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.

Fluorodeoxyglucose (FDG)-avid pericardial effusion is frequently associated with malignancy, but inflammation and reactive mesothelial proliferation may produce similar imaging and histologic findings, creating diagnostic uncertainty. This overlap may lead to unnecessary invasive procedures if metabolic imaging is overemphasized. A 76-year-old man presented with progressive bilateral lower extremity edema and was found to have a large pericardial effusion. Imaging demonstrated FDG-avid pericardial and pleural thickening with hypermetabolic lymphadenopathy on PET-CT. Serial cytology, bronchoscopic biopsies, and immunohistochemistry did not demonstrate malignancy. Cardiac MRI showed pericardial inflammation without myocardial involvement. The patient was treated with pericardial drainage and corticosteroids, resulting in clinical improvement and resolution of the effusion. This case is unique because FDG-avid pleuropericardial abnormalities, hypermetabolic lymphadenopathy, and reactive mesothelial proliferation closely simulated malignant disease but ultimately represented a non-malignant inflammatory process. FDG uptake in pericardial effusion is not synonymous with malignancy, and PET-CT findings alone are insufficient for diagnosis. Integrating metabolic imaging with pathology and dedicated cardiac imaging can prevent misdiagnosis and avoid unnecessary invasive interventions, particularly in older or frail patients.

Iatrogenic central venous dissection during cardiac pacing procedures is exceptional. We present the case of a 75-year-old woman with a single-chamber pacemaker since 2004, who underwent generator replacement and new ventricular lead implantation in 2025. During the procedure, anomalous resistance to lead advancement was identified. Immediate venography revealed innominate vein dissection with intramural hematoma. The procedure was discontinued, and the patient remained stable. Computed tomography angiography at 24 hours confirmed complete occlusion of the left subclavian and innominate veins due to thrombotic progression. Conservative management with deferred anticoagulation was adopted after confirming clinical stability and absence of pericardial effusion progression. Given that the patient was not pacemaker-dependent (ventricular pacing, 2.6%) and the existing ventricular lead retained adequate electrical parameters, a new generator was connected to the previous lead without adding a new lead, deferring any further transvenous implantation attempt to avoid additional manipulation of the recently injured venous system. The patient evolved favorably, with confirmation of right contralateral access patency as a viable alternative for potential future implantation if clinically required. This case illustrates the importance of early recognition of acute venous injuries and individualization of therapeutic management.

We report a case of an exceedingly rare form of conjoined twinning in a 37-year-old patient who underwent a single euploid embryo transfer for severe male factor infertility. The male partner presented with congenital bilateral absence of the vas deferens, absence of the right seminal vesicle, and right renal agenesis. The sperm used to create the couple's embryos were obtained by TESE and cryopreserved with subsequent thawing. The patient had an unremarkable IVF and medicated frozen embryo transfer cycle. The serum βHCG trend was unremarkable, and pregnancy ultrasound revealed a single fetal pole visualized until 8 weeks of gestation, when two fetal poles were noted. A comprehensive ultrasound evaluation at 9 weeks and 6 days revealed monochorionic, monoamniotic ischiopagus conjoined twins. Twin B demonstrated significant skin edema, a large pericardial effusion, and possible abnormal intracranial anatomy. The couple elected to terminate the pregnancy. Monoamniotic, monochorionic twinning is a rare complication after single embryo transfer, with conjoined twinning exceptionally rare. While several mechanisms underlying monochorionic, monoamniotic twinning after single embryo transfer has been proposed, the development of conjoined twins following embryo transfer is poorly understood. Further investigation is needed to understand the underlying pathophysiologic processes responsible for this phenomenon. These data will aid clinicians in counseling, risk-stratifying, and ultimately, managing rare occurrences of conjoined twinning after SET.