***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background — Aortic stiffness is a marker of cardiovascular disease and an independent predictor of cardiovascular risk . Although an association between inflammatory markers and increased arterial stiffness has been suggested , the causative relationship between inflammation and arterial stiffness has not been investigated . Methods and Results — One hundred healthy individuals were studied according to a r and omized , double-blind , sham procedure-controlled design . Each sub study consisted of 2 treatment arms , 1 with Salmonella typhi vaccination and 1 with sham vaccination . Vaccination produced a significant ( P<0.01 ) increase in pulse wave velocity ( at 8 hours by 0.43 m/s ) , denoting an increase in aortic stiffness . Wave reflections were reduced significantly ( P<0.01 ) by vaccination ( decrease in augmentation index of 5.0 % at 8 hours and 2.5 % at 32 hours ) as a result of peripheral vasodilatation . These effects were associated with significant increases in inflammatory markers such as high-sensitivity C-reactive protein ( P<0.001 ) , high-sensitivity interleukin-6 ( P<0.001 ) , and matrix metalloproteinase-9 ( P<0.01 ) . With aspirin pretreatment ( 1200 mg PO ) , neither pulse wave velocity nor augmentation index changed significantly after vaccination ( increase of 0.11 m/s and 0.4 % , respectively ; P = NS for both ) . Conclusions — This is the first study to show through a cause- and -effect relationship that acute systemic inflammation leads to deterioration of large-artery stiffness and to a decrease in wave reflections . These findings have important implication s , given the importance of aortic stiffness for cardiovascular function and risk and the potential of therapeutic interventions with antiinflammatory properties Background New 2007 European Society of Hypertension guidelines recommend measuring arterial stiffness in patients with arterial hypertension , suggesting a carotid – femoral pulse wave velocity over 12 m/s as an estimate of sub clinical organ damage . Considering this cutoff point , it is worth exploring whether or not there are significant differences in results obtained using various techniques for measuring aortic pulse wave velocity . The aim of the study was to compare aortic pulse wave velocity measurements using Complior , SphygmoCor , and Arteriograph devices , and to assess the effect of pulse wave transit time and traveled distance on pulse wave velocity values . Methods Aortic pulse wave velocity was measured on a single visit , using these devices , in r and omized order , in a group of 64 patients with grade 1 or 2 arterial hypertension . Results Aortic pulse wave velocity measured using Complior ( 10.1 ± 1.7 m/s ) was significantly higher than that obtained using SphygmoCor ( 8.1 ± 1.1 m/s ) or Arteriograph ( 8.6 ± 1.3 m/s ) . No differences were noted between pulse wave velocity measurements using SphygmoCor and Arteriograph . Between- method comparison revealed that differences in traveled distance were significant : Complior versus Arteriograph [ 0.09 m , Confidence interval ( CI ) : 0.08–0.12 m , P < 0.05 ] , Complior versus SphygmoCor ( 0.15 m , CI : 0.13–0.16 m , P < 0.05 ) , Arteriograph versus SphygmoCor ( 0.05 m , CI : 0.03–0.07 m , P < 0.05 ) . No between- method differences were found for transit times . Conclusion Differences in pulse wave velocity obtained by compared devices result ed primarily from using various methods for measuring traveled distance . It appears reasonable to establish uniform principles for the measurement of traveled distance . Because a large number of prognosis/survival studies used direct distance between carotid and femoral sites of pulse wave recording , this distance should be mostly recommended Background — Rheumatoid arthritis ( RA ) is associated with increased cardiovascular risk , which is not explained by traditional cardiovascular risk factors but may be due in part to increased aortic stiffness , an independent predictor of cardiovascular mortality . In the present study , our aim was to establish whether aortic stiffness is increased in RA and to investigate the relationship between inflammation and aortic stiffness . In addition , we tested the hypothesis that aortic stiffness could be reduced with anti – tumor necrosis factor-&agr ; ( TNF-&agr ; ) therapy . Methods and Results — Aortic pulse-wave velocity ( PWV ) , augmentation index , and blood pressure were measured in 77 patients with RA and in 142 healthy individuals . Both acute and chronic inflammatory measures and disease activity were determined . The effect of anti-TNF-&agr ; therapy on PWV and endothelial function was measured in 9 RA patients at 0 , 4 , and 12 