Background/Objectives: Vitamin D insufficiency is common in patients with spondyloarthritis (SpA). We analyzed the relationship between vitamin D, disease activity, and left ventricular (LV) function in patients with SpA. Methods: A total of 298 patients with SpA and 57 healthy controls were enrolled. Serum vitamin D and laboratory cardiovascular risk factors were analyzed, and LV function was assessed by echocardiography. Vitamin D, the Ankylosing Spondylitis Disease Activity Score (ASDAS), and the Disease Activity Index for Psoriatic Arthritis (DAPSA) were examined for mutual correlations using univariate and multivariate linear regression models and were compared between groups. Results: Vitamin D levels did not differ between the SpA group and controls, although vitamin D supplementation was more frequent among SpA patients. Vitamin D was not associated with SpA activity. ASDAS and DAPSA were positively correlated with isovolumic relaxation time, and DAPSA was inversely correlated with peak early diastolic mitral annular velocity (e'), after adjustment for age, sex, metabolic factors, and/or therapy. Patients with insufficient serum vitamin D levels (<75 nmol/L) showed greater impairment of systolic and diastolic LV function and a diabetic-like lipid profile compared with those with sufficient vitamin D levels. The e' wave was positively correlated with vitamin D after controlling for confounding factors. These findings in patients with SpA are consistent with those previously reported in patients with psoriatic arthritis (PsA). Conclusions: Patients with SpA were characterized by vitamin D supplementation, increased disease activity parameters, and impaired LV function. SpA activity, independent of vitamin D, was associated with LV functional impairment, and vitamin D was associated with an increase in the e' wave after adjustment for confounding factors. However, causal inferences cannot be drawn from correlational analyses.

Objective: The oral cavity is the beginning of the digestive tract and the composition of saliva could indicate immune events in the gut and joints. The objective of this research was to evaluate the diagnostic accuracy of salivary interleukin (IL)-17A for temporomandibular joint (TMJ) internal derangements (IDs) in patients with spondyloarthritis (SpA). Methods: SpA disease activity was assessed using the Bath Ankylosing Disease Activity Index (BASDAI), Ankylosing Spondylitis Disease Activity Score (ASDAS) and Disease Activity Index for Psoriatic Arthritis (DAPSA). Salivary cytokines were analyzed using enzyme-linked immunosorbent assay. TMJ conditions were evaluated using The Diagnostic Criteria for Temporomandibular Disorder (DC/TMD) protocol. A symptomatic TMJ-ID group with intracapsular arthralgia (n = 64) and asymptomatic TMJ-ID group without intracapsular arthralgia (n = 50), regardless of joint sounds, were compared with controls (healthy TMJs, n = 86). Results: Women were more prevalent and salivary IL-17A concentration was higher in both ID groups than in controls. Salivary IL-17A levels positively correlated with erythrocyte sedimentation rate, anti-streptolysin-O titer, salivary IL-12/23 p40 and matrix metalloproteinase-3 levels, sore and swollen joint counts, BASDAI, chronic TMJ pain and anxiety. IL-17A demonstrated diagnostic accuracy for currently symptomatic (cutoff, 11 pg/mL) and asymptomatic (cutoff, 11.6 pg/mL) TMJ-ID vs. controls. Patients with IL-17A levels above these cutoffs more frequently exhibited disc displacement with reduction and degenerative TMJ disease, higher self-reported spinal pain and higher SpA activity, as assessed by ASDAS, than patients with IL-17A levels ≤ cutoffs. TMJ-related headache and somatization contributed to greater TMJ pain in those with IL-17A > cutoffs, when compared with dichotomous controls. Conclusions: Salivary IL-17A concentration provides an accurate laboratory marker of SpA activity and enables the diagnosis of both currently symptomatic and asymptomatic TMJ-IDs in patients with SpA.

Purpose: The widely spread membrane and soluble Klotho protein plays a pivotal role in vascular calcification by orchestrating calcium/phosphate/magnesium homeostasis mediated by the Klotho/fibroblast growth factor 23 receptor complex. Our aim was to review new scientific data and discuss the role(s) of Klotho in vascular calcification. The basic procedures were to review the literature concerning Klotho and its mechanisms of action during physiological and pathological aging. Main findings: A lack of Klotho shortens the lifespan, increases vascular calcification and the frequency of cardiovascular diseases with multiple organ degeneration and weakness in experimental animal models. In humans, the most prominent decrease of Klotho protein and mRNA is found in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD), which shows accelerated aging due to increased vascular calcification. Additionally, Klotho acts in an endocrine manner participating in different signaling pathways as an anti-inflammatory, antioxidant, anti-fibrotic and anti-aging mediator, preserving vascular structure and function. Principal conclusions: Klotho is a possible early marker for the detection and monitoring of subclinical arterial calcification in patients with CKD-MBD and in the general population.

