***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: OBJECTIVE Our aim was to ascertain the efficacy of golimumab compared with placebo in the prevention of atherosclerosis and arterial stiffness in AS . METHODS A r and omized , double-blind , placebo-controlled pilot study was performed in which AS patients were treated with  golimumab ( n = 20 ) and placebo  ( n = 21 ) for 12 months . Patients from the placebo group who failed to achieve a 20 % response to Assessment of SpondyloArthritis international Society criteria ( ASAS20 ) at 6 months received open-label golimumab .  Intima-media thickness ( IMT ) , pulse wave velocity ( PWV ) and augmentation index ( AIx ) were measured at baseline , 6 and 12 months . RESULTS At 6 months , 11/20 ( 55 % ) and 3/21 ( 14 % ) patients from the golimumab and placebo groups achieved an ASAS20 response , respectively ( P = 0.006 ) . There was no significant difference in the change of the vascular parameters between the two groups . In the placebo group , significantly greater progression of the mean IMT [ from 0.51 mm ( S.D. 0.07 ) at baseline to 0.53 mm ( S.D. 0.08 ) at 6 months , P = 0.044 ] and PWV ( from 12.2 m/s ( S.D. 1.6 ) at baseline to 12.6 m/s ( S.D. 1.3 ) , P = 0.028 ] were observed . There was a trend towards progression of the mean IMT in the golimumab group ( P = 0.099 ) but the maximum IMT , PWV and AIx remained unchanged . At 12 months the changes in vascular parameters were similar between the early and delayed ( or no ) golimumab groups . CONCLUSION Uncontrolled inflammation may result in a significant progression in IMT and PWV in patients with AS . Arterial dysfunction may be prevented by golimumab over a period of 6 months , probably because of effective suppression of inflammation . TRIAL REGISTRATION clinical trials.gov ( NCT01212653 Objective . To determine the efficacy of methotrexate ( MTX ) with infliximab ( IFX ) compared with MTX alone in the prevention of atherosclerosis and arterial stiffness in patients with early rheumatoid arthritis ( RA ) . Methods . A r and omized , open-label study in which early RA patients with active disease were treated with MTX alone ( n = 20 ) and MTX plus IFX ( n = 20 ) for 6 months . Patients were assessed every 3 months . Patients from the MTX-alone group who failed to achieve 28-joint Disease Activity Score remission ( DAS28 ≤ 2.6 ) at 6 months were permitted to escape to open-label IFX . Intima-media thickness ( IMT ) , pulse wave velocity ( PWV ) , and augmentation index ( AIx ) were measured at baseline , 6 months , and 12 months . Results . At 6 months , there was a significantly greater reduction in PWV in the MTX-alone group ( 0.18 ± 1.59 m/s ) compared with the MTX plus IFX group ( −0.78 ± 1.13 m/s ; p = 0.044 ) , accompanied by significantly greater reduction in patient ’s global assessment , number of swollen joints , C-reactive protein , and DAS28 in the MTX plus IFX group compared to the MTX-alone group . The changes in IMT and AIx were similar between the 2 groups . At 12 months , there was a trend favoring early combination treatment with regard to the reduction in PWV ( p = 0.06 ) . Conclusion . MTX plus IFX causes a more significant reduction in PWV than MTX alone in patients with early RA after 6-month treatment , and further improvement may be achieved in patients who continued on longterm tumor necrosis factor-α blockers , suggesting that early , effective suppression of inflammation may prevent progression of atherosclerosis by improving vascular function The objective of the study is to evaluate the effect of TNF inhibition on carotid thickness over a 2-year period . 144 women with RA diagnosed according to ACR criteria , without clinical evidence of cardiac and /or vascular disease were enrolled and compared with 78 matched controls . All patients received methotrexate ( 15–20 mg weekly ) for 3 months . Responders ( n = 79 ) continued to be treated with methotrexate , non-responders ( n = 40 ) moved to methotrexate plus a TNF alpha antagonist .  Echosonographic studies of carotids were obtained before and after 2-year follow-up . A significant decrease of ca-IMT was observed in anti-TNF-treated patients ( P < 0.001 ) ; on the other h and , no significant variation of ca-IMT was observed after 2 years in MTX-treated patients . Our study indicates that anti-TNF blocking agents , but not methotrexate , are capable of reducing IMT of carotid arteries in female RA patients in a 2-year follow-up Objectives : Vascular endothelial function and common carotid artery intima – medial thickness ( CCA‐IMT ) are well‐established surrogate markers for early atherosclerotic disease , which accounts for 30–40 % of excess mortality in rheumatoid arthritis ( RA ) patients . Our aim was to investigate whether long‐term treatment with anti‐tumour necrosis factor (TNF)α agents can modulate endothelial function and CCA‐IMT . Methods : Twelve patients with RA ( mean age 54.8±15 years ) on anti‐TNFα treatment ( seven adalimumab , five infliximab ) due to uncontrolled disease activity , with mean Disease Activity Score ( DAS28 ) 5.7 ( range 4.6–6.9 ) despite disease‐modifying anti‐rheumatic drugs ( DMARDs )  , were studied prospect ively . Patients were assessed at baseline and