Background and Clinical Significance: Inflammatory myopericardial syndrome is an umbrella term recently introduced by the European Society of Cardiology, which encapsulates the overlap that exists in clinical practice between myocardial and pericardial disease. It has a heterogeneous aetiology and a broad spectrum of severity in terms of its clinical features. Toxoplasma gondii is a rare but recognised infectious cause of myopericarditis and is typically seen in immunocompromised individuals. Case Presentation: We present the case of a young, immunocompetent male, presenting with pleuritic chest pain following a recent flu-like illness. Investigations revealed an acute myocardial injury based on elevated troponin T levels, in the absence of ventricular dysfunction. Toxoplasma immunoserology was consistent with primary toxoplasma infection. The remainder of his viral panel was negative. There was prompt symptom improvement following commencement of treatment with colchicine and a non-steroidal anti-inflammatory agent. Cardiac magnetic resonance imaging post-discharge revealed findings consistent with prior myocarditis. Conclusions: This case is an example of the rare occurrence of toxoplasma myopericarditis in an immunocompetent individual. Cardiac MRI is an invaluable imaging modality used to evaluate myocardial function and tissue characteristics in patients presenting with inflammatory myopericardial syndrome.

Autoimmune myocarditis frequently progresses to inflammatory cardiomyopathy through dysregulated immune-stromal interactions. This study employs single-nuclei RNA-sequencing (snRNA-seq) to profile 46,233 cardiac nuclei from the experimental autoimmune myocarditis (EAM) mouse model at four timepoints: day 0 (healthy), day 14 (inflammation), day 21 (acute inflammation), and day 40 (late cardiac remodelling). Single-nuclei RNA profiling identified 18 transcriptionally distinct cell populations. Global cell-cell communication analysis revealed a dramatic peak of intercellular signalling at day 14 (5907 interactions), with fibroblast subpopulations and macrophages as dominant hubs, followed by partial resolution at day 21 (2264 interactions) and renewed remodelling at day 40 (4862 interactions). Subclustering of the macrophage compartment identified five subpopulations: Mac-TLF, Mac-MHCII, Mac-rMHCII, Mac-ResL, and Classical Monocytes. Tissue-resident macrophages (Mac-TLF, CCR2-) dominated at healthy state (~55%) but were rapidly depleted at day 14, coinciding with a dramatic influx of recruited CCR2[+] macrophages (Mac-rMHCII), which expanded to over 70% of the compartment and maintained dominance through day 40. At inflammation (day 14), the expanded Mac-rMHCII subpopulation displayed a strongly pro-inflammatory signature (Il1b, Stat2, Parp14, Apoe), and the overall macrophage compartment was enriched for cytokine response, Fc-gamma receptor, and Notch signalling pathways, while downregulating homeostatic and mitochondrial metabolic programmes, potentially contributing to impaired efferocytosis and cardiomyocyte dysfunction. Macrophage-centred communication networks expanded markedly at day 14 (1047 interactions), with resting fibroblasts (FB-R) as the primary signalling partner, driving pro-inflammatory stromal activation marked by upregulation of Ccl2, Ccl7, and Csf2. Intra-macrophage subcluster communication also intensified at this timepoint (447 interactions). These findings delineate the temporal and functional heterogeneity of cardiac macrophages during EAM progression and identify key immune-stromal interactions driving pathological cardiac remodelling. The coexistence of pro-inflammatory and transitional reparative macrophage subsets highlights the limitations of broad immunosuppression and supports precision strategies targeting CCR2-mediated recruitment, the SPP1 signalling axis, and macrophage-fibroblast crosstalk as therapeutic avenues in myocarditis and its progression.

Acute myocarditis (AM) shows sex-specific differences in prevalence, clinical phenotype, and outcomes. This review summarizes evidence from studies published between 2000 and 2026 reporting sex-stratified data on AM epidemiology, presentation, and prognosis to guide future research and a more personalized management.