Objectives: The group of spondyloarthritis (SpA) disorders shares common clinical manifestations, including internal derangement (ID) of temporomandibular joint (TMJ). This study aimed to investigate SpA activity in patients with ID of TMJ. Materials and Methods: We assessed 200 patients with neck pain using the Assessment of Spondyloarthritis International Society (ASAS) criteria. TMJ was examined using Diagnostic Criteria for Temporomandibular Disorders (DC/TMD protocol). Patients with SpA were divided into three groups: symptomatic ID of TMJ, asymptomatic ID of TMJ, or healthy TMJ (controls). Activity of SpA was evaluated using the Ankylosing Spondylitis Disease Activity Score (ASDAS), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Disease Activity Index in Psoriatic Arthritis (DAPSA), patients’ self-estimated SpA activity, difficulties in performing daily activities, pain intensity (visual analogue scale) and laboratory parameters. Results: Patients with symptomatic and asymptomatic ID showed statistically significantly increased ASDAS, anti-streptolysin titer, patients’ self-estimated axial pain and activity of SpA, and decreased hematocrit than the control. Patients with symptomatic ID also had statistically significant earlier onset of SpA, along with increased BASDAI and DAPSA, total body pain, difficulties in performing daily activities, platelet count, and serum alpha-amylase but lower hemoglobin concentration than controls. Patients with asymptomatic ID had higher frequencies of exacerbated axial SpA and sacroiliac joint ankylosis compared to the control. Conclusion: All patients with SpA and ID showed increased axial disease activity.

Surgical myocardial revascularization, regardless of the technique used, causes ischemia–reperfusion injury (IRI) in the myocardium mediated by inflammation and degradation of the endothelial glycocalyx (EG). We investigated the difference between on-pump and off-pump techniques in terms of the concentration of proinflammatory interleukin (IL)-18 and the EG degradation products syndecan-1 and hyaluronic acid measured by ELISA in the peripheral and cardiac circulation during open heart surgery and in the early postoperative period. The concentration of IL-18, C-reactive protein (CRP), and cardiac troponin T (cTnT) and the leukocyte count increased statistically significantly in revascularized patients at 24 and 72 h after revascularization compared to the beginning of the procedure and was always statistically significantly higher in on-pump patients. Syndecan-1 and hyaluronic acid only increased in on-pump patients 24 and 72 h after revascularization. IL-18 correlated positively with syndecan-1 and CRP only in the pump setting and with the number of leukocytes in both revascularization regimens 24 and 72 h after the surgery. cTnT and hyaluronic acid did not correlate with IL-18. Our results suggest that IL-18 plays an important role in the early inflammatory response in patients during open heart surgery and in the early postoperative period, leading to additional damage to the EG, while it is probably not responsible for myocardial necrosis. It could serve as a biomarker to identify high-risk patients and as a therapeutic target to reduce inflammation and EG degradation. In addition, measurement of IL-18 could help improve the treatment, recovery, and outcomes of patients after heart surgery.

Background/Objectives: Knee osteoarthritis (KOA) is a progressive degenerative joint disease characterised by low-grade inflammation and is associated with increased cardiovascular (CV) risk and arterial stiffness. Pulse wave velocity (PWV) is a quantitative measure of arterial stiffness and an important tool for detecting subclinical arterial calcification and CV risk. This study aimed to determine whether PWV can distinguish radiographically mild KOA (Kellgren–Lawrence grades 1-2) from severe KAO (Kellgren–Lawrence grades 3-4) in terms of CV risk factors. Methods: A total of 223 postmenopausal women with KOA participated in this cross-sectional study. Assessments included anthropometry, laboratory analyses, blood pressure and PWV measurements, a 6 min walk test, pain evaluation using a visual analogue scale (VAS), and completion of the International Physical Activity Questionnaire (IPAQ). Results: PWV was significantly higher in the severe KOA group (10.53 m/s vs. 8.78 m/s, p < 0.001). A cut-off value of 8.4 m/s effectively distinguished between severe and mild forms of KOA (AUC = 0.798, p = 0.001). OA grade, pain, age, waist circumference, WHR, SCORE 2/SCORE 2OP, systolic blood pressure, serum glucose, HbA1c, uric acid, creatinine, and erythrocyte sedimentation rate were increased in the group with PWV > 8.4 m/s, compared to the group with PWV ≤ 8.4 m/s. Conversely, eGFR, the 6 min walk test and physical activity of patients were reduced in the group with PWV > 8.4 m/s. A patient with a PWV > 8.4 m/s has a 1.77 times higher chance of developing a more severe form of the disease than a patient with a lower PWV. Conclusions: Patients with a higher PWV are more likely to develop a more severe form of KOA, which is associated with increased cardiovascular risk.

