OBJECTIVE:To investigate the effects of achieving minimal disease activity (MDA) on the progression of subclinical atherosclerosis and arterial stiffness in patients with psoriatic arthritis (PsA).METHODS:A total of 101 consecutive patients with PsA were recruited for this prospective cohort study. All patients received protocolized treatment targeting MDA for a period of 2 years. High-resolution carotid ultrasound and arterial stiffness markers were assessed annually. The primary outcome measure was the effect of achieving MDA at 12 months (MDA group) on the progression of subclinical atherosclerosis over a period of 24 months. Secondary objectives were to compare the changes in arterial stiffness markers over 24 months between the MDA and non-MDA groups, as well as the changes in subclinical atherosclerosis and arterial stiffness markers in patients who achieved MDA at each visit from month 12 through month 24 (sustained MDA [sMDA]).RESULTS:Ninety PsA patients (mean ± SD age 50 ± 11 years, 58% male [n = 52]) who completed 24 months of follow-up were included in this analysis. Fifty-seven patients (63%) had achieved MDA at 12 months. Subclinical atherosclerosis and arterial stiffness outcomes were similar between the MDA and non-MDA groups. Forty-one patients (46%) achieved sMDA. As shown by multivariate analysis, achieving sMDA had a protective effect on plaque progression (odds ratio 0.273 [95% confidence interval 0.088-0.846], P = 0.024), and less of an increase in total plaque area, mean intima-media thickness, and augmentation index values after adjustment for covariates.CONCLUSION:Our results support the recommendation that once MDA is achieved, it should ideally be maintained for a prolonged period in order to prevent progression of carotid atherosclerosis and arterial stiffness in patients with PsA.

Cardiovascular disease is the most common cause of death in patients with psoriatic arthritis (PsA) [(1)][1]. An overactive immune response in PsA together with traditional cardiovascular risk factors accelerates early atherosclerosis via a shared inflammatory pathway [(2)][2]. Inflammation may also

Background PsA patients have higher CVD risk due to underlying inflammation.While achieving MDA was associated with articular benefits, its effect on CVD risk remained uncertain Objectives To investigate effect of achieving MDA on subclinical atherosclerosis and arterial stiffness Methods Subjects without CVD were recruited and received protocolised treatment aiming at MDA for 2 years. High-resolution ultrasound(for subclinical atherosclerosis) and arterial stiffness were assessed yearly. The primary objective was to investigate the effect of achieving MDA(MDA group)at 12 months on the progression of subclinical atherosclerosis(carotid intima-media thickness[IMT] and plaque)over 2 years. Secondary objectives were to compare1)changes in arterial stiffness(branchial-ankle pulse wave velocity[PWV] and augmentation index[AIX])over 2 years between MDA and non-MDA group;2)changes in vascular outcomes in patients who could or could not achieved sustained MDA(sMDA,defined as achievingMDA from month12 to24).Carotid plaque progression was defined as an increase in number/region harbouring plaque compared with baseline Results 90 patients [male:52(58%); age: 50±11] were included. At 24 months, 62 (69%)were on csDMARDs, 20 (22%)were on anti-TNF-α and 8 (9%)were on Secukinumab. Proportion of patient achieved MDA increased significantly(baseline:17%;12 months:64%;24 months:69%) after intensive treatment. Vascular outcomes were similar between MDA and non-MDA group (figure 1).41 (46%)patients achieved sMDA. At baseline, a higher prevalence of subjects in the non-sMDA group were smokers, treated with NSAIDS and csDMARDs;fewer subjects were on bDMARDs, and they had higher disease activity compared with the sMDA group. 34 (38%)of them had plaque progression and prevalence was numerically higher in the non-sMDA group[22 (45%)vs 12 (29%), p=0.13]. Using multivariate analysis, achieving sMDA had protective effect on plaque progression[OR=0.27, 95% CI: 0.09 to 0.84, p=0.03]after adjustment of baseline difference(table 1). Achieving sMDA was also related to less progression of total plaque area(TPA),mean and maxIMT,PWV and AIX(table 1) Conclusions Effective suppression of inflammation by achieving sustained MDA may prevent subclinical atherosclerosis and arterial stiffness progression in PsA patients Acknowledgements Health and Medical Research Fund for funding support Disclosure of Interest None declared

Background Patients with rheumatoid arthritis(RA) had increased risk of cardiovascular disease(CVD). IL-33, a member of the IL-1 family, plays an important role in the pathogenesis of RA and development of CVD. Yet, plasma IL-33 level was not detectable in most subjects which limits it’s utility as a biomarker for CVD. Meanwhile, microRNAs(miRNAs) targeting IL-33 gene expression might play a role. Objectives To ascertain if dysregulated miRNAs targeting IL-33 gene expression in earlyRA patients were associated with subclinical atherosclerosis progression Methods 73 ERA patients were recruited for this 1 year cohort study. Potential miRNAs binding to IL-33 gene were predicted by miRanda. 10 miRNAs with the highest possibility of targeting functional sites of IL-33 gene were quantified in cell free plasma samples. cel-miR-39 was used as spike-in control. Carotid plaque(CP) was identified using high-resolution ultrasound annually. Plaque progression(PP) was defined as an increased region harbouring plaque. Results CPs were identified in 25 (34%) and 31 (43%) subjects at baseline and month 12 respectively. 16 (22%) subject had plaque progression(PP +group). At baseline, subjects in PP +group were older, with lower pain and patient global scores, a higher proportion on conventional synthetic DMARDs, and higher cardiovascular risk compared to patients without plaque progression (PP-) (table 1). Plasma level of miR-382–5 p in the PP +group was significantly higher than that in the PP- group after adjusting for baseline difference (table 1). Using multivariate logistic regression, miRNA-382–5 p was an independent predictor for plaque progression(OR:2.534, 95%CI=1.079–5.952, p=0.033) after adjustment of baseline characteristics. [AUC:0.66,95% CI:0.51–0.81,p=0.048]. Other independent predictor included higher baseline Framingham risk score, diastolic BP and lower pain score. Conclusions miR-382–5 p was an independent predictor for progression of subclinical atherosclerosis and may serve as a novel biomarker for cardiovascular risk assessment in ERA patients. Acknowledgements Acknowledgement to Hong Kong Society of Rheumatology Project Fund for supporting this project. Disclosure of Interest None declared

Background Carotid Atherosclerosis is associated with compromised volumetric bone mineral density and microstructures in patients with inflammatory arthritis Objectives The aim of this study was to explore the relationship between volumetric bone mineral density (vBMD)/microstructural features and presence of carotid plaque (CP) in patients with inflammatory arthritis. Methods 175 inflammatory arthritis patients (81 [46%] PsA, 94 [54%] RA; 70 [40%] males; age: 53±12 years) were recruited into an ongoing prospective study assessing the relationship between inflammation, osteoporosis and carotid atherosclerosis. Carotid plaque and intima-media thickness (IMT) were measured by carotid ultrasound. Areal BMD (aBMD) was measured by dual energy X-ray absorptiometry (DXA). Microstructure features and vBMD of distal radius were measured using high-resolution peripheral quantitative computed tomography (HR-pQCT). Results No patients had established cardiovascular disease (CVD). Data from 172 patients at baseline were analyzed for this cross-sectional study. Patients were sub grouped according to the presence or absence of carotid plaque (CP+ group, n=68 [40%]) and CP- group, n=132 [60%]). CP+ group were older (59±10 vs 49±11, p<0.001), more likely to be male (54% vs 31%, p=0.002), had higher systolic blood pressure (130±19 vs 124±17 mmHg, p=0.034) and CVD risk (15.7±14.2 vs 7.9±8.6, p<0.001) according to the Framingham Risk Score (FRS) then the CP- group. aBMD, vBMD and microstructure were significantly compromised in the CP+ group. Distal radius aBMD, distal radius total vBMD, trabecular (Tb) vBMD, Tb thickness, cortical (Ct.) vBMD, Ct. thickness and bone volume fraction were 5% (p=0.004), 12% (p<0.001), 8% (p=0.007), 8% (p=0.004), 4% (p=0.007), 10% (p=0.001) and 8% (p=0.007) lower in the CP+ group. The differences remained significant after adjustment for gender, disease type and FRS (Table 1). Conclusions Inflammatory arthritis patients with carotid plaque had lower aBMD, vBMD and compromised bone microstructure in the distal radius even after adjustment for gender, disease type and FRS, suggesting that inflammation may be the common link for both conditions. Disclosure of Interest None declared

Cardiovascular disease is the most common cause of death in patients with psoriatic arthritis (PsA) [(1)][1]. An overactive immune response in PsA together with traditional cardiovascular risk factors accelerates early atherosclerosis via a shared inflammatory pathway [(2)][2]. Inflammation may also

