No significant changes in arterial stiffness in patients with ankylosing spondylitis after tumour necrosis factor alpha blockade treatment for 6 and 12 months.
OBJECTIVE
The increased cardiovascular risk associated with AS is attributable to multiple factors: disease activity, systemic inflammation, traditional risk factors and NSAIDs. This study aimed to investigate the effects of 24 and 52 weeks of TNF-α inhibitor treatment on arterial stiffness and cardiovascular risk factors.


METHODS
Arterial stiffness was measured using the augmentation index (AIx) and pulse wave velocity (PWV), while other cardiovascular risk factors [lipid profile, blood pressure (BP) and BMI] were collected for active AS patients.


RESULTS
In total, 49 patients, comprising 30 men, were included in the study, with a mean age of 46.9 (12.1) years. Of these, 20 (40.8%) patients were current smokers, while 10 were treated for hypertension. Patients had long-standing [11.9 (9.2) years] and active AS, with a high initial BASDAI [55.0 (18.2)]. Regarding treatment, 26 patients received etanercept, 17 adalimumab and 6 infliximab. No changes were observed in PWV and AIx after 6 or 12 months following TNF-α blockade [PWV 6.97 (2.03) m/s, 6.92 (1.81) m/s and 7.10 (1.95) m/s at baseline, 6 months and 1 year, respectively, P = 0.64; AIx 19.5 (13.1%), 20.2 (12.8%), 18.3 (13.5%), respectively, P = 0.87]. Lipid profiles and other cardiovascular risk factors were unchanged. However, BASDAI, BASFI and biological inflammation were significantly improved.


CONCLUSIONS
Arterial stiffness was not improved after 6 and 12 months of anti-TNF-α therapy. However, treatment decreased biological inflammation and disease activity without causing any changes in lipid profiles and other traditional cardiovascular risk factors.
Gabriel Montpied Teaching Hospital, Rheumatology Department, Place H. Dunant, Clermont-Ferrand, 63000, France. smathieu@chu-clermontferrand.fr
Sylvain
S
Mathieu
Bruno
B
Pereira
Marion
M
Couderc
Emilie
E
Rabois
Jean-Jacques
JJ
Dubost
Martin
M
Soubrier
D000068879:Adalimumab; D000328:Adult; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000494:pharmacology / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000494:pharmacology / Q000627:therapeutic use; D007249:Inflammation / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D000069285:Infliximab; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D063177:Pulse Wave Analysis; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012307:Risk Factors; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D059289:Vascular Stiffness / Q000187:drug effects* / Q000502:physiology
D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D008055:Lipids; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept