Etanercept improves inflammation-associated arterial stiffness in rheumatoid arthritis.
OBJECTIVE
Increased arterial stiffness, an independent risk factor for premature coronary artery disease, has been reported in patients with RA. The objectives of this study were first to assess, in patients with RA, the relationship between disease activity, inflammation and augmentation index, which is a combined measure of arterial stiffness and pulse wave reflection. The second objective was to establish any effect anti-rheumatic treatment may have on augmentation index.


METHODS
One hundred and forty-eight RA patients with no previous history of cardiovascular disease (CVD) had their augmentation index corrected for a heart rate of 75 beats per minute (AIx@75), and parameters of RA disease activity and CV risk measured. Forty-seven patients were then treated with either MTX (n = 21) or etanercept (ETAN) (n = 26), and assessments were repeated at 2 and 4 months.


RESULTS
Patients with high CRP (> 10 mg/l) showed significantly higher mean AIx@75 than those with low CRP (< or = 10 mg/l) (33 +/- 8 vs 30 +/- 8%; P = 0.033). On regression analysis, log(10) CRP (beta = 0.298; P = 0.002), gender (beta = 0.257; P = 0.007), BMI (beta = -0.292; P = 0.004), diastolic blood pressure (beta = 0.260; P = 0.009) and age (beta = 0.194; P = 0.046) were independently associated with AIx@75. Treatment with ETAN (35 +/- 9, 32.5 +/- 1 and 32.5 +/- 8%; P = 0.025) but not MTX (31 +/- 1, 31 +/- 1 and 31 +/- 1%; P = 0.971) attenuated the AIx@75 significantly from baseline to Visits 2 and 3.


CONCLUSIONS
Systemic inflammation (CRP) is an independent predictor of arterial stiffness and pulse wave reflection in patients with RA. ETAN but not MTX therapy reduces arterial stiffness and pulse wave reflection and may thus improve CV morbidity in RA.
Galarraga
Bernat
B
The Institute of Cardiovascular Research, Vascular and Inflammatory Diseases Research Unit, Ninewells Hospital and Medical School, Dundee DD1 9SY, UK. lauberdoc@hotmail.com.
Khan
Faisel
F
Kumar
Pradeep
P
Pullar
Tom
T
Belch
Jill J F
JJ
D000368:Aged; D018501:Antirheumatic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D002097:C-Reactive Protein / Q000378:metabolism; D004548:Elasticity / Q000187:drug effects; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology* / Q000627:therapeutic use; D007249:Inflammation / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; 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; D016896:Treatment Outcome; D014655:Vascular Resistance / Q000187:drug effects
D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D018124:Receptors, Tumor Necrosis Factor; D002097:C-Reactive Protein; D000068800:Etanercept