Objective. To determine the efficacy of 2 tight control treatment strategies aiming at Simplified Disease Activity Score (SDAI) remission (SDAI ≤ 3.3) compared to 28-joint count Disease Activity Score (DAS28) remission (DAS28 < 2.6) in the prevention of arterial stiffness in patients with early rheumatoid arthritis (RA). Methods. This was an open-label study in which 120 patients with early RA were randomized to receive 1 year of tight control treatment. Group 1 (n = 60) aimed to achieve SDAI ≤ 3.3 and Group 2 (n = 60), DAS28 < 2.6. Pulse wave velocity (PWV) and augmentation index (AIx) were measured at baseline and 12 months. A posthoc analysis was also performed to ascertain whether achieving sustained remission could prevent progression in arterial stiffness. Results. The proportions of patients receiving methotrexate monotherapy were significantly lower in Group 1 throughout the study period. At 12 months, the proportions of patients achieving DAS28 and SDAI remission, and the change in PWV and AIx, were comparable between the 2 groups. In view of the lack of differences between the 2 groups, a posthoc analysis was performed at Month 12, including all 110 patients with PWV, to elucidate the independent predictors associated with the change in PWV. Multivariate analysis revealed that achieving sustained DAS28 remission at months 6, 9, and 12 and a shorter disease duration were independent explanatory variables associated with less progression of PWV. Conclusion. With limited access to biologic disease-modifying antirheumatic drugs, treatment efforts toward DAS28 and SDAI remission had similar effects in preventing the progression of arterial stiffness at 1 year. However, achieving sustained DAS28 remission was associated with a significantly greater improvement in PWV. [Clinical Trial registration: Clinicaltrial.gov NCT01768923.]

Background PsA patients have increased morbidity & mortality due to cardiovascular disease (CVD). However, their CV risk were underestimated by various CV risk score1. Subclinical carotid atherosclerosis may be considered as surrogate marker of coronary artery disease (CAD) in the general population2while it remained uncertain for PsA patients Objectives To assess the relationship between carotid artery disease by ultrasound (US) and CAD by coronary computed tomography angiography (CCTA) and identify US parameters predictive of significant CAD Methods 91subjects (56 males; age: 50±11 years; disease duration 9.4±9.2 years) without overt CVD who underwent CCTA & carotid US (interval between two exams:2 [1–7] months) were recruited. Carotid intima-media thickness (cIMT)& the presence of plaque were determined by high resolution US in the distal CCA, bulb & proximal ICA bilaterally. Significant coronary artery stenosis was defined as stenosis of the lumen >50% Results Carotid plaque was present in 33 (36%) patients & coronary plaque was present in 55 (60%) patients while 9 (10%) patients had significant coronary artery stenosis. 36 (40%) patients had non-zero calcium score (CAC+ group).The mean cIMT was significantly higher in CAC+ group compared to CAC=0 group [0.70±0.11mm vs0.64±0.11mm, p=0.031]. There was a trend suggesting the mean cIMT increases with increasing CAC score, while the prevalence of carotid plaque increased significantly with rising calcium score (Table1). The mean cIMT increased significantly with number of coronary vessels habouring plaque, while there was a trend suggesting the max cIMT and the prevalence of carotid plaque may increase in patients with rising number of coronary vessels harboring plaques The mean & max cIMT were significantly higher in SS+ group than SS- group [mean cIMT: 0.76±0.07mm vs0.65±0.12mm, p=0.011; max cIMT: 0.93±0.14mm vs 0.80±0.16mm, p=0.020] (Table1). The prevalence of carotid plaque was similar between SS+ & SS- group [29 (35.4%) vs 4 (44.4%), p=0.421]. Using multivariate logistic regression, mean & max cIMT were independent explanatory variable of significant coronary stenosis after adjusting age, gender, disease duration & damaged joint count. The OR of significant coronary stenosis of every 0.01mm increase in mean & max cIMT were 1.07 (95% CI: 1.00–1.15, p=0.042) and 1.06 (95% CI: 1.00–1.11,p=0.036). Mean cIMT of 0.66mm was the optimal cut off for discriminating patients with significant coronary stenosis (sensitivity: 100%; specificity: 44%). ROC analyses demonstrated that mean cIMT (AUC=0.801, p=0.003)has higher power than Framingham CVD risk score (FRS) (AUC=0.756, p=0.012) Conclusions Increased cIMT is associated with the presence & severity of coronary calcification & obstructive coronary disease on CCTA in PsA patients. cIMT measurement can discriminate PsA patient with significant coronary stenosis better than FRS. PsA patients with moderate CVD risk should have carotid US for better CV risk stratification References LamHM, ShenJ., et al., Framingham Risk Score Discriminates Coronary Atherosclerosis in PsA Patient Better Than Other Cardiovascular Scores Do [abstract]. Arthritis Rheumatol. 2016;68. Cohen, G.I., et al., Relationship between carotid disease on ultrasound and coronary disease on CT angiography. JACC Cardiovasc Imaging, 2013.6(11). Disclosure of Interest None declared

