combination of terms related to exposure to gaseous [nitrogen dioxide (NO2), nitrogen oxides (NOx) and sulphur dioxide (SO2)] or particulate matter pollutants (PM2.5, PM10 and PM10-2.5), arterial stiffness (pulse wave velocity) and reflected waves (augmentation index, augmentation pressure). Pertinent information were extracted from selected studies. In this systematic review were included 8 studies with available data on air pollution and arterial stiffness/reflected waves parameters (8 studies explored the effects of exposure to particulate matter pollutants, 3 studies the effects of exposure to gaseous pollutants); seven of them reported increased arterial stiffness/reflected waves after exposure to air pollution (6 of 8 studies after particulate matter pollutants; 2 of 3 studies after gaseous pollutants). Arterial stiffness and reflected waves were increased in the majority of the studies after both short- and long-term exposure to air pollutants. In conclusion, available evidence supports an association of main air pollutants with increased arterial stiffness and reflected waves. This finding may have implications for population-based strategies for the reduction of arterial stiffness, a vascular biomarker and an intermediate endpoint for cardiovascular disease. [ABSTRACT FROM AUTHOR]

An editorial is presented on growing interest regarding the link between arterial stiffness and cardiovascular risk in this area of research was the publication in 2006 of an expert consensus document on methodological issues and clinical applications of arterial stiffness. Topics include the major vessel of interest when determining regional arterial stiffness and aortic pulse wave velocity, and the increased aortic stiffness was considered as a measure of subclinical target organ damage.

An editorial is presented on the Angiology provide an interesting contribution with regard to the relationship between arterial and cardiac dysfunction in patients with premature coronary artery disease (CAD). Topics include the lower at baseline in patients with CAD who developed cardiovascular (CV) events, and the agreement with the concept that increased arterial stiffness is a CV risk factor.

Background: Inflammatory bowel diseases (IBD) are associated with an increased cardiovascular risk that is not fully explained by traditional cardiovascular risk factors but may be due to inflammation and mediated by an increased arterial stiffness. Aims: Study 1, to investigate the relationship between inflammation and arterial stiffening; Study 2, to look whether aortic stiffening is reduced by immunomodulatory therapy in IBD. Methods: Study 1 (Cross-sectional study): pulse wave velocity (PWV) was measured in 74 IBD subjects (40 ulcerative colitis and 34 Crohn's disease) and 80 matched controls. Study 2 (Longitudinal study): the effect of therapy on PWV was measured at baseline and 3.4 ± 0.5 years later in 14 IBD subjects treated only with salicylates, 11 subjects treated with steroids and azathioprine, 7 subjects treated with anti TNF-alpha and 30 matched controls. Results: Study 1: All parameters were comparable between subjects with ulcerative colitis and Crohn's disease. Compared to controls, subjects with ulcerative colitis and those with Crohn's disease have both higher carotid-femoral PWV (7.0 ± 1.1, 7.8 ± 1.7 and 8.0 ± 1.6 m/s, respectively; P < 0.001) and carotid-radial PWV (7.2 ± 0.9, 8.8 ± 1.4 and 8.8 ± 1.3 m/s, respectively; P < 0.001). In fully adjusted models carotid-femoral PWV was positively associated with disease duration whereas carotid-radial PWV was associated with C-reactive protein and history of relapse. Study 2: in fully adjusted model carotid-femoral PWV increased significantly at follow-up in IBD subjects treated with salicylates but not in those treated with steroids and azathioprine or anti TNF-alpha. Conclusion: Increased arterial stiffness in IBD is dependent upon inflammation and reduced by immunomodulatory drugs. [ABSTRACT FROM AUTHOR]

Osteoporosis and cardiovascular disease are worldwide public health issues. Recent evidence indicates a possible role of the canonical Wnt/β-catenin signalling pathway as a common mediator between these two diseases. The aim of the present study was to investigate the relationship between serum concentrations of sclerostin and Dkk1, two extracellular inhibitors of Wnt/β-catenin signalling, with carotid intima-media thickness (CIMT) and with arterial stiffness, evaluated by measuring the pulse wave velocity (PWV) in an ambulatory population of adults. To this aim, 67 subjects were recruited in the 'Atherosclerosis and osteoporosis: identification of common pathogenetic factors' investigation. Serum sclerostin levels correlated positively with CIMT (r=0.314, p=0.03) and inversely with the augmentation index, a marker of arterial stiffness (r=-0.286, p<0.05), whereas Dkk1 did not. Moreover, in a multivariate linear regression model, sclerostin [β -0.1472; p=0.0023; standard error (SE)=0.04620] was an independent predictor of PWV in the study subjects. Our study shows that, following adjustment for confounders, sclerostin is an independent predictor of arterial stiffness in an ambulatory population, whereas Dkk1 is not. [ABSTRACT FROM AUTHOR]