3.5 Improvement in Aortic Stiffness after One Year of Anti-Tumor Necrosis Factor- Therapy in Patients with Inflammatory Arthropathies is Associated with Reduction in Calprotectin (A Proinflammatory S100 Protein)

Abstract

Background

Chronic inflammatory arthropathies such as rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are associated with an increased risk of cardiovascular disease. TNF-α antagonists are previously reported to improve vascular function in these patients and thus be beneficial with regard to cardiovascular disease.

Aims:

To examine the effect of one year treatment with Tumor Necrosis Factor (TNF)-α antagonists on arterial stiffness and carotid intima media thickness (cIMT) in patients with inflammatory arthropathies, and furthermore to explore possible associations between changes in the vascular measurements and Calprotectin which is a proinflammatory protein (S100A8/S100A9) associated with both inflammatory arthropathies, endothelial dysfunction and acute coronary events.

Methods and Results:

A total of 53 patients with RA, AS or PsA and clinical indication for anti-TNF-α therapy were included. 36 patients started with anti-TNF-α therapy and were compared with a non-treatment group of 17 patients. Aortic pulse wave velocity (aPWV), augmentation index (AIx) (Sphygmocor), cIMT (ArtLab) and Calprotectin were measured at baseline and after one year. aPWV (mean ± SD) was reduced in the treatment group, but not in the control group (−0.51 ± 0.80 m/s versus 0.11 ± 0.48 m/s, respectively; P = 0.001). AIx and cIMT did not change in any of the groups. In the treatment group, change in aPWV correlated with change in Calprotectin (r = 0.36, P = 0.04).

Conclusion:

These findings indicate that long term anti-TNF-α therapy improves aortic stiffness in patients with inflammatory arthropathies, and that the improvement is correlated with reduction in the proinflammatory protein Calprotectin.