Pericarditis is the most common cardiovascular manifestation of systemic lupus erythematosus and affects a substantial proportion of patients during the course of the disease. Although it is often mild and self-limiting, lupus-associated pericarditis can result in substantial morbidity due to recurrent episodes and potentially life-threatening complications, including cardiac tamponade and constrictive pericarditis. Recent advances have expanded our understanding of its immunopathogenesis, highlighting the interplay between immune complex deposition, complement activation, type I interferon signaling, and dysregulated cell death pathways. Diagnostic evaluation relies on clinical assessment supported by electrocardiography and transthoracic echocardiography, while cardiac MRI has emerged as a valuable modality for detecting active inflammation, characterizing pericardial tissue involvement, and identifying constrictive physiology. In contrast to idiopathic pericarditis, management strategies should address both pericardial inflammation and the underlying autoimmune disease activity. Colchicine has become a cornerstone of therapy owing to its effectiveness in symptom control and recurrence prevention, whereas glucocorticoids and immunosuppressive agents remain essential for selected patients with active systemic disease. Emerging targeted therapies, including anifrolumab, belimumab, and IL-1 inhibitors, offer promising alternatives for refractory or recurrent cases, although disease-specific evidence remains limited. This review provides a comprehensive overview of the current understanding of lupus-associated pericarditis, encompassing its pathophysiology, clinical manifestations, diagnostic approach, and therapeutic management, while highlighting recent advances and key areas for future research.

Congenital complete atrioventricular block (CCAVB) is a well-recognized manifestation of neonatal lupus erythematosus (NLE), caused by transplacental transfer of maternal anti-Ro/Sjögren's Syndrome Type A (SSA) and anti-La/Sjögren's Syndrome Type B (SSB) antibodies. Although non-cardiac manifestations of NLE typically resolve within the first year of life, the long-term autoimmune risk in affected offspring remains unclear. We report a 24-year-old woman with CCAVB secondary to maternal Sjögren's disease who presented with acute heart failure, nephrotic-range proteinuria, bicytopenia, pericardial effusion, and findings concerning for Libman-Sacks endocarditis. Despite negative conventional lupus serologies, renal biopsy demonstrated Class IV/V lupus-like immune-complex glomerulonephritis with full-house immune complex deposition, leading the multidisciplinary team to favor seronegative lupus nephritis. This case demonstrates the diagnostic limitations of serology-based approaches in atypical lupus presentations and underscores the critical role of tissue biopsy. The case also raises questions regarding long-term autoimmune risk after autoimmune congenital heart block, an area for which prospective data and evidence-based surveillance strategies remain limited.

We report the case of a 70-year-old female with a history of hypothyroidism who presented following an unwitnessed fall with bradycardia and hypothermia. She was found to have myxedema coma complicated by signs of early cardiac tamponade, requiring urgent pericardiocentesis. Myxedema coma is a rare but life-threatening manifestation of severe decompensated hypothyroidism, carrying a high mortality rate despite treatment. It commonly presents with hypothermia and altered mental status and may be precipitated by infection, trauma, medication nonadherence, or cold exposure. Early recognition and prompt treatment with intravenous stress-dose steroids and thyroid hormone replacement are essential to improve outcomes. This case highlights the potentially severe complications of inadequately treated hypothyroidism. It emphasizes the importance of considering cardiac tamponade as a rare but life-threatening consequence of this disease, requiring a high index of suspicion, timely diagnosis, and urgent intervention.

A right ventricular pseudoaneurysm is a rare and serious complication secondary to central venous catheterisation and can present as subtle nonspecific cardiopulmonary symptoms. This case reports an 88-year-old woman on chronic haemodialysis via a right internal jugular tunnelled catheter which was described as a technically difficult insertion. Although initially asymptomatic, three months later, the patient developed orthopnoea and progressive dyspnoea with an incidental new onset of atrial fibrillation. Transthoracic echocardiography and computed tomography demonstrated a right ventricular pseudoaneurysm with an associated pericardial effusion and pulmonary emboli. At the time of admission, whilst the patient's diagnosis was being established, she became haemodynamically unstable. Surgical management and haemodialysis then became unfeasible, which led to the patient's demise during hospitalisation. This case highlights the importance of early imaging and a high clinical suspicion, given the high mortality rates associated with a right ventricular pseudoaneurysm.

