Key result
In patients with active ankylosing spondylitis, 24 weeks of anti-TNF-α therapy did not significantly improve arterial stiffness (pulse wave velocity 7.9 vs 7.7 m/s; P=0.412).
Why the study?
Does 24-week anti-TNF-α therapy improve arterial stiffness in patients with active ankylosing spondylitis?
Cohort (n=28)
Does 24-week anti-TNF-α therapy improve arterial stiffness in patients with active ankylosing spondylitis?
Absolute Event Rate: 7.7% vs 7.9%
p-value: p=0.412
Anti-TNF-α therapy does not appear to improve arterial stiffness in patients with active ankylosing spondylitis despite improving disease activity markers.
No improvement in arterial stiffness after 24-week anti-TNF-α in active ankylosing spondylitis; leaves open longer-term cardiovascular effects.
OBJECTIVE: The availability of new-generation drugs has provided significant success reflected by disease activity markers and clinical status in AS, but controversial reports necessitate further assessment of associated increased risk of cardiovascular burden that might persist. Hence this prospective clinical study evaluated the effectiveness of a 24-week anti-TNF-α therapy on vascular stiffness [pulse wave velocity (PWV)] in AS. METHODS: A total of 28 active AS patients (21 males, 7 females) were enrolled before the start of biologic therapy. Demographic and clinical characteristics were recorded. Arterial stiffness was assessed using PWV. Patients were evaluated before and 24 weeks after anti-TNF-α therapy. RESULTS: The mean disease duration was 8.4 (4.9) years. After 24 weeks of anti-TNF-α therapy, despite significant improvements in patients' symptoms and clinical activity parameters, including BASDAI score [4.9 (0.9) vs 1.9 (0.5), P = 0.0001], ESR [35.5 (23.1) vs 13.8 (9.2) mm/h, P = 0.0001) and CRP level [2.1 (1.6) vs 0.4 (0.3) ng/dl, P = 0.0001], no significant change was seen in arterial stiffness parameters [7.9 (1.3) vs 7.7 (1.3) m/s, P = 0.412]. Significant correlation was determined between arterial stiffness and age, systolic blood pressure and high-density lipoprotein cholesterol levels. CONCLUSION: Despite significant improvement in markers of disease activity, anti-TNF-α therapy does not seem to improve arterial stiffness, a significant AS-associated cardiovascular burden. Thus, when treating AS, significant end-points other than DASs should also be considered, and any hidden threat like arterial stiffness should be addressed further.
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Çapkın et al. (2012) conducted a cohort in Ankylosing Spondylitis (AS) (n=28). Anti-TNF-α therapy vs. Baseline (before therapy) was evaluated on Arterial stiffness assessed by pulse wave velocity (PWV) (p=0.412). In patients with active ankylosing spondylitis, 24 weeks of anti-TNF-α therapy did not significantly improve arterial stiffness (pulse wave velocity 7.9 vs 7.7 m/s; P=0.412).
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