Background Patients with rheumatoid arthritis (RA) have higher incidence of cardiovascular disease (CVD) and prevalence of arterial stiffness (AS) due to underlying inflammation. Effective immunosuppression using anti-TNF was shown to improve AS in early RA (ERA) patients.Whether it is a specific effect by blocking the TNFα pathway or suppression of inflammation remains uncertain. While achieving Disease Activity Score in 28joints (DAS) remission was associated with significant benefits in articular disease, its effect on co-morbidities such as CVD risk is uncertain. Objectives To investigate the effect of achieving sustained DAS remission on AS. Methods This randomized control trial investigates the effect of 2 tight-control treatment strategies aiming 1.Simplified disease activity score [SDAI≤3.3]or 2.minimal disease activity [DAS<2.6] on AS in ERA patients.120 patients with active disease (DAS≥3.2), symptoms onset <2years and bDMARDs naive were recruited and received 1-year treatment.Treatment are adjusted based on the standardized protocol every 3month aiming at either 1 of the 2 targets. AS is measured by branchial-ankle pulse wave velocity (baPWV) using a dedicated tonometry system (Omron VP-2000). Results In the interim analysis, results of 100 patients [male (23.0%); 52.8±13 years] completed 1year follow-up were analyzed. No significant differences between groups in clinical features, DMARD use and baPWV at month12 (M12) was observed yet significant improvement in disease activity was found in both groups.Hence,results from the 2 groups were combined to ascertain if achieving sustained DAS remission can prevent AS progression.The disease activity improved significantly [DAS: 4.8 (4.2,5.6) at baseline (BL) vs 2.38 (1.6,3.0) at M12, p<0.001]. 57% patients achieved DAS remission at M12 and 36% patients achieved DAS remission over 3 consecutive visits (sustained remission). No significant differences were found in disease activity, cardiovascular risk factors (CRF) and baPWV at BL between groups who can (CA) or cannot achieve (NA) sustained remission. At M12, no significant differences in CRF and baPWV were found between groups.However, the change in baPWV was significantly different between CA and NA group [-65.5 (-147.25, 44.0) cm/s vs 39 (-65.25, 124.75) cm/s, p=0.005]. The differences remained significant in the %change of baPWV [-4.4 (-9.67–2.84)% vs 2.51 (-4.34–10.28)%, p=0.006].I n univariate analysis,assocation of change in baPWV and potential predictors included BL baPWV, blood pressure (systolic & diastolic) and sustained DAS remission was found.By multivariate analysis,achieving sustained DAS remission was an independent predictor for baPWV reduction. Conclusions Effective suppression of inflammation by achieving sustained DAS remission may prevent progression of AS in ERA patients. Disclosure of Interest None declared