weeks . Median ( interquartile range ) aortic PWV was significantly higher in subjects with RA than in control subjects ( 8.35 [ 7.14 to 10.24 ] versus 7.52 [ 6.56 to 9.18 ] m/s , respectively ; P=0.005 ) . In multiple regression analyses , aortic PWV correlated independently with age , mean arterial pressure , and log-transformed C-reactive protein ( R2=0.701 ; P<0.0001 ) . Aortic PWV was reduced significantly by anti-TNF-&agr ; therapy ( 8.82±2.04 versus 7.94±1.86 versus 7.68±1.56 m/s at weeks 0 , 4 , and 12 , respectively ; P<0.001 ) ; concomitantly , endothelial function improved . Conclusions — RA is associated with increased aortic stiffness , which correlates with current but not historical measures of inflammation , suggesting that increased aortic stiffness may be reversible . Indeed , anti-TNF-&agr ; therapy  reduced aortic stiffness to a level comparable to that of healthy individuals . Therefore , effective control of inflammation may be of benefit in reducing cardiovascular risk in patients with RA Arterial stiffness , estimated by  pulse wave velocity ( PWV ) , is an independent predictor of cardiovascular mortality and morbidity . However , the clinical applicability of these measurements and the elaboration of reference PWV values are difficult due to differences between the various devices used . In a population of 50 subjects aged 20–84 years , we compared PWV measurements with three frequently used devices : the Complior and the PulsePen , both of which determine aortic PWV as the delay between carotid and femoral pressure wave and the PulseTrace , which estimates the Stiffness Index ( SI ) by analyzing photoplethysmographic waves acquired on the fingertip . PWV was measured twice by each device . Coefficient of variation of PWV was 12.3 , 12.4 and 14.5 % for PulsePen , Complior and PulseTrace , respectively . These measurements were compared with the reference method , that is , a simultaneous acquisition of pressure waves using two tonometers . High correlation coefficients with the reference method were observed for PulsePen ( r=0.99 ) and Complior ( r=0.83 ) , whereas for PulseTrace correlation with the reference method was much lower ( r=0.55 ) . Upon Bl and –Altman analysis , mean differences of values±2s.d . versus the reference method were −0.15±0.62 m/s , 2.09±2.68 m/s and −1.12±4.92 m/s , for PulsePen , Complior and PulseTrace , respectively . This study confirms the reliability of Complior and PulsePen devices in estimating PWV , while the SI determined by the PulseTrace device was found to be inappropriate as a surrogate of PWV . The present results indicate the urgent need for evaluation and comparison of the different devices to st and ardize PWV measurements and establish reference values BACKGROUND Premature arterial stiffening and atherosclerosis are increased in patients with inflammatory arthropathies such as rheumatoid arthritis ( RA ) , ankylosing spondylitis ( AS ) and psoriatic arthritis ( PsA ) . The proinflammatory protein calprotectin is associated with inflammatory arthropathies , vascular pathology , and acute coronary events . We examined the long-term effects of treatment with tumor necrosis factor (TNF)-α antagonists on aortic stiffness and carotid intima media thickness ( CIMT ) in patients with inflammatory arthropathies , and the relationships to the levels of calprotectin . METHODS Fifty-five patients with RA , AS , or PsA and a clinical indication for anti-TNF-α therapy  were included and followed with regular examinations for 1 year . Thirty-six patients starting with anti-TNF-α therapy  were compared with a nontreatment group of 19 patients . Examinations included assessment s of aortic stiffness ( aortic pulse wave velocity , aPWV ) , CIMT , and plasma calprotectin . RESULTS After 1 year , aPWV ( mean ( s.d . ) ) was improved in the treatment group , but not in the control group ( -0.54 [ 0.79 ] m/s vs. 0.06 [ 0.61 ] m/s , respectively ; P = 0.004 ) , and CIMT progression ( median ( quartile cut-points , 25th and 75th percentiles ) ) was reduced in the treatment group compared to the control group ( -0.002 [ -0.038 , 0.030 ] mm vs. 0.030 [ 0.011 , 0.043 ] mm , respectively ; P = 0.01 ) . In multivariable analyses , anti-TNF-α therapy over time was associated with improved aPWV ( P = 0.02 ) and reduced CIMT progression ( P = 0.04 ) , and calprotectin was longitudinally associated with aPWV ( P = 0.02 ) . CONCLUSIONS Long-term anti-TNF-α therapy improved aortic stiffness and CIMT progression in patients with inflammatory arthropathies . Calprotectin may be a soluble biomarker reflecting aortic stiffening in these patients 
    Output:
    
CONCLUSION cf-PWV is increased in both ulcerative colitis and Crohn 's disease patients