We investigated the polarisation of CD68+ macrophages and perforin and granulysin distributions in kidney lymphocyte subsets of children with IgA vasculitis nephritis (IgAVN). Pro-inflammatory macrophage (M)1 (CD68/iNOS) or regulatory M2 (CD68/arginase-1) polarisation; spatial arrangement of macrophages and lymphocytes; and perforin and granulysin distribution in CD3+ and CD56+ cells were visulaised using double-labelled immunofluorescence. In contrast to the tubules, iNOS+ cells were more abundant than the arginase-1+ cells in the glomeruli. CD68+ macrophage numbers fluctuated in the glomeruli and were mostly labelled with iNOS. CD68+/arginase-1+ cells are abundant in the tubules. CD56+ cells, enclosed by CD68+ cells, were more abundant in the glomeruli than in the tubuli, and co-expressed NKp44. The glomerular and interstitial/intratubular CD56+ cells express perforin and granulysin, respectively. The CD3+ cells did not express perforin, while a minority expressed granulysin. Innate immunity, represented by M1 macrophages and CD56+ cells rich in perforin and granulysin, plays a pivotal role in the acute phase of IgAVN.

The endothelial glycocalyx (EGC) is a layer of proteoglycans (associated with glycosaminoglycans) and glycoproteins, which adsorbs plasma proteins on the luminal surface of endothelial cells. Its main function is to participate in separating the circulating blood from the inner layers of the vessels and the surrounding tissues. Physiologically, the EGC stimulates mechanotransduction, the endothelial charge, thrombocyte adhesion, leukocyte tissue recruitment, and molecule extravasation. Hence, severe impairment of the EGC has been implicated in various pathological conditions, including sepsis, diabetes, chronic kidney disease, inflammatory disorders, hypernatremia, hypervolemia, atherosclerosis, and ischemia/reperfusion injury. Moreover, alterations in EGC have been associated with altered responses to therapeutic interventions in conditions such as cardiovascular diseases. Investigation into the function of the glycocalyx has expanded knowledge about vascular disorders and indicated the need to consider new approaches in the treatment of severe endothelial dysfunction. This review aims to present the current understanding of the molecular mechanisms underlying cardiovascular diseases and to elucidate the impact of heart surgery on EGC dysfunction.

Heat shock proteins (hsps), in certain circumstances, could shape unique features of decidual dendritic cells (DCs) that play a key role in inducing immunity as well as maintaining tolerance. The aim of the study was to assess the binding of gp96 to Toll-like receptor (TLR) 4 and CD91 receptors on decidual CD1a+ DCs present at the maternal-fetal interface in vitro as well as the influence of CD1a+ DCs maturation status. Immunohistology and immunofluorescence of paraffin-embedded first-trimester decidua tissue sections of normal and pathological (missed abortion MA and blighted ovum BO) pregnancies were performed together with flow cytometry detection of antigens in CD1a+ DCs after gp96 stimulation of decidual mononuclear cells. Gp96 efficiently bound CD91 and TLR4 receptors on decidual CD1a+ DCs in a dose-dependent manner and increased the expression of CD83 and HLA-DR. The highest concentration of gp96 (1000 ng/mL) increased the percentage of Interferon-γ (INF-γ) and IL-15 expressing gp96+ cells. Gp96 binds CD91 and TLR4 on decidual CD1a+ DCs, which causes their maturation and significantly increases INF-γ and IL-15 in the context of Th1 cytokine/chemokine domination, which could support immune response harmful for ongoing pregnancy.

