A 52-year-old gentleman presenting with tachycardia was found to have a large pericardial effusion and cardiac tamponade. This case was on a background of long-standing myelofibrosis managed with ruxolitinib, which was recently withheld for an orthopaedic procedure. He was diagnosed with presumed ruxolitinib discontinuation syndrome (RDS), resulting in a large pericardial effusion due to an increased inflammatory response. He was managed with a pericardial window and prompt recommencement of ruxolitinib and steroids. This case highlights the importance and increasing prevalence of RDS with the serious consequence of cardiac tamponade. Symptoms of RDS should be recognised and managed with recommencement of a JAK inhibitor and steroids.

Fluid retention due to tyrosine kinase inhibitor administration might lead to pericardial effusion and right heart failure. Here, we present the case of a 63-year-old man with subacute cardiac tamponade complicated with heart failure, acute kidney injury, and generalized edema due to the bosutinib treatment.

Introduction Transcatheter mitral valve repair (TMVR) creates an iatrogenic atrial septal defect (iASD) that may persist and affect hemodynamics. Although the MITHRAS (Closure of Iatrogenic Atrial Septal Defects Following Transcatheter Mitral Valve Repair) trial showed no benefit of routine closure, its small size and selective population limit generalizability, and observational data remain conflicting. We hypothesized that percutaneous iASD closure (PC-iASD) would be associated with differences in in-hospital clinical and hemodynamic outcomes compared with no closure. Methods Using the National Inpatient Sample (NIS), we evaluated national prevalence, baseline characteristics, and in-hospital outcomes of PC-iASD among patients undergoing TMVR from 2020 to 2022. Results We identified 4,965 weighted TMVR hospitalizations; 431 (8.7%) underwent PC‑iASD closure during the same admission. Compared with TMVR only, the closure cohort had a higher prevalence of pulmonary hypertension (245 (56.9%) vs. 1735 (40.5%), p = 0.0034) and heart failure (411 (95.4%) vs. 3767 (87.9%), p = 0.0396). There were no significant differences in chronic obstructive pulmonary disease, coronary artery disease, end-stage renal disease, or tricuspid regurgitation between the two groups. After multivariate adjustment, there was no difference in in‑hospital mortality, cardiogenic shock, acute heart failure, acute right heart failure, cardiac tamponade, or need for mechanical circulatory support among the two cohorts. Conclusion There have been conflicting results over numerous retrospective and prospective studies regarding the outcomes of post-TMVR iASD closure. Potential benefits of right-sided volume overload may be offset by higher left-atrial pressures after closure. The wide confidence (albeit nonsignificant) toward the development of acute right heart failure, pericardial effusion, and cardiac tamponade raises the possibility of better patient selection or some iASD closure procedural modifications that can help improve outcomes.

Canine babesiosis is an important and potentially life-threatening disease of worldwide significance. European babesiosis encompasses all protozoan parasites of the genus Babesia that have been reported to cause canine disease in Europe. Despite its importance, cardiac pathology associated with European babesiosis remains poorly characterized. The aim of this study was to assess cardiac lesions in dogs that succumbed to European babesiosis. For this study, the archive of the Department of Veterinary Pathology, Faculty of Veterinary Medicine Zagreb, was retrospectively searched for necropsied dogs which died as a consequence of naturally acquired European babesiosis. Babesiosis was diagnosed by detection of trophozoites within erythrocytes, but not lymphocytes, in cytological and/or histological slides. Necropsy reports, photographs of cardiac gross lesions, and histologic slides of the heart were reviewed, and all changes were noted. The most common gross pathologies were hemorrhage and pericardial effusion, while intravascular monocytic leukostasis, hemorrhage, endomysial edema, myocardial necrosis, congestion, and myocarditis were the most frequent histologic findings. Based on results of the current study, cardiac lesions in clinical cases of complicated European babesiosis should be expected and patients should be evaluated for such damage.

