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Abstract Number: 596

Evolution of Atherosclerosis in Psoriatic Arthritis: Is the Former an Independent Inflammatory Process?

Roberta Ramonda1, Massimo Puato2, Valentina Modesti3, Mariagrazia Lorenzin4, Paola Frallonardo4, Augusta Ortolan4, Carla Campana3, Alessandro Lo Nigro3 and Leonardo Punzi5, 1Rheumatology Unit, University of Padova, Padova, Italy, 2Department of Internal Medicine, University of Padova, Padova, Italy, 3Unit of Rheumatology, University of Padova, Padova, Italy, 4Rheumatology Unit, Department of Medicine, University of Padova, Padova, Italy, 5Clinical and Experimental Medicine, Rheumatology Unit - University of Padova, Padova, Italy

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: anti-TNF therapy, Atherosclerosis, Cardiovascular disease, psoriatic arthritis and spondylarthropathy

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Session Information

Title: Spondylarthritis and Psoriatic Arthritis - Pathogenesis, Etiology

Session Type: Abstract Submissions (ACR)

Background/Purpose:

A non-invasive study focusing on the structural and functional properties of the carotid arteries was carried out in psoriatic arthritis (PsA) patients. Increased cardiovascular morbidity and mortality and accelerated atherosclerosis were observed in patients with several rheumatic diseases, including PsA. The impact of two years of Tumor Necrosis factor alpha (TNF-a) blockade treatment on vascular structure and function was assessed.

The aim of this study was to evaluate the presence of subclinical atherosclerosis in PsA patients before and after 24 months of TNF blockade therapy and to investigate the efficacy of treatment not only with regard to disease activity but also in improving atherosclerotic indexes.

Methods:

Thirty-two PsA patients were studied before and after 24 months of TNF blockade therapy. Subclinical atherosclerosis was investigated on the basis of B-mode ultrasound measurements of the carotid intima-media thickness (IMT) expressed as the mean IMT value (the mean IMT measured bilaterally at 3 levels: the common carotid artery, the carotid artery bulb and the internal carotid artery,) and as the MMax (the mean maximum IMT). Post-occlusion flow mediated dilation (FMD) of the brachial artery was evaluated by high-sensitivity brachial ultrasonography and endothelial independent dilatation (GTN) using carotid duplex scanning. Response to therapy was studied by evaluating the tender and swollen joints (Tj and Sj), DAS 28, ESR and CRP. Patients’ lipid profiles before and after the 24 month treatment period were also evaluated. Differences in parameters over the observation period were assessed using the Wilcoxon test.

Results:

After a 24 month treatment period there was no improvement in ultrasonographic parameters with respect to baseline values. Indeed, there was a significant deterioration in both mean IMT and MMAX (respectively 0.75±0.20 vs 0.96±0.40 and 0.91±0.25 vs 1.09±0.44, p<0.01), while no alterations were observed in the FMD (5.81±2.07 vs 5.29±2.64, ns) or the GTN (7.76±2.96 vs 7.84±3.08, ns). There was instead a good response to therapy with significant reduction in the Tj (8.10±5.56 vs 2.09±2.32, p<0.01), the Sj (3.85±3.84 vs 0.25±0.72, p<0.01), the DAS 28 (4.16±0.66 vs2.30±0.82, p<0.01), the ESR (26.3±16.4 vs 14.88±13.99, p<0.01) and the CRP (11.25±9.16 vs 2.91±1.72, p<0.01). There were no significant alteration with regard to lipid profile after the two year treatment period.

Conclusion:

PsA per se implies a pro-atherogenic remodelling of carotid arteries that did not seem to be affected by the 2 year anti-TNF blockade therapy despite clinical improvement. There was in fact a slight progression in subclinical atherosclerosis as assessed by ultrasonography. Both the mean IMT and the MMAX showed a slight worsening over the two year period, while FMD, which we expected to be improved, was instead stable. Other inflammatory mechanisms not related to TNF may be responsible for the progression in atherosclerotic disease and the possible role of a genetic predisposition should not be underestimated. PsA patients seem, in fact, to have a higher risk of atherosclerosis compared to subjects with other inflammatory rheumatic diseases.


Disclosure:

R. Ramonda,
None;

M. Puato,
None;

V. Modesti,
None;

M. Lorenzin,
None;

P. Frallonardo,
None;

A. Ortolan,
None;

C. Campana,
None;

A. Lo Nigro,
None;

L. Punzi,
None.

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