Osteoarthritis (OA) is a chronic joint disease caused by both mechanical damage and metabolic factors, which intertwine in their pathogenetic pathways. We hypothesise that the oxidised cholesterol derivative, 7-ketocholesterol (7-KCh), represents a danger signal in the synovia of patients with OA and promotes low-grade inflammation. The study would aim to elucidate the possible immune mechanisms initiated by 7-KCh that contribute to oxidative stress and inflammation in the synovia and synovial CD68+ cells, which are mostly macrophages. The polarisation of synovial CD68+ cells, their tissue distribution in relation to T and natural killer (NK) cells, and the influence of 7-KCh on the phenotype and intracellular cytokine and chemokine production in suspension is worth analysing. We envisage that this research would contribute to a better understanding of the biology of CD68+ macrophages influenced by 7-KCh and encourage the development of therapeutic approaches based on directing macrophage polarisation.

Spondyloarthritis (SpA) is a group of autoinflammatory/autoimmune diseases that affects the spine and peripheral joints. Involvement of the cervical spine correlates with occurrence of temporomandibular disorders (TMDs). Proinflammatory cytokines, interleukin (IL)-23, IL-17A, and tumour necrosis factor-alpha (TNF-α) are significantly involved in the immunopathogenesis of SpA, and inflammation is one of the causes of TMDs. We hypothesised that internal derangement (ID) of temporomandibular joints (TMJs), as the most frequent TMDs in patients with SpA, could be associated with salivary pro-inflammatory markers and clinical activity of axial SpA, measured with laboratory methods or rheumatological indexes. If a statistically significant difference in the concentration of salivary IL-23, IL-17A or TNF-α exists between patients with symptomatic or asymptomatic ID and patients without TMDs, the diagnostic accuracy of certain cytokine(s) for ID can be calculated. The diagnostic accuracy of the cytokine(s) could emphasise the inflammatory background of ID and possibly broaden therapeutic approaches for symptomatic ID in patients with SpA with biological drugs in addition to the routine application of occlusal splint and/or physical therapy.

Cardiac surgery is one of the highest-risk procedures, usually involving cardiopulmonary bypass and commonly inducing endothelial injury that contributes to the development of perioperative and postoperative organ dysfunction. Substantial scientific efforts are being made to unravel the complex interaction of biomolecules involved in endothelial dysfunction to find new therapeutic targets and biomarkers and to develop therapeutic strategies to protect and restore the endothelium. This review highlights the current state-of-the-art knowledge on the structure and function of the endothelial glycocalyx and mechanisms of endothelial glycocalyx shedding in cardiac surgery. Particular emphasis is placed on potential strategies to protect and restore the endothelial glycocalyx in cardiac surgery. In addition, we have summarized and elaborated the latest evidence on conventional and potential biomarkers of endothelial dysfunction to provide a comprehensive synthesis of crucial mechanisms of endothelial dysfunction in patients undergoing cardiac surgery, and to highlight their clinical implications.

Psoriatic arthritis (PsA) is influenced by a complex genetic predisposition. In patients with PsA, interleukin (IL) -17A plays a key role in triggering a complex autoimmune/autoinflammatory immune response in conjunction with other pro-inflammatory cytokines (such as tumor necrosis factor-alpha, IL-23, monocyte chemotactic protein-1, and IL-6). PsA manifests with various clinical symptoms, including musculoskeletal diseases and extra-articular manifestations. In particular, mediated by the soluble IL-17A presents a higher cardiovascular risk, suggesting connection between inflammation and cardiovascular diseases beyond the traditional risk factors. Moreover, studies have shown that patients with psoriasis are ten times at higher risk of developing dilated cardiomyopathy than those without psoriasis. Therefore, owing to the prominent role of IL-17A and psoriasis in the pathogenesis of PsA and endothelial dysfunction, we hypothesized that IL-17A is crucial in the early development of diastolic dysfunction (DD) and could serve as a tool to identify patients with asymptomatic DD and PsA. Although transthoracic echocardiography is the primary evaluation method for DD, it requires skilled personnel, routine parameters assessment, such as mitral inflow, and tissue Doppler imaging. As a result, assessing parameters such as left atrial deformity using novel techniques could be valuable for a more specific evaluation and diagnosis of DD. Clinical characteristics and laboratory parameters of PsA activity, cardiac ultrasound parameters, or cardiac functional markers like N-terminal pro-brain natriuretic peptide (NT-pro-BNP) can be correlated with the concentration of serum IL-17A. Moreover, determining the diagnostic accuracy of circulating IL-17A for early DD can also serve as a laboratory biomarker for diagnosing DD in asymptomatic patients. Thus, if the diagnostic accuracy of IL-17A for DD can be proven, the identification of biological drugs that inhibit IL-17A could be advantageous in treating patients with PsA and echocardiography-verified asymptomatic DD.

