SAT0400 EVIDENCE FOR “DEEP KOEBNERISATION” AT BOTH THE ENTHESIS AND VASCULAR BIFURCATIONS AS A NOVEL MECHANISTIC LINK BETWEEN PSORIATIC ARTHRITIS AND CARDIOVASCULAR DISEASE- RESULTS OF PILOT ULTRASOUND STUDIES OF JOINTS AND ARTERIES
Authors: I. Tinazzi, G. Citriniti, N. Girolimetto, F. Martinis, C. Salvarani, D. Mcgonagle, P. Macchioni
Journal: Annals of the Rheumatic Diseases (2020)

Background: The association between PsA and cardiovascular disease is generally thought to be greater than the risk between psoriasis and cardiovascular disease. Vascular calcifications (VC) are considered an early marker of atherogenesis and accurate VC scores including Carotid, Aortic and Lower limbs vascular Calcifications (CALC) were published 2 . PsA localises to entheses that are sites of high physical stressing, analogous to artery bifurcations which are sites of high vascular stress. Entheseal calcification is a feature of the post-inflammatory changes. We hypothesised that there may be common “deep koebernisation” responses in the entheses and vessels in PsA as a common biomechanical response specifically linking PsA with cardiovascular disease Objectives: To quantify non-coronary VC in a consecutive series of PsA patients using CALC score (CALCs) and compare PsA patients with CV risk factors to the group without. To independently evaluate sonographic entheseal changes including new bone formation and to determine if the magnitude of vascular and entheseal lesions was linked Methods: 122 adult PsA patients diagnosed according to the CASPAR criteria underwent US assessment for the presence of VC according to CALCs. Carotids arteries intima-media thickness (IMT) was also measured. Blinded to this US assessment, further US imaging of 12 large entheseal sites was performed. The presence of enthesophytes was scored dichotomously for each site and summed up to generate the ARES score. Enthesophytes were scored semiquantitatively in a 0-3 scale according to previous studies 3 to generate RESS score. Enthesal inflammatory changes were identified according with OMERACT definitions Results: Overall, 83 patients were female (68%), mean age 58.6±10.3 y and mean PsA duration 9.5±7.0 y. PsA with obesity, metabolic syndrome and hypertension presented higher IMT values. The IMT scores correlated significantly with entheseal thickness (p&lt; 0.001). A statistical significant correlation was found between CALCs with enthesophytes scores ARES and RESS (spearman rho = 0.665, p &lt; 0.001 and 0.634, p &lt; 0.001 respectively). CALCs, ARES and RESS were significantly increased in patients with CV risk factors or an history of CV events, compared with patients without (table 1). No significant correlation was found between CALCs and PsA duration (Spearman rho = 0.132, p = 0.135) PATIENTS, N. (%) CALCs ARES RESS Hypertension 50 (41%) 8.18 ± 6.20 ** 6.55 ± 2.59 ** 12.06 ± 5.91 ** No hypertension 72 (59%) 3.82 ± 4.24 ** 4.79 ± 2.61 ** 8.05 ± 5.40 ** Positive history of CV events 16 (13%) 11.5 ± 5.34 ** 7.56 ± 2.50 * 13.56 ± 4.97 * No CV events 106 (87%) 4.70 ± 5.02 ** 5.16 ±2.64 * 9.06 ± 5.86 * Obesity 31 (25%) 6.55 ± 5.03 6.63 ± 1.86 * 12.03 ± 4.96 * No obesity 91 (75%) 5.48 ± 5.77 5.32 ± 2.85 * 9.17 ± 6.07 * Hyperuricemia 14 (11%) 11.86 ± 8.15 * 7.43 ± 2.56 * 15.00 ± 5.33 ** No hyperuricemia 108 (89%) 4.65 ± 4.55 * 5.23 ± 2.68 * 8.97 ± 5.69 ** Dyslipidemia 54 (44%) 7.47 ± 6.43 ** 5.90 ± 2.70 10.84 ± 6.13 * No Dyslipidemia 68 (56%) 3.92 ± 4.03 ** 5.11 ± 2.73 8.59 ± 5.58 * Diabetes 11 (9%) 10.09 ± 7.29 * 7.18 ± 2.14 * 14.55 ± 5.20 * No diabetes 111 (91%) 5.08 ± 5.16 * 5.31 ± 2.73 * 9.14 ± 5.79 * * = p&lt;0.05, ** = p&lt;0.001 Conclusion: In PsA patients vascular and entheseal calcifications are significantly correlated. Patients with CV risk factors and/or history of CV events have higher values of CALCs, ARES and RESS. This suggests possible commonalites between entheses and vessels that might represent a deep Koebnerisation response in arteries and entheses. This raises the possibilities that the primary joint inflammatory responses and what is viewed as a comorbidity are closely linked References: [1]Eder L, et al. J Rheumatol Suppl. 2019;95:20-27. [2]Flore R, et al. Eur Rev Med Pharmacol Sci. 2018;22(3):736-742. [3]Aydin SZ, et al. Rheumatol Int. 2016;36(3):397-404. Disclosure of Interests: Ilaria Tinazzi: None declared, Giorgia Citriniti: None declared, Nicolò Girolimetto: None declared, Federica Martinis: None declared, Carlo Salvarani: None declared, Dennis McGonagle Grant/research support from: Janssen Research &amp; Development, LLC, Pierluigi Macchioni: None declared