Background/Objectives: Pericardial effusion (PEf) is a frequent finding after cardiac surgery. Progression to cardiac tamponade (CT) is a rare but life-threatening complication. Current evidence remains limited due to insufficient data on prevalence, progression predictors and management strategies. Methods: We retrospectively analyzed anamnestic, clinical, laboratory, echocardiographic and therapeutic data from 2662 patients (74 ± 11 years) admitted to the Cardiac Rehabilitation ward between 2022 and 2024. Results: Among 2152 (81%) cardiac surgery patients, 382 (18%) developed PEf: 58% mild, 38% moderate, and 4% severe. Patients developing PEf tended to be younger and more frequently male. In addition, PEf development was seen more commonly after aortic and combined surgeries. All patients with severe PEf or CT had undergone surgery via sternotomy, whereas minithoracotomy was inversely associated with PEf severity. Postoperative complications occurred in 92% of PEf patients, mainly due to arrhythmia, hemodynamic deterioration, or heart failure. Overall outcome was favourable in 98% of patients. CT occurred in eight patients (2%). Anticoagulation therapy was more frequent among patients who developed PEf or CT. Preventive colchicine was prescribed in only 16% of cases. No PEf-specific therapy was administered in 56% of PEf patients, while corticosteroids and nonsteroidal anti-inflammatory drugs were used in 28% and 8% of cases, respectively, without surgical wound complications. No PEf recurrences were observed during follow up (517 ± 424 days). Conclusions: PEf is a common complication after cardiac surgery, more frequently in young males, usually of mild or moderate severity. The majority of these cases resolve using either a conservative or pharmacological approach, predominantly via corticosteroids. Patients undergoing aortic surgery, experiencing postoperative complications (especially arrhythmias), and receiving anticoagulation therapy were associated with severe PEf or CT. Despite guideline recommendations, colchicine remains markedly underutilized.

Primary cardiac tumors are extremely rare in fetal life, with rhabdomyomas being the most frequently encountered. In contrast, fetal cardiac myxomas are exceptionally uncommon, and reports of diagnosis during the first trimester are exceedingly rare. We report a fetal right atrial myxoma diagnosed at 12 weeks' gestation. Fetal echocardiography revealed a hyperechoic, pedunculated mass originating from the right atrial wall. Serial follow-up demonstrated rapid tumor growth, with increasing pericardial effusion and reversed A-wave flow in the ductus venosus by 14 weeks' gestation, indicating early and severe hemodynamic compromise. After detailed parental counseling regarding the poor prognosis, the pregnancy was electively terminated. Postmortem examination revealed a gelatinous intracardiac mass, and histopathological analysis confirmed the diagnosis of cardiac myxoma, showing stellate cells embedded in a myxoid stroma. To our knowledge, this represents the earliest gestational age at which a fetal cardiac myxoma has been diagnosed and histopathologically confirmed. This case highlights that fetal cardiac myxomas, although histologically benign, may demonstrate rapid progression and lead to significant hemodynamic deterioration even in the first trimester, underscoring the importance of early fetal echocardiographic evaluation and timely parental counseling.

Cholesterol pericardial effusion is a rare diagnosis and typically not associated with the development of pericardial constriction. However, covariate factors, such as Rheumatoid arthritis, myxoedema, and comorbid disease requiring anticoagulation, can predispose to developing dense adhesions that ultimately can cause pericardial constriction and constrictive physiology. This can develop without preceding symptoms but ultimately may declare itself with a variety of clinical presentations including syncope.

Atrial fibrillation (AF) affects approximately 3%-5% of adults and is projected to double in prevalence by 2060, significantly increasing the burden of thromboembolic stroke. This risk is largely attributed to thrombus formation within the left atrial appendage (LAA), particularly in nonvalvular AF, where the LAA's trabeculated anatomy, diverse morphologies (e.g., chicken wing, windsock, cactus, cauliflower), and impaired contractility allows for blood stasis and thrombogenesis. As a result, the LAA has become a focus for stroke prevention strategies. This review demonstrates current evidence on LAA closure by discussing patient selection, anatomical feasibility, procedural workflow, imaging guidance (transesophageal echocardiography vs. intracardiac echocardiography), device platforms (Amplatzer Amulet, Watchman 2.5, Watchman FLX/FLX Pro), and complication profiles. P procedural success rates exceed 95%, with improving safety profiles. Nonetheless, adverse events such as pericardial effusion, device-related thrombus (DRT), peri-device leak (PDL), device embolization, and periprocedural stroke remain important considerations. Post-implant antithrombotic strategies are evolving beyond the traditional warfarin/aspirin → DAPT → SAPT pathway toward more individualized regimens, including simplified DOAC or antiplatelet-based approaches tailored to bleeding and thrombotic risk especially in complex scenarios like concurrent coronary stenting. Ongoing device innovations (e.g., FLX Pro, expanded size matrices, thromboresistant coatings), CT-led surveillance algorithms, and randomized studies of post-implant pharmacotherapy aim to reduce DRT/bleeding, harmonize follow-up, and expand indications. Collectively, these advances refine patient-centered LAA closure by aligning anatomic complexity, procedural technique, and pharmacology to improve stroke prevention and safety in AF.