U fiziološkim uvjetima, endotel predstavlja dinamičku strukturu važnu u održavanju tonusa krvnih žila, regulaciji protoka krvi uz stijenke krvnih žila, vaskularne propusnosti, puteva zgrušavanja i adhezije leukocita. U sepsi, djelovanjem patogena i njihovih topljivih čimbenika dolazi do aktivacije endotela, oštećenja endotelnog glikokaliksa (EG) te pokretanja brojnih mehanizama koji imaju ključnu ulogu u razvoju i progresiji sepse. Nadalje, disfunkcija endotela i oštećenje EG ima za posljedicu snažni proupalni, prokagulacijski, proadhezivni i proapoptotični odgovor koji dovodi do disregualacije vaskularnog tonusa, povećane propusnosti krvnih žila, povećane adhezije i migracije leukocita uzrokujući razvoj šoka i višeorganskog zatajenja. U ovom preglednom radu prikazani su struktura i funkcija endotela i EG, opisani su mehanizmi njihovoga oštećenja tijekom sepse te posljedice koje nastaju njihovom disfunkcijom. Nadalje, iznijete su do sada poznate činjenice o metodama detekcije endotelne disfunkcije te mogućnostima njenog liječenja u sepsi s ciljem unapređenja liječenja septičnih bolesnika.

Background Oxidized low-density lipoprotein (oxLDL) particles support low-grade inflammation and have been found in synovial fluid from osteoarthritis (OA) joints [1]. Their component is 7-ketocholesterol (7-KC), which arises as the result of the oxidation of cholesterol [1]. 7-KC acts proinflammatory and it binds to Toll-like receptor (TLR) 4 expressed on macrophages [1]. Activation of TLR4 stimulates the classical macrophage maturation program, resulting in a specific phenotype of inducible nitric oxide synthase positive (iNOS+) and macrophage (M) 1 function, which produce and secrete proinflammatory chemokines and cytokines [2]. M2 macrophages are associated with wound healing by the production of arginase-1 [2,3]. Synovial macrophages are of critical importance in the symptomatology and structural progression of OA since M1 polarized macrophages accumulate in human OA synovial tissue during exacerbation [3]. However, it is not known whether 7-KC can re-program synovial tissue macrophages and support M1 polarization. Objectives We analyzed the influence of 7-KC on the polarization of CD68+ macrophages in the suspension of synovial mononuclear cells (SMCs) in respect to lipopolysaccharide (LPS), as M1 inducer. Methods Mature synovial tissue samples were obtained during alloarthroplasty of the knee (N = 56). Paraffin embedded tissue sections were labelled by double immunofluorescence using a combination of antibodies directed toward CD68 and iNOS, arginase-1, CCL2 or CCL22. Suspension of SMCs was prepared by enzymatic digestion of tissue samples using collagenase IV and gradient density centrifugation. We analyzed intracellular (iNOS, arginase-1, CCL2, and CCL22) and surface (CD91, mannose receptor, HLA-DR, CD80, CD86 and decoy D6) antigens expression in CD68+ cells in the suspension of freshly isolated or 18 hour-cultured SMCs with 7-KC (25 μM), LPS (10 ng/ml), their combination or in the medium only. Results iNOS and CCL2 were more frequently labelled in lymphocyte clusters, while arginase-1 and CCL22 were labelled in synovial lining CD68+ cells. Phenotype of CD68+ cells did not change significantly after the 18 hour- culture in the medium only, except the decrease of mannose receptor and CD91, when compared with freshly isolated cells. 7-KC increased the percentage of CD86 expressing CD68+ cells, whereas decreased surface expression of CD91 and chemokine decoy D6, like in the culture with LPS, when compared with cells cultured in the medium only. 7-KC decreased the frequency of arginase-1+/CD68+ cells in the suspension and did not change iNOS+ in CD68+ cells, thus increasing the ratio of iNOS+/arginase-1+ in CD68+ subset. 7-KC was unable to increase CCL2 like LPS in comparison with cells cultured in the medium only. Neither 7-KC nor LPS affected CCL22 expression in the CD68+ subset. Conclusion These data provide a new perspective in understanding the polarization of macrophages toward the M1 phenotype mediated with oxysterol 7-KC in vitro . References [1]Niki E. Biomarkers of lipid peroxidation in clinical material. Biochim Biophys Acta. 2014;1840(2):809-17. [2]Fernandes TL, Gomoll AH, Lattermann C, Hernandez AJ, Bueno DF, Amano MT. Macrophage: A Potential Target on Cartilage Regeneration. Front Immunol. 2020;11:111. [3]Zhang H, Cai D, Bai X. Macrophages regulate the progression of osteoarthritis. Osteoarthritis Cartilage. 2020;28(5):555-561. Acknowledgements The University of Rijeka supported the research by the grants No. Uni-ri-biomed-18-110 and No. Uni-ri-biomed-18-160. Disclosure of Interests None declared.