Carcinoid heart disease (CHD) is a serious cardiac manifestation of carcinoid syndrome (CS), characterized by progressive fibrotic degeneration of cardiac valves and right-sided heart failure. We report the case of a 72-year-old man with a history of metastatic small-intestinal neuroendocrine tumor and CS diagnosed four years earlier, who presented with worsening dyspnea and peripheral edema. Transthoracic echocardiography revealed characteristic findings of advanced CHD, including severely thickened, retracted, and immobile tricuspid and pulmonary valve leaflets, resulting in severe tricuspid and pulmonary regurgitation. Additional findings included right ventricular dilatation, severe biatrial enlargement, moderate mitral regurgitation, a small pericardial effusion, and a 7-cm ascending aortic aneurysm. The diagnosis was established based on the characteristic echocardiographic appearance and elevated N-terminal pro-B-type natriuretic peptide levels. Notably, no routine cardiological surveillance had been performed following the diagnosis of CS. The patient was managed conservatively with intravenous diuretic therapy and optimization of heart failure treatment. Following multidisciplinary evaluation, surgical intervention was not pursued because of the patient's advanced disease stage, clinical instability, and concomitant ascending aortic aneurysm, which collectively rendered him a prohibitive surgical candidate. His clinical course was subsequently complicated by acute kidney injury with progressive renal dysfunction and anuria, and he ultimately died during hospitalization. This case highlights the importance of regular cardiovascular follow-up in patients with CS, as delayed recognition of cardiac involvement may lead to advanced and potentially irreversible valvular disease. Early detection remains crucial for timely intervention and may improve clinical outcomes.

We report a 31-year-old woman with cirrhosis who developed bilateral pleural and pericardial effusions caused by Curvularia hawaiiensis. The patient developed worsening shock and multiorgan failure during hospitalization despite broad-spectrum antibacterial and antifungal therapy. Her course was complicated further by development of bilateral pleural effusions and pericardial effusion. Pericardiocentesis and thoracentesis were performed, with cultures initially demonstrating scant mold growth. Liposomal amphotericin B was subsequently initiated; however, the patient ultimately died following transition to comfort-focused care. Postmortem identification of both pleural and pericardial isolates revealed Curvularia hawaiiensis, a rare dematiaceous mold infrequently associated with invasive disease. This case highlights the profound immune dysfunction associated with acute-on-chronic liver failure and demonstrates the potential for rare molds to cause rapidly progressive invasive infection in cirrhotic patients. Additionally, it underscores the diagnostic and therapeutic challenges posed by delayed organism identification and limited susceptibility data for uncommon fungal pathogens. This is the first reported pericardial infection due to this human pathogen.

Primary purulent pericarditis due to Streptococcus pyogenes is exceedingly rare in adults, with fewer than 10 cases reported in the literature to date. Most reported cases have occurred in the setting of an immunocompromised state, thoracic procedures, or identifiable infectious foci.

Melioidosis is a serious infectious disease caused by Burkholderia pseudomallei, a bacterium endemic to tropical regions, including Taiwan. The disease can involve multiple organs; however, cardiac involvement, particularly cardiac tamponade, is rare. To date, only four cases of melioidosis presenting with cardiac tamponade have been reported in the literature. Here, we report an extremely rare case of melioidosis complicated by pericardial effusion and cardiac tamponade, which was successfully treated with pericardiocentesis and appropriate antimicrobial therapy.

ObjectivesTo determine the prevalence of increased serum high-sensitivity cardiac troponin I (hs-cTnI) concentrations in cats with acute blunt trauma and assess associations with trauma severity, clinicopathological variables, echocardiographic findings, and short-term outcome.MethodsThirty-nine cats presenting within 48 hours of blunt trauma were prospectively enrolled. All cats underwent physical examination, Animal Trauma Triage scoring, thoracic radiography, electrocardiography, echocardiography, complete blood count, serum biochemistry, NTproBNP testing, and hs-cTnI measurement. Associations between hs-cTnI concentrations and clinical, laboratory, echocardiographic, and outcome variables were assessed. Receiver operating characteristic (ROC) analysis was performed as an exploratory assessment of prognostic performance.ResultsIncreased hs-cTnI concentrations were detected in 34/39 cats (87%; 95% CI 72-96%). A significant ordinal association was identified between trauma severity and hs-cTnI class (linear-by-linear association, p=0.036), although the overall Fisher-Freeman-Halton test was not significant (p=0.088). Hs-cTnI concentrations correlated positively with urea, creatinine, neutrophil count, ALT, NLR, blood glucose, IVSd, and LVPWd, and negatively with LVIDd. Increased left ventricular wall thickness was identified in 10/39 cats and was associated with higher hs-cTnI concentrations (p=0.033). No traumatic cardiac rupture, pericardial effusion, or pleural effusion were observed. Electrocardiographic abnormalities were detected in 6/39 cats and were not associated with hs-cTnI concentrations. Seven cats (18%) died during hospitalization. Increased urea concentration , white blood cell count, and neutrophil count were associated with non-survival. ROC analyses were considered exploratory because of the limited number of outcome events.Conclusions and relevanceIncreased hs-cTnI concentrations were common in cats with acute blunt trauma and were associated with leukocyte variables, renal function markers, and subtle echocardiographic abnormalities. These findings suggest that hs-cTnI may reflect a multifactorial biological response involving myocardial stress or injury, systemic disease severity, altered renal handling, and possible underlying subclinical cardiac disease. Further studies are needed to clarify the relative contribution and clinical significance of these mechanisms.