Post-mortem computed tomography (PMCT) is increasingly used in forensic investigations as a non-invasive screening tool; however, its ability to assess the vascular system remains limited. Multiphase post-mortem computed tomography angiography (MPMCTA) was developed to overcome these limitations, but its contribution to routine medico-legal investigations requires further evaluation. This monocentric observational study included 37 non-hospitalized individuals who died suddenly and underwent non-contrast PMCT, MPMCTA, and subsequent blinded medico-legal autopsy with histological and toxicological examinations at the Legal Medicine Institute of the University of Modena and Reggio Emilia. Imaging findings were correlated with autopsy and histological results. MPMCTA showed a high degree of concordance with autopsy for major vascular lesions, enabling accurate pre-autopsy visualization and localization of coronary thrombosis, aortic rupture/dissection, pulmonary arterial filling defects, and neoplastic vascular involvement. By contrast, several pathological conditions, including myocardiosclerosis, myocarditis, pneumonia, and some cases of acute or previous myocardial infarction, could only be definitively diagnosed through histological examination. These findings support the role of MPMCTA as a valuable adjunct to conventional autopsy in cases of sudden natural death. By improving the pre-autopsy assessment of vascular pathology, MPMCTA may facilitate lesion localization and support a more targeted post-mortem investigation.

McConnell's sign is a classic echocardiographic finding most often encountered in the context of acute pulmonary embolism and is defined by severe hypokinesis or akinesis of the right ventricular free wall and hypercontractility of the apex. Despite having a high specificity for pulmonary embolism, other causes of McConnell's sign have been reported. This case is a rare presentation of McConnell's sign in association with myopericarditis. The patient presented with a systemic lupus erythematosus flare as well as acute pleuritic chest pain and was found to have significantly elevated high-sensitivity troponin, pericardial effusion, and McConnell's sign on echocardiography. Pulmonary embolism and underlying pulmonary hypertension were ruled out. The patient improved clinically with treatment of a systemic lupus erythematosus flare, and short-term follow-up echocardiography demonstrated resolution of right ventricular dysfunction. This case challenges the conventional diagnostic specificity attributed to McConnell's sign for pulmonary embolism by describing a similar pattern of regional right ventricular wall motion abnormalities in the setting of an inflammatory myopericardial syndrome. Additionally, it underscores the utility of speckle-tracking strain analysis to help differentiate potential etiologies in right ventricular dysfunction. This case demonstrates the importance of having a broad differential when encountering McConnell's sign and represents an underappreciated cause of McConnell's sign associated with myopericarditis.

Autoimmune pericarditis is commonly idiopathic but may represent the initial manifestation of systemic autoimmune disease. Hepatic autoimmune disorders rarely present with primary cardiac involvement, and recognition of extrahepatic presentations is essential for early diagnosis and prevention of organ damage. Autoimmune hepatitis-primary biliary cholangitis (AIH-PBC) overlap syndrome is an uncommon entity characterized by combined hepatocellular and cholestatic immune-mediated injury. A previously healthy young woman presented with progressive pleuritic chest pain and dyspnea and was found to have a large pericardial effusion causing hemodynamic compromise requiring surgical drainage. Pericardial pathology demonstrated acute and chronic fibrinous pericarditis. Initial evaluation revealed elevated inflammatory markers and mild transaminitis with positive autoimmune serologies including antinuclear antibody and anti-smooth muscle antibody. Following clinical improvement, she developed recurrent pericarditis accompanied by worsening liver enzyme abnormalities. Liver biopsy demonstrated chronic active hepatitis with bile duct injury and bridging fibrosis, consistent with autoimmune hepatitis-primary biliary cholangitis overlap syndrome. Cardiac magnetic resonance imaging confirmed active pericardial inflammation without myocarditis. Immunosuppressive therapy with corticosteroids followed by azathioprine resulted in clinical stabilization. This case highlights autoimmune pericarditis as the presenting manifestation of AIH-PBC overlap syndrome and underscores the importance of evaluating unexplained pericarditis for systemic autoimmune disease. Early recognition of cardio-hepatic autoimmune overlap allows timely immunosuppressive therapy and may prevent progression to advanced hepatic fibrosis.

