Faculty Bibliography

Platelets, classically defined by their hemostatic function, are increasingly recognized as immune effectors that shape chronic inflammation and vascular pathology in immune-mediated inflammatory diseases. In conditions such as systemic lupus erythematosus, rheumatoid arthritis, and psoriasis, immune activation skews platelet adhesion, secretion, and procoagulant activity, while persistent interferon signaling and immune complex engagement (via receptors such as FcγRIIA) amplify thromboinflammation. Platelets orchestrate leukocyte recruitment and endothelial activation through P-selectin/PSGL-1 (P-selectin glycoprotein ligand-1) interactions, CD40 ligand, interleukin-1β, and the release of extracellular vesicles carrying cytokines and RNAs. Platelet involvement manifests differently across immune-mediated inflammatory diseases. In systemic lupus erythematosus, they promote type I interferon priming, neutrophil extracellular trap formation, and endothelial dysfunction. In rheumatoid arthritis, they generate abundant synovial microparticles and systemic vascular changes. In psoriasis, they accumulate within skin lesions, enhance platelet-leukocyte aggregation and activate proatherogenic endothelial responses. These pathways promote, independent of traditional cardiovascular risk factors, atherothrombosis including myocardial infarction, stroke, and venous thromboembolism. Limited translational data suggest that hydroxychloroquine may attenuate platelet activation and improve endothelial function. P2Y₁₂ inhibition may blunt interferon-linked platelet RNA signatures and leukocyte-platelet interactions. However, some therapies targeting inflammation, such as Janus kinase inhibitors, may promote thrombosis, the mechanisms of which are not fully known. Advances in multiomics, single-cell and spatial profiling, and in vivo models are delineating targets for intervention and enabling biomarker-driven risk stratification. Collectively, platelets function as central translators between autoimmunity and atherothrombosis. Defining and modulating platelet-immune crosstalk holds the potential to reduce cardiovascular risk in rheumatologic populations.

BACKGROUND/UNASSIGNED:Psoriasis is a chronic immune-mediated inflammatory disease associated with heightened cardiovascular risk. Platelets are increasingly implicated in this link through their capacity to amplify vascular inflammation and interact with leukocytes. Circulating leukocyte-platelet aggregates are elevated in psoriasis, although the biological significance of these aggregates remains incompletely understood. We investigated whether increased leukocyte-platelet aggregates is associated with alterations in the platelet transcriptomic profile in psoriasis. METHODS/UNASSIGNED:Leukocyte-platelet aggregate levels were compared between psoriasis patients (n = 42) and healthy controls (n = 29). Psoriasis patients were stratified by the cohort median lymphocyte-platelet aggregate (LyPA) or neutrophil-platelet aggregate (NPA) levels into high vs low aggregate groups. Platelet RNA sequencing was then performed to define transcriptomic differences in high-vs low-aggregate psoriasis. RESULTS/UNASSIGNED:= 0.04) compared with healthy controls (mean age 42; 55% male; 69% Caucasian). Platelet RNA sequencing revealed that psoriasis patients with high LyPA or high NPA had downregulation of platelet inflammatory pathways, including interferon, tumor necrosis factor (TNF), IL-8, and IL-6 signaling. CONCLUSION/UNASSIGNED:These findings identify inflammatory platelet transcriptomic alterations associated with elevated lymphocyte-platelet and neutrophil-platelet aggregates in psoriasis and motivate further work to define the functional consequences of leukocyte-platelet aggregates in psoriasis.

Pericardial disease is common in patients with immune-mediated inflammatory diseases (IMIDs), especially in systemic lupus erythematosus. Pericardial disease may present as an asymptomatic pericardial effusion or acute and recurrent pericarditis, and may sometimes lead to complications (cardiac tamponade and constrictive pericarditis). Pathophysiology of pericarditis in IMIDs is likely related to the underlying immune dysregulation. Diagnosis of IMID-related pericarditis relies on general diagnostic criteria, supported by inflammatory biomarkers and non-invasive multimodality imaging. Initial management of IMID-related pericarditis overlaps with idiopathic pericarditis (nonsteroidal anti-inflammatory drugs and colchicine) together with treatment of the underlying IMID. Glucocorticoids are used in cases of poor response to first-line treatments. The use of immunosuppressive therapies is driven by the underlying IMID and systemic organ involvement beyond the pericardium. Multi-disciplinary care collaboration between cardiologists, radiologists, internists, and rheumatologists is pivotal to develop an appropriate, common treatment plan based on the individual features of each patient with IMIDs.

IMPORTANCE/UNASSIGNED:Psoriasis is a chronic immune-mediated disease associated with cardiovascular, metabolic, musculoskeletal, psychiatric, hepatic, kidney, and pulmonary comorbidities. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) are approved by the US Food and Drug Administration for type 2 diabetes, obesity, cardiovascular risk reduction, chronic kidney disease, obstructive sleep apnea, and metabolic dysfunction-associated steatohepatitis-conditions common in psoriasis. Emerging evidence suggests GLP-1 RAs and dual glucose-dependent insulinotropic polypeptide/GLP-1 agonists may improve psoriatic skin disease, partly through immune modulation. If confirmed in larger randomized clinical trials, GLP-1-based therapies may offer an opportunity to address both cutaneous disease and cardiometabolic comorbidities. This primer from the US National Psoriasis Foundation Medical Board sought to provide an evidence-informed narrative synthesis and practical considerations to introduce dermatologists to GLP-1 RAs for psoriasis treatment. OBSERVATIONS/UNASSIGNED:GLP-1 RAs have been associated with reductions in Psoriasis Area and Severity Index (PASI) scores, particularly in patients with obesity or type 2 diabetes. Studies report relative PASI reductions ranging from approximately 40% to 80% with parallel quality-of-life gains, although most of these studies are small (7-48 patients), short term (≤6 months), and lack a control group. Semaglutide and liraglutide have been associated with reductions in C-reactive protein, interleukin-6, lipids, and visceral adiposity. In small, translational cohorts, PASI improvement has been correlated with reductions in superficial adiposity and dermal γδ T-cell density. GLP-1 RAs combine safely with methotrexate, cyclosporine, and biologics. Adverse effects are mainly transient gastrointestinal symptoms; pancreatitis and gallbladder events are rare. Early data show both metabolic and immunomodulatory benefits. CONCLUSIONS AND RELEVANCE/UNASSIGNED:This review found that GLP-1-based therapies target shared metabolic and inflammatory pathways in psoriasis. Current evidence supports consideration of adjunctive use in selected patients with metabolic comorbidities, although definitive conclusions await larger randomized clinical trials.

