Tumour necrosis factor antagonists improve disease activity but not arterial stiffness in rheumatoid arthritis.
OBJECTIVE
Systemic inflammation may play an important role in the accelerated atherosclerosis and increased cardiovascular mortality of rheumatoid arthritis (RA). Atorvastatin reduced arterial stiffness in RA patients after only 6 weeks, an effect that may be partially mediated by the immunomodulatory effects of this drug. Suppression of inflammation with tumour necrosis factor (TNF) antagonists may therefore also improve vascular function in RA; however, TNF antagonists have also been shown to cause or exacerbate congestive heart failure in patients with RA and heart failure. The aim of the present study was to examine the effect of treatment with TNF antagonists on arterial stiffness in RA patients with active disease.


METHODS
Fourteen RA patients (age 55.1 +/- 3.8 yr; disease duration 7.9 +/- 1.3 yr) with high disease activity [disease activity score (DAS28) 7.1 +/- 0.3] commencing treatment with TNF antagonists for the first time were studied. Clinical status and arterial stiffness were measured before and after 6 weeks of TNF antagonist therapy (etanercept, adalimumab or infliximab).


RESULTS
Arterial stiffness did not change during the study period (the mean augmentation index was 29.1 +/- 2.2% at baseline vs 30.1 +/- 1.8% at week 6; P = 0.504). The DAS28 improved significantly from 7.1 +/- 0.3 to 4.3 +/- 0.4 (P < 0.0001). The erythrocyte sedimentation rate and C-reactive protein [median (range)] were reduced from 44 (12-85) to 15 (3-82) mm/h (P = 0.02) and from 34 (3-95) to 10 (2-61) mg/l (P = 0.007), respectively.


CONCLUSIONS
Despite significant reductions in synovitis and inflammatory markers in these RA patients, arterial stiffness was not improved by 6 weeks of treatment with TNF antagonists. This result is of relevance given recent reports of potential adverse cardiovascular effects of TNF antagonists in some RA patients.
Van Doornum
S
S
Department of Medicine (RMH/WH), The University of Melbourne, Post Office, Royal Melbourne Hospital, Victoria 3050 Australia. svd@unimelb.edu.au
McColl
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G
Wicks
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IP
D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000503:physiopathology*; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow / Q000187:drug effects; D017534:Radial Artery / Q000187:drug effects / Q000503:physiopathology; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014655:Vascular Resistance / Q000187:drug effects
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept