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Objectives: (i) To estimate the prevalence and severity of coronary artery disease and (ii) to assess the risk of cardiovascular events and mortality, in patients with psoriasis and psoriatic arthritis (PsA) in a large-scale cohort of patients referred to coronary computed tomography angiography (CTA). Methods: This was a cross-sectional study with follow-up of 46,022 patients based on data from a Danish national CTA registry. Exposure was defined as psoriasis or PsA. A group of patients without psoriasis, PsA or any other inflammatory disease was used as reference. Cross-sectional primary outcomes were a coronary artery calcium score (CACS) >0 and CACS ≥400, and secondary outcome was obstructive CAD. At follow-up, the primary outcome was a composite endpoint of cardiovascular events and all-cause mortality. All outcomes were adjusted for traditional cardiovascular risk factors. Results: We identified 1356 psoriasis and 370 PsA patients. The adjusted odds ratio (OR) for psoriasis patients for CACS >0, CACS ≥400 and obstructive CAD was 1.26 (1.10–1.46), 1.25 (1.04–1.50) and 1.14 (0.98–1.33), respectively. For PsA patients, OR for CACS >0 was 1.28 (1.00–1.64). We found a crude hazard ratio (HR) of 1.49 (1.21–1.85) and adjusted HR of 1.14 (0.92–1.41) for the primary outcome in psoriasis patients. Conclusions: In this population, both psoriasis and PsA were associated with an increased prevalence of coronary calcification. Psoriasis patients also showed an increased prevalence of severe calcification. Psoriasis patients were at increased risk for cardiovascular events and death, however not after adjusting for the effect of other predictors.

Background The left atrial appendage (LAA) is the main source of thromboembolism in atrial fibrillation (AF). Transcatheter closure is non-inferior to warfarin therapy in preventing stroke. Case summary A patient with two consecutive strokes associated with AF was referred for transcatheter LAA occlusion (LAAO). Preprocedural cardiac CT and transoesophageal echocardiography demonstrated a spontaneously occluded LAA with a smooth left atrial surface, with stationary results at 6- and 12-month imaging follow-up. Warfarin was discontinued, and life-long aspirin instigated. Discussion Left atrial appendage occlusion has shown non-inferiority to warfarin for prevention of stroke, cardiovascular death, and all-cause mortality. No benefits from anticoagulation have been demonstrated in patients with embolic stroke of undetermined source. In the present case, we observed that the LAA was occluded and, therefore, treated with aspirin monotherapy assuming similar efficacy as transcatheter LAAO.

Andreas Bugge Tinggaard,1 Annette de Thurah,2 Ina Trolle Andersen,3 Anders Hammerich Riis,3 Josephine Therkildsen,1 Simon Winther,4 Ellen-Margrethe Hauge,2 Morten Bøttcher1 1Department of Cardiology, Hospital Unit West, Herning, Denmark; 2Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark; 3Department of Clinical Epidemiology, Aarhus University Hospital, Aarhus, Denmark; 4Department of Cardiology, Aarhus University Hospital, Aarhus, DenmarkCorrespondence: Andreas Bugge Tinggaard Tel +0045 30272717Email andreas.bugge@midt.rm.dkPurpose: To examine the occurrence and severity of coronary artery disease (CAD) in patients with rheumatoid arthritis (RA) compared to non-RA patients in a population referred for coronary computed tomography angiography (CTA) due to chest pain.Patients and Methods: In this cross-sectional study, 46,210 patients from a national CTA database were included. Patients with RA were stratified on serology, treatment with conventional synthetic or biological disease-modifying antirheumatic drugs (DMARDs), and the need for relapse or flare treatment with intraarticular or -muscular glucocorticoid injections (GCIs). Primary outcomes were coronary artery calcium score (CACS) > 0 and CACS ≥ 400, and secondary outcome was obstructive CAD. Associations between RA and outcomes were examined using logistic regression and results were adjusted for age, sex, cardiovascular risk factors and comorbidities.Results: A total of 395 (0.9%) RA patients were identified. In overall RA, crude odds ratio (OR) for having CACS > 0 was 1.48 (1.21– 1.82) and 1.52 (1.15– 2.01) for CACS ≥ 400, whereas adjusted ORs were 1.08 (0.86– 1.36) and 1.21 (0.89– 1.65), respectively. Seropositive RA patients had adjusted OR of 1.16 (0.89– 1.50) for CACS > 0 and 1.37 (0.98– 1.90) for CACS ≥ 400. Patients who had received ≥ 1 GCI in the period of 3 years prior to the CTA had an adjusted OR of 1.37 (0.94– 2.00) for having CACS > 0 and 1.46 (0.92– 2.31) for CACS ≥ 400.Conclusion: This is the first large-scale, CTA-based study examining the occurrence and severity of CAD in RA patients with symptoms suggestive of cardiovascular disease. A higher prevalence of coronary artery calcification was found in RA patients. After adjusting for age, sex, cardiovascular risk factors and comorbidities, the tendency was less pronounced. We found a trend for increased coronary calcification in RA patients being seropositive or needing treatment with GCI for a relapse or flare.Keywords: rheumatoid arthritis, computed tomography angiography, coronary artery disease, coronary artery calcium score, cross-sectional

Background Inflammation plays a central role in the development of atherosclerosis and inflammatory disease might promote progression of CAD. Objectives To examine the impact of the most frequent systemic inflammatory disease, rheumatoid arthritis (RA), on the prevalence and severity of coronary artery disease (CAD) in patients referred for rule out of CAD by cardiac computed tomography (CCT). Methods In total, 39,534 patients from a mandatory national CCT database were included. Patients with a validated RA diagnosis were subgrouped based on serology, treatment with biological disease-modifying anti-rheumatic drugs (DMARDs), and the need for flare treatment with intraarticular and intramuskular glucocorticoid injections (GCIs). Outcomes were coronary artery calcium score (CACS) > 0 and CACS > 400. Differences in prevalences were assessed by odds ratios (OR). Outcomes were adjusted for cardiovascular risk factors and comorbidities. Results A total of 337 (0.9%) patients with RA were identified. OR for having CACS > 0 was 1.17 (0.91-1.50) for overall RA and 1.33 (1.00-1.77) for seropositive RA. Patients who had received ≥1 GCI in the period 3 years prior to the CCT had an OR of 1.49 (0.99-2.27) for having CACS > 0. The OR for having CACS > 400 was 1.31 (0.95-1.81) for overall RA and 1.49 (1.04-2.12) for seropositive RA. OR for having CACS > 400 was 1.43 (0.99-2.07) for RA patients treated with conventional synthetic DMARDs, but 1.01 (0.51-1.99) for patients treated with biological DMARDs. Conclusion Coronary artery calcifications are more frequent in RA patients being seropositive or needing flare treatment. The occurrence of severe calcification is more frequent in seropositive RA patients and in RA patients not escalated to biological DMARDs. These findings support the hypothesis that systemic inflammation accelerates the atherosclerotic process leading to increased coronary artery calcium, which may explain the increased risk of cardiovascular events among RA patients. Disclosure of Interests None declared

Background: Rheumatoid arthritis (RA) is a known risk factor for developing coronary artery disease (CAD). The influence of RA on the prognosis after initial diagnosis and treatment of CAD is however largely unknown. Objectives: To examined the risk of major cardiovascular events among RA and non-RA patients with chest pain referred to cardiac computed tomography (CCT). Methods: This was a follow-up study, using data from the Western Denmark Heart Registry[1]. Information on RA diagnosis and co-variates were identified through nationwide administrative registers. The primary outcome was a combined outcome including, myocardial infarction, ischemic or uspecified stroke, coronary artery bypass grafting, percutaneus coronary intervention, and all-cause mortality. In the studied region, RA-flares are controlled through escalation of disease modifying drugs and intra-articular or intramuscular glucocorticoid injections (GCI). Hence, the number of times a patient had received GCIs 3 years prior to the CCT were used as a surrogate marker of disease activity. Analyses were performed for overall RA and the serological subtypes: ‘seropositive RA’(ICD-10: M05) and ‘other RA’(ICD-10: M06). Median time until events or censoring was 3.5 years (min/max: 0.0: 9.2). Cox proportional hazard models were used to examine the association between RA/non-RA patients and outcomes. Results: Among 42,257 patients, referred between 2008 and 2016, we identified 358 (0.8%) with RA. An increased risk was seen in RA compared to non-RA (adjusted hazard ratio (HR) 1.35 (95% CI: 0.93; 1;96)). An additional risk was found among patients who had received flare treatment more than once prior to CCT (adjusted HR 1.80 (95% CI: 1.08; 3.00)), and in patients with sero-positive RA (adjusted HR: 1.42 (95% CI: 0.93; 2.16)). Conclusion: In patients with low-intermediate a priori risk of CAD, we found an association between RA and the combined primary outcome, supporting that RA per se, but in particular sero-positive and active RA, increase the risk of cardiovascular events even after initial CAD diagnosis and treatment. References [1] Nielsen LH, et al. The Western Denmark cardiac Computed Tomography Registry: a review and validation study. Clinical epidemiology2014, Dec31; 53-64 Disclosure of Interests: None declared

Background MicroRNAs (MiRs) play an important role in the pathogenesis of chronic inflammatory diseases. This study is the first to investigate miR expression profiles in purified CD4+ T lymphocytes and CD14+ monocytes from patients with axial spondyloarthritis (axSpA) using a high-throughput qPCR approach. Methods A total of 81 axSpA patients fulfilling the 2009 ASAS classification criteria, and 55 controls were recruited from October 2014 to July 2017. CD14+ monocytes and CD4+ T lymphocytes were isolated from peripheral blood mononuclear cells. MiR expression was investigated by qPCR using the Exiqon Human MiRnome panel I analyzing 372 miRNAs. Differentially expressed miRNAs identified in the discovery cohort were validated in the replication cohort. Results We found a major difference in miR expression patterns between T lymphocytes and monocytes regardless of the patient or control status. Comparing disease-specific differentially expressed miRs, 13 miRs were found consistently deregulated in CD14+ cells in both cohorts with miR-361-3p, miR-223-3p, miR-484, and miR-16-5p being the most differentially expressed. In CD4+ T cells, 11 miRs were differentially expressed between patients and controls with miR-16-1-3p, miR-28-5p, miR-199a-5p, and miR-126-3p were the most strongly upregulated miRs among patients. These miRs are involved in disease relevant pathways such as inflammation, intestinal permeability or bone formation. Mir-146a-5p levels correlated inversely with the degree of inflammation in axSpA patients. Conclusions We demonstrate a consistent deregulation of miRs in both monocytes and CD4+ T cells from axSpA patients, which could contribute to the pathophysiology of the disease with potential interest from a therapeutic perspective. Electronic supplementary material The online version of this article (10.1186/s13075-019-1829-7) contains supplementary material, which is available to authorized users.

ObjectiveMicroRNAs (miRNAs) play an important role in the pathogenesis of autoimmune diseases such as primary Sjögren’s syndrome (pSS). This study is the first to investigate miRNA expression patterns in purified T and B lymphocytes from patients with pSS using a high-throughput quantitative PCR (qPCR) approach.MethodsTwo independent cohorts of both patients with pSS and controls, one for discovery and one for replication, were included in this study. CD4+ T cells and CD19+ B cells were isolated from peripheral blood mononuclear cells by magnetic microbeads and expression of miRNAs was profiled using the Exiqon Human miRNome panel I analysing 372 miRNAs. A selection of differentially expressed miRNAs was replicated in the second cohort using specific qPCR assays.ResultsA major difference in miRNA expression patterns was observed between the lymphocyte populations from patients with pSS and controls. In CD4 T lymphocytes, hsa-let-7d-3p, hsa-miR-155–5 p, hsa-miR-222–3 p, hsa-miR-30c-5p, hsa-miR-146a-5p, hsa-miR-378a-3p and hsa-miR-28–5 p were significantly differentially expressed in both the discovery and the replication cohort. In B lymphocytes, hsa-miR-378a-3p, hsa-miR-222–3 p, hsa-miR-26a-5p, hsa-miR-30b-5p and hsa-miR-19b-3p were significantly differentially expressed. Potential target mRNAs were enriched in disease relevant pathways. Expression of B-cell activating factor (BAFF) mRNA was inversely correlated with the expression of hsa-miR-30b-5p in B lymphocytes from patients with pSS and functional experiments showed increased expression of BAFF after inhibiting hsa-miR-30b-5p.ConclusionsThis study demonstrates major miRNAs deregulation in T and B cells from patients with pSS in two independent cohorts, which might target genes known to be involved in the pathogenesis of pSS.