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Inflammatory myocardial and pericardial syndromes (IMPS), including myocarditis, pericarditis, and overlapping myopericardial syndromes, constitute a heterogeneous group of immune-mediated cardiac disorders with clinical trajectories ranging from complete recovery to progressive heart failure and sudden death. This state-of-the-art review synthesizes current insights into immunopathogenesis, emphasizing the interplay among genetic susceptibility, environmental factors, and systemic inflammatory drivers, including rheumatological diseases. A pragmatic diagnostic framework is presented; it integrates targeted serological evaluation, genetic testing, multimodality imaging, and selective endomyocardial biopsy to enable precise etiologic classification. Therapeutic strategies are examined across the spectrum of disease severity, including guideline-directed medical therapy for heart failure, immunosuppression for autoimmune and fulminant phenotypes, and cytokine-directed biologics for recurrent pericarditis. Prognostic determinants, indications for advanced heart failure therapies, and emerging directions in precision immunology, molecular profiling, and AI-enabled risk stratification are discussed to guide future clinical and translational advances.

Pericarditis is the most frequent manifestation of pericardial disease and accounts for up to 5% of emergency department visits for chest pain. Although traditionally considered a benign and self-limited condition, it is a heterogeneous syndrome with a broad aetiological spectrum and potentially significant morbidity. While mortality is low, the burden of complications like recurrent disease, cardiac tamponade or constrictive pericarditis, and the frequent need for hospitalisation underscore its clinical relevance. The growing availability of multimodality imaging and the publication of updated international guidelines in 2025 have recently renewed attention to pericardial diseases, refining diagnostic criteria, risk stratification and therapeutic approaches. In high-income settings, idiopathic or presumed viral pericarditis remains the most common presentation. However, a substantial proportion of patients harbour alternative aetiologies that carry distinct prognostic implications and require tailored diagnostic and management strategies. In this review, we use the ABCDE mnemonic as a pragmatic framework to highlight five clinically important and often under-recognised forms of pericardial disease. Pericarditis associated with autoimmune and systemic inflammatory diseases is typically characterised by recurrent or refractory inflammatory courses and frequent extracardiac involvement. Bacterial pericarditis, although rare, represents a life-threatening condition requiring rapid aetiological identification and aggressive therapy. Cancer-related pericardial disease often presents with large pericardial effusions or cardiac tamponade and is associated with a poor prognosis largely determined by the underlying malignancy. Damage-related and drug-related pericarditis encompasses postcardiac injury syndromes and pharmacological toxicity. Finally, endocrine and metabolic disorders, including uraemia, hypothyroidism and infiltrative conditions such as amyloidosis, are associated with pericardial disease that manifests with atypical features and effusion. Early recognition of these entities is critical, as management extends beyond standard anti-inflammatory therapy and often requires correction of the underlying cause and close multidisciplinary collaboration. This ABCDE approach can aid clinicians in identifying these uncommon high-risk forms of pericarditis and optimising patient-centred care.

UNLABELLED:Systemic lupus erythematosus (SLE) is associated with increased cardiac morbidity and mortality and involves a range of cardiac pathologies. The most common of these is a simple pericardial effusion, though rarely this can be complicated by constrictive pericarditis. We present a case illustrating a rare SLE-mediated effusive-constrictive pericarditis. A 70-year-old female with a history of a prior stroke and coronary artery disease presented with 2 weeks of dyspnea, pleuritic chest pain, and fever. Her labs were notable for acute kidney injury with hematuria and proteinuria, elevated inflammatory markers, positive anti-nuclear antibody, low complement levels, and positive double-stranded DNA. CT scan of the chest showed circumferential pericardial effusion with echocardiogram and right heart catheterization confirming effusive-constrictive pericarditis. Clinically, she met diagnostic criteria for SLE and additionally underwent renal biopsy that confirmed SLE nephritis. The patient was started on colchicine, hydroxychloroquine, mycophenolate mofetil, and prednisone. A 3-month follow-up echocardiogram demonstrated resolution of the pericardial effusion and constrictive physiology. Effusive-constrictive pericarditis is a rare but important manifestation of pericardial disease in SLE. Treatment of the underlying SLE led to the resolution of the pericardial pathology. LEARNING OBJECTIVE/UNASSIGNED:Systemic lupus erythematosus (SLE) is a heterogeneous illness that causes significant morbidity and mortality across a variety of organ systems. Our aim is to educate clinicians on the spectrum of cardiac manifestations in SLE with a particular focus on pericardial disease. Using our case as a reference, we hope to highlight developments in diagnosis and management of pericardial disease in SLE.