Objectives To evaluate coronary atherosclerosis in patients with psoriatic arthritis (PsA) and control subjects using coronary CT angiography (CCTA). Methods Ninety consecutive patients with PsA (male: 56(62.2%); 50.3±11.1 years) were recruited. 240 controls (male: 137(57.1%); 49.6±10.7 years) without known cardiovascular (CV) diseases who underwent CCTA due to chest pain and/or multiple CV risk factors were recruited for comparison. Results Patients with PsA and controls were matched in age, gender and traditional CV risk factors (all p>0.2). The prevalence of overall plaque (54(60%)/84(35%), p<0.001), calcified plaque (CP) (29(32%)/40(17%), p=0.002), mixed plaque (MP) (20(22%)/18(8%), p<0.001), non-calcified plaque (NCP) (39(43%)/53(22%), p<0.001) and combined MP/NCP (46(51%)/62(26%), p<0.001) were all significantly higher in patients with PsA. Three-vessel disease was diagnosed in 12(13%) patients with PsA and 7(3%) controls (p<0.001), while obstructive plaques (>50% stenosis) were observed in 8(9%) patients with PsA and 7(3%) controls (p=0.033). After adjusting for traditional CV risk factors, PsA remained an independent explanatory variable for all types of coronary plaques (OR: 2.730 to 4.064, all p<0.001). PsA was also an independent explanatory variable for three-vessel disease (OR: 10.798, p<0.001) and obstructive plaque (3.939, p=0.024). In patients with PsA, disease duration was the only disease-specific characteristic associated with more vulnerable plaques (MP/NCP) in multivariate analysis (1.063, p=0.031). The other independent explanatory variables were age ≥55 years (5.636, p=0.005) and male gender (8.197, p=0.001). Conclusions Patients with PsA have increased prevalence, burden and severity of coronary atherosclerosis as documented by CCTA. Longer disease duration was independently associated with the presence of vulnerable MP/NCP plaques in patients with PsA. Trial registration number NCT02232321.

Objective. To test the performances of established cardiovascular (CV) risk scores in discriminating subclinical atherosclerosis (SCA) in patients with psoriatic arthritis. Methods. These scores were calculated: Framingham risk score (FRS), QRISK2, Systematic COronary Risk Evaluation (SCORE), 10-year atherosclerotic cardiovascular disease risk algorithm (ASCVD) from the American College of Cardiology and the American Heart Association, and the European League Against Rheumatism (EULAR)–recommended modified versions (by 1.5 multiplication factor, m-). Carotid intima-media thickness > 0.9 mm and/or the presence of plaque determined by ultrasound were classified as SCA+. Results. We recruited 146 patients [49.4 ± 10.2 yrs, male: 90 (61.6%)], of whom 142/137/128/118 patients were eligible to calculate FRS/QRISK2/SCORE/ASCVD. Further, 62 (42.5%) patients were SCA+ and were significantly older, with higher systolic blood pressure and higher low-density lipoprotein cholesterol (all p < 0.05). All CV risk scores were significantly higher in patients with SCA+ [FRS: 7.8 (3.9–16.5) vs 2.7 (1.1–7.8), p < 0.001; QRISK2: 5.5 (3.1–10.2) vs 2.9 (1.2–6.3), p < 0.001; SCORE: 1 (0–2) vs 0 (0–1), p < 0.001; ASCVD: 5.6 (2.6–12.4) vs 3.4 (1.4–6.1), p = 0.001]. The Hosmer-Lemeshow test revealed moderate goodness of fit for the 4 CV scores (p ranged from 0.087 to 0.686). However, of the patients with SCA+, those identified as high risk were only 44.1% (by FRS > 10%), 1.8% (QRISK2 > 20%), 10.9% (SCORE > 5%), and 43.6% (ASCVD > 7.5%). By applying the EULAR multiplication factor, 50.8%/14.3%/14.5%/54.5% of the patients with SCA+ were identified as high risk by m-FRS/m-QRISK2/m-SCORE/m-ASCVD, respectively. EULAR modification increased the sensitivity of FRS and ASCVD in discriminating SCA+ from 44% to 51%, and 44% to 55%, respectively. Conclusion. All CV risk scores underestimated the SCA+ risk. EULAR–recommended modification improved the sensitivity of FRS and ASCVD only to a moderate level.

Background Patients with rheumatoid arthritis (RA) die prematurely compared with the general population, primarily because of cardiovascular diseases (CVD). Interleukin-33 (IL-33) is a member of the IL-1 cytokine family which was important in the pathogenesis of RA and development of CVD. Blood IL-33 protein was not detectable in most subjects, even in RA patients. Thus, the usability of IL-33 as a biomarker for CVD is limited. MicroRNAs (miRNAs) are small non-coding RNAs that function as post-transcriptional regulators of gene expression. Objectives This study was to ascertain if dysregulated miRNAs targeting IL-33 gene in early RA (ERA) patients were associated with subclinical atherosclerosis in ERA patients. Methods 76 ERA patients were recruited in this cross-sessional study. Potential miRNAs binding to 39UTR of the IL-33 gene were predicted by miRanda (www.microRNA.org). 10 miRNAs with highest possibility targeting functional sites of IL-33 gene were quantified in cell free plasma samples using a 2Δ Ct method. Caenorhabditis elegans miR-39 (cel-miR-39) was used as spike-in control. The results were then log transferd. Carotid plaque (CP) was measured and identified at bilateral common carotid artery, bulb, and proximal internal carotid artery using a high-resolution B mode ultrasound. Receiver-operating characteristic curve (ROC) analysis was performed to determine the discriminating power of the miRNA for the presence of CP. Results CPs were identified in 26/76 (34%) subjects (CP+ group). Subjects in the CP+ group were older [58±10 vs 48±11 years old, p=0.001], predominantly male [48 (42.3%) vs 43 (14.0%), p=0.006], with a higher C-reactive protein (CRP) level [24.9±25.0 vs 11.8±13.7 mg/dL, p=0.018] and higher cardiovascular risk [Framingham risk score (FRS): 12.8±11.6 vs 5.7±6.8, p=0.008] (Table 1). All miRNAs were detected in >80% of subjects in both group. Plasma level of miR-186–5p in the CP+ group was significantly higher than that in the CP- group [log miRNA: 3.28±3.21 vs 2.58±1.13 p=0.008]. It was still significant after adjusting age, sex, plasma CRP and FRS (p=0.030) (Table 1). Using multivariate logistic regression, miRNA-186–5p was an independent predictor of the presence of carotid plaque (OR: 1.919, 95% CI=1.096–3.361, p=0.023) after adjustment of FRS and CRP level. [Area under the ROC (AUC) 0.66, 95% CI: 0.60–0.80 p=0.024]. Conclusions miR-186–5p was an independent predictor for presence of subclinical atherosclerosis and may serve as a novel biomarker for risk stratification in ERA patients with mild to moderate cardiovascular risk. Disclosure of Interest None declared

Patients with inflammatory arthritis have increased risk of cardiovascular diseases (CVDs) compared with the general population. Subclinical carotid atherosclerosis and increased arterial stiffness are also common in these patients, which may serve as surrogate end points for cardiovascular (CV) events in clinical trials. Although exact mechanisms are still unclear, persistent systemic inflammation in patients with inflammatory arthritis may contribute to the development of CVD. Dysregulated innate immunity pathways in these patients may also play a role in accelerating atherosclerosis. During the last decade, effective suppression of inflammation by biological disease-modifying antirheumatic drugs has improved the disease outcome dramatically in patients with inflammatory arthritis. Growing evidence suggests that antitumor necrosis factor (TNF) therapy may prevent CVD in patients with rheumatoid arthritis. Nonetheless, data on non-TNF biologics are limited. Whether anti-TNF therapy may prevent CVD in patients with spondyloarthritis also remained unclear. In this review, we summarized the effect of both anti-INF and non-TNF biologics on the CV system, including traditional CVD risk factors, endothelial function, arterial stiffness, subclinical atherosclerosis, and clinical CVD in patients with inflammatory arthritis.

Psoriatic arthritis (PsA) patients have increased risk of both atherosclerosis and osteoporosis. Previous studies revealed that IL-33/ST2 axis may be related to both conditions; however, these associations were never evaluated in a single patients’ group. Here we explored the association among plasma levels of IL-33 and its decoy receptor soluble ST2 (sST2), carotid plaque determined by ultrasound and volumetric bone mineral density (vBMD)/microstructure of distal radius measured by high-resolution peripheral quantitative computed tomography (HR-pQCT) in 80 PsA patients (55% male; 53.0 ± 10.1 years). Plasma sST2 levels were significantly higher in 33 (41%) patients with carotid plaques (11.2 ± 4.5 vs 7.7 ± 3.7 ng/ml, P < 0.001). In multivariate analysis, sST2 was an independent explanatory variable associated with carotid plaques (OR = 1.296, 95% CI: [1.091,1.540]; P = 0.003). After adjustment for the osteoporotic risk factors, sST2 was significantly associated with higher cortical porosity (β = 0.184, [0.042,0.325]; P = 0.012) and cortical pore volume (2.247, [0.434,4.060]; P = 0.016); and had a trend to be associated with lower cortical vBMD (−2.918, [−6.111,0.275]; P = 0.073). IL-33 was not associated with carotid plaque or vBMD/microstructure. In conclusion, plasma sST2 levels were independently correlated with both carotid plaque and compromised cortical vBMD/microstructure in PsA patients. IL-33/ST2 axis may be a link between accelerated atherosclerosis and osteoporosis in PsA.