after 3 and 18 months for endothelial‐dependent vasodilatation , assessed by flow‐mediated vasodilatation ( FMD ) , endothelial‐independent vasodilatation and CCA‐IMT . RA disease activity and response to therapy were assessed by the DAS28 index . Results : After 18 months of treatment , 67 % of the patients were responders according to European League Against Rheumatism ( EULAR ) response criteria  . Anti‐TNFα treatment improved FMD ( from 7±4.3 % to 11.1±3.8 % , p = 0.026 ) whereas CCA‐IMT did not change significantly [ from 0.67 ( 0.4–1 ) to 0.68 ( 0.39–1.2 ) mm ; mean change 0.01 ( −0.06 to 0.08 ) mm ] . Endothelial‐independent vasodilatation remained stable ( 20.4±7.3 % to 22.9±6.5 % , p = 0.4 ) . Conclusions : In this small cohort of patients with RA and no clinical ly overt cardiovascular disease ( CVD ) , after 18 months of treatment with anti‐TNFα agents , endothelial function improved significantly while CCA‐IMT remained stable . Longitudinal studies using more patients are needed to determine the clinical significance of these findings in relation to the risk of atherosclerosis To determine whether treatment with the anti-TNF-alpha blocker adalimumab yields persistent improvement of endothelial function and prevents from morphological progression of sub clinical atherosclerosis in patients with rheumatoid arthritis ( RA ) refractory to conventional therapy , a series of 34 consecutive RA patients , attending hospital outpatient clinics and who were switched from disease modifying antirheumatic drug therapy to anti-TNF-alpha-adalimumab treatment because of severe disease , were assessed by ultrasonography techniques before the onset of adalimumab therapy ( at day 0 ) and then at day 14 and at month 12 . Values of flow-mediated endothelium-dependent vasodilatation at day 14 and at month 12 were significantly higher ( mean ± st and ard deviation ( SD ) : 6.1 ± 3.9 % ; median : 5.7 % at day 14 , and mean ± SD : 7.4 ± 2.8 % ; median : 6.9 % at month 12 ) than those obtained at day 0 ( mean : 4.5 ± 4.0 % ; median : 3.6 % ; P = 0.03 and P < 0.001 , resp . ) . Endothelium-independent vasodilatation results did not significantly change compared with those obtained at day 0 . No significant differences were observed when carotid artery intima-media wall thickness values obtained at month 12 ( mean ± SD : 0.69 ± 0.21 mm ) were compared with those found at day 0 ( 0.65 ± 0.16 mm ) ( P = 0.3 ) . In conclusion , anti-TNF-alpha-adalimumab therapy has beneficial effects on the development of the sub clinical atherosclerosis disease in RA 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 OBJECTIVE To investigate prognostic factors associated with mortality in patients with psoriatic arthritis ( PsA ) . METHODS Patients followed up at the Toronto PsA Clinic between 1978 and 1994 were included . Patients were review ed at initial clinic entry and at 6-month intervals using a st and ard protocol . Data on deaths were collected in a prospect i ve manner , and death certificates were used to identify the primary and antecedent cause(s ) of death . All death information was recorded in the clinic 's computerized data base . Only factors that represented st and ard clinical measures of disease activity and progression were studied . The relationship between potential prognostic factors recorded at the time of the first clinic visit and the mortality rate was determined using the Cox relative risk regression model . RESULTS There were 428 patients ( 234 men and 194 women ) , of whom 68 % were known to be alive on September 1 , 1994 , 20 % were lost to followup but assumed to be alive , and 12 % had died . Multivariate analysis revealed that an erythrocyte sedimentation rate ( ESR ) > 15 mm/hour , medications used prior to initial clinic visit , radiologic damage , and the absence of nail lesions were associated with an increased overall mortality rate . There is some suggestion that prior medication use was least important for deaths associated with the circulatory system , while radiologic damage was particularly important for such deaths . A marked sex-associated effect was noted among deaths caused by injuries/poisoning , since 6 of the deaths occurred in men and only 1 was in a woman . CONCLUSION Patients with PsA are at an increased risk of death compared with the general population . Evidence of previously active and severe disease , as manifested by the prior use of medications and by radiologic changes as well as an elevated ESR at presentation , are prognostic indicators for death . The presence of nail lesions appears to be a protective factor that has the most clinical importance in the context of previously active and severe disease Background Cardiovascular mortality is increased in patients with rheumatoid arthritis ( RA ) . RA is associated with an increased left ventricular mass index ( LVMI ) , a 
    Output:
    
The balance of evidence suggests that TNF-a antagonists may have a beneficial effect on preventing the progression of sub clinical atherosclerosis and arterial stiffness .
It remains unknown whether this effect is specific to TNF-a antagonists or relates to better control of inflammation irrespective of the disease modification strategy by which this is achieved