Osteoarthritis (OA) is a chronic joint disease caused by mechanical damage and metabolic factors that support the development of low-grade inflammation. Increased levels of T helper 1 pro-inflammatory cytokines in the serum of OA patients may support granulysin (GNLY) mediated cytotoxicity, which in-turn may contribute to the pathogenesis of OA. In the present study, GNLY expression and cytotoxic/apoptotic mechanisms mediated by GNLY in the peripheral blood of OA patients were assessed. A total of 40 non-obese women (median age of 64 years old) with knee OA, and 40 controls (median age 62 years old) were enrolled in the study. GNLY, IFN-γ and IL-4 expression levels were investigated in peripheral blood lymphocytes (PBLs) using flow cytometry, immunocytochemistry and/or confocal microscopy. Natural killer (NK) GNLY-mediated apoptosis through NK effectors against K-562 targets was analyzed using the PKH-26 18-h cytotoxicity assay. Serum GNLY levels were assessed using ELISA. The percentage of GNLY+PBLs was higher in the OA patients than that in the controls due to the increase in the proportions of GNLY+ cells in the natural killer (NK), T and natural killer T (NKT) subsets. GNLY localization inside exocytotic lysosomal-associated membrane protein-1+ granules was ~40% in both groups. However, the intensity of GNLY labeling in PBLs was higher in OA patients than in the controls, and it was supported by the increased expression of IFN-γ relative to IL-4 in NK and T cells from OA patients. The serum GNLY concentration was <0.3 ng/ml in both groups. RC8 anti-GNLY mAb by itself was unable to significantly alter early apoptosis, whereas RC8 anti-GNLY mAb combined with anti-perforin mAb significantly reduced NK-mediated early apoptosis of K-562 targets in the OA patients, whilst not exerting a notable effect in the controls. Anti-perforin mAb by itself did not affect apoptosis significantly. These results suggest that in women with knee OA, GNLY expression in the PBL subsets and GNLY-mediated early apoptosis of K-562 targets are increased compared with the controls and accompanied by intracellular dominance of IFN-γ over IL-4 in NK cells.

We aimed to evaluate the diagnostic accuracy of the proinflammatory monocyte chemotactic protein-1 (MCP-1) in the diagnosis of asymptomatic diastolic dysfunction (DD) in patients with psoriatic arthritis (PsA). The disease activity in psoriatic arthritis (DAPSA) was determined using clinical and laboratory parameters, and echocardiography was performed to estimate DD. Serum MCP-1 concentrations were elevated in PsA patients with DD diagnosed with ultrasound (median (25th percentile, 75th percentile): 366.6 pg/mL (283, 407.1 pg/mL) vs. 277.5 pg/mL (223.5, 319.1 pg/mL) in controls; P < 0.0017 ). PsA patients with serum MCP-1 concentration higher than the cut-off value of 347.6 pg/mL had a 7.74-fold higher chance of developing DD than PsA patients with lower serum MCP-1 concentrations (controls), with a specificity of 86.36% and sensitivity of 55%, as verified using ultrasound. The group with MCP-1 concentrations above the cut-off value also showed a higher late peak diastolic mitral inflow velocity, A-wave value ( P = 0.000005 ), E/E ′ ratio ( P = 0.00005 ), and a lower E/A ratio ( P = 0.000002 ), peak systolic left atrial reservoir strain, SA value ( P = 0.0066 ), early peak diastolic displacement of the mitral septal annulus, E ′ wave value ( P = 0.003 ), than controls. Systolic blood pressure ( P = 0.01 ), LDL cholesterol concentration ( P = 0.012 ), glucose concentration ( P = 0.011 ), and DAPSA ( P = 0.0000 ) increased in the PsA group with higher MCP-1 concentrations, although there were no differences in comorbidities and therapy between the groups compared. Thus, the serum MCP-1 concentration was a significant and independent prognostic indicator for asymptomatic DD in PsA patients ( area under the curve = 0.730 , P = 0.001 ). The DAPSA score in PsA patients might indicate the need for echocardiography and adjustment of anti-inflammatory treatment in terms of DD prevention.