Myocarditis is a heterogeneous inflammatory syndrome with aetiologies ranging from viral infection and drug hypersensitivity to systemic autoimmune/autoinflammatory disease and immune checkpoint inhibitor (ICI) therapy. In response to these triggers, the innate immune response and inflammasome activation can amplify myocardial injury via IL-1, providing a mechanistic rationale for IL-1 pathway inhibition as a targeted therapeutic strategy. This review synthesizes preclinical and clinical evidence for IL-1 blockade in myocarditis and related inflammatory cardiac syndromes.

Pericardial effusions can progress to cardiac tamponade, a life-threatening condition that requires immediate management. Although the first-line treatment for cardiac tamponade is pericardiocentesis, a surgical approach becomes necessary to create a pericardial window in cases of failure to drain, recurrence, or loculated effusions or in unsafe percutaneous procedures. We present two cases of hemodynamically significant pericardial effusions treated with different techniques to emphasize the determinants in choosing the most appropriate surgical approach. The first case is a 46-year-old male patient with pneumonia and a progressively increasing pericardial effusion with early signs of tamponade who underwent a left anterior mini-thoracotomy for the creation of a pericardial window. The second case is a 50-year-old male patient with a past medical history of bilateral lung transplantation who developed a loculated pericardial effusion and signs of tamponade. Because of previous thoracic surgery and an unsafe percutaneous access, a subxiphoid window with xiphoidectomy and a small wedge sternotomy was performed. The patients in both cases showed resolution of tamponade physiology and symptomatic relief after surgical drainage. Pathologic evaluation in both patients revealed fibrous pericarditis, with no evidence of malignancy or infection. These two cases showcase that the choice of surgical method for pericardial window depends on patient-specific factors, which include previous thoracic surgery, percutaneous accessibility, and the nature of pericardial effusion. Thus, careful operative planning is key to optimize outcomes and minimize procedural risks.

We report an autopsy case of a man in his early 80s who was found deceased, submerged in a bathtub at home. He had no history of regular medical care or smoking. One month before death, he experienced vomiting, malaise, and reduced appetite; however, due to limited clinical information, it was unclear whether he exhibited symptoms suggestive of cerebellar dysfunction. The autopsy showed fibrinous pericarditis resulted from left atrial metastasis from lung squamous cell carcinoma (LSCC) originating in the left lower lobe, which was determined to be the cause of death. Neuropathological examination exhibited no gross abnormalities in the cerebrum or brainstem; however, mild atrophy of the cerebellar vermis, extending from the lobulus centralis to the culmen, was observed. Histologically, focal loss of Purkinje cells accompanied by gliosis was noted, predominantly affecting the superficial layers of the superior vermis and simple lobule, while other cerebellar regions were largely preserved. Mild-to-moderate CD8-positive T-lymphocyte-predominant perivascular infiltration was present in the cerebellar white matter and leptomeninges, whereas no significant inflammation was detected in the cerebrum or brainstem. No abnormal protein aggregates (phosphorylated tau, α-synuclein, polyglutamine, or p62) were identified in the cerebellum. Postmortem serum testing revealed the presence of anti-amphiphysin antibodies. Collectively, although the clinical manifestations were unclear and a definitive diagnosis remains difficult, these findings support a pathological diagnosis of paraneoplastic cerebellar degeneration (PCD) associated with previously undiagnosed LSCC. Although autopsy data are limited, the preferential involvement of the superficial superior vermis may represent an early-stage pattern of PCD. This case highlights the importance of autopsy with detailed neuropathological examination in patients with malignancy, even when cerebellar symptoms are mild or absent and imaging or gross abnormalities are lacking. To our knowledge, this is the first reported autopsy case of anti-amphiphysin antibody-associated PCD in association with LSCC.

Pericarditis is the most frequent pericardial syndrome and a common cause of chest pain in emergency and cardiology practice. During the past two decades, management has moved from largely empirical anti-inflammatory treatment towards a mechanism-based, risk-stratified, and imaging-supported approach. Diagnosis remains clinical, based on typical chest pain, pericardial rub, electrocardiographic changes and pericardial effusion, but inflammatory biomarkers and multimodality imaging, especially cardiac magnetic resonance, increasingly support diagnostic confidence, differential diagnosis, and therapeutic decisions. For most patients with acute idiopathic or presumed viral pericarditis, aspirin or a non-steroidal anti-inflammatory drug combined with colchicine is first-line therapy, with exercise restriction and follow-up guided by symptoms and C-reactive protein. Corticosteroids should be avoided when possible or used at low-to-moderate doses only for selected indications, because they promote chronicity and recurrence in unselected cases. The major recent advance is the recognition of recurrent pericarditis as an autoinflammatory, interleukin (IL)-1-mediated disease in a substantial proportion of patients with an inflammatory phenotype. Randomized and registry data now support IL-1 inhibition (eg, anakinra or rilonacept) for corticosteroid-dependent and colchicine-resistant recurrent pericarditis, allowing rapid symptom control, withdrawal of corticosteroids, and marked reduction in recurrences. Remaining challenges include optimal treatment duration, cost and access to biologics, management of patients without overt systemic inflammation, and personalized strategies for tapering and return to activity.

Postcardiac injury syndrome (PCIS) is an uncommon inflammatory complication after catheter ablation for atrial fibrillation (AF). While pericarditis is well described following thermal ablation, reports after pulsed-field ablation (PFA) remain rare.