The present study aimed to investigate the therapeutic efficacy and underlying mechanism of olive oil-based lipid emulsions (OOLE) in mitigating immune checkpoint inhibitor (ICI)-induced myocarditis triggered by ipilimumab (IPI) and nivolumab (NIVO). An in vitro model of inflammatory cardiomyocytes was established by co-culturing HL-1 cells with CD4[+]/CD8[+] T cells isolated from ICI-treated mice. Cells were treated with 10% OOLE, followed by flow cytometry for apoptosis, ELISA for cytokine profiling (TNF-α, IL-1β, IL-6), and Western blot/qPCR for pathway analysis (NF-κB, NLRP3, IL-1β). In vivo, myocarditis was induced in mice via IPI/NIVO administration. Cardiac function was assessed using echocardiography, and inflammatory markers were evaluated in serum and myocardial tissue. The results showed that OOLE significantly reduced T cell-induced apoptosis and suppressed inflammatory cytokine production in HL-1 cells, while the expression of NF-κB, NLRP3, and IL-1β was downregulated. In vivo., OOLE improved left ventricular functional parameters and attenuated systemic inflammation. Molecular analyses confirmed that these protective effects were mediated via the inhibition of the NF-κB/NLRP3/IL-1β signaling axis. In conclusion, OOLE mitigates acute ICI-induced myocarditis by targeting the NF-κB/NLRP3/IL-1β pathway, demonstrating its potential in suppressing early inflammatory cascades and providing rapid cardioprotection. These findings highlight its promise as an adjunctive therapy for immune-related cardiac injury.

This manuscript describes a rare case of undifferentiated connective tissue disease (UCTD)-associated fulminant myocarditis presenting with isolated diplopia as the sole initial manifestation. A 66-year-old Chinese woman presented with a 17-day history of isolated diplopia. Initial evaluation revealed markedly elevated cardiac enzyme profile and electrocardiographic changes suggestive of acute myocardial infarction. However, coronary angiography revealed no coronary stenosis. Cardiac magnetic resonance imaging (MRI) was consistent with myocarditis. The initial diagnoses included Miller-Fisher syndrome and inflammatory cardiomyopathy. The patient underwent plasma exchange, intravenous methylprednisolone (20 mg daily), and intravenous immunoglobulin (IVIg). Her condition improved. After discharge, oral prednisone was initiated at 20 mg daily, with a weekly taper of 5 mg. However, 12 days after discharge, she was readmitted with abdominal distension. At that time, she also presented with hypotension and ophthalmoplegia. Brain MRI revealed abnormal signals in the medial and lateral rectus muscles bilaterally. Echocardiography revealed a reduced left ventricular ejection fraction (LVEF) of 38%. Endomyocardial biopsy confirmed lymphocytic myocarditis, and serology was positive for anti-SSA/Ro52 antibodies and borderline positive for anti-PL-7 antibody, leading to a diagnosis of UCTD-associated fulminant myocarditis. Treatment with methylprednisolone (60 mg daily) and IVIg resulted in clinical recovery. At three-year follow-up, the patient remained in remission, with complete resolution of diplopia, normalization of cardiac enzyme profile, and no progression to any definite connective tissue disease. This case suggests that isolated diplopia as the sole initial manifestation of UCTD-associated fulminant myocarditis is exceedingly rare. For autoimmune myocarditis, endomyocardial biopsy is crucial to guide treatment. Premature tapering of low-dose corticosteroids led to rapid relapse, highlighting the importance of starting with an adequate dose, tapering slowly, and maintaining the minimal effective dose.

Cardiac magnetic resonance (CMR) is a key modality for diagnosing and monitoring myocarditis, including cases related to COVID-19 infection and Multisystem Inflammatory Syndrome in Children (MIS-C). While acute findings are often favorable, the persistence of abnormalities over time remains uncertain. This retrospective study included 21 pediatric patients with suspected COVID-19-related myocarditis between March 2020 and July 2023. All underwent CMR as part of clinical evaluation. Imaging findings were analyzed at early (< 30 days), mid (30-364 days), and long-term (≥ 365 days) intervals. Myocarditis was defined using the 2009 Lake Louise criteria. Of the 21 patients (mean age 13.1 years, 57% male), 8 had follow-up CMRs (median time to follow-up 347 days). Etiologies included MIS-C (57%), confirmed COVID-19 (19%), and suspected COVID-19 (24%). A total of 30 CMR studies were analyzed. Initial CMR met 2009 Lake Louise criteria in 8 patients (38%). Across temporally categorized studies, LGE declined from 46% of early studies to 25% of mid-term studies and was absent on long-term studies; pericardial effusions similarly declined from 46% to 25% to 0%. EGE remained frequent across timepoints (77%, 83%, and 80%, respectively). Among patients with serial CMR, no patient had edema on follow-up, LGE persisted in 1 of 8 (13%), pericardial effusion in 1 of 8 (13%), and only 1 of 8 (13%) continued to meet Lake Louise criteria. Biventricular systolic function remained normal on follow-up imaging. Initial LGE demonstrated marked lateral wall predominance (Cochran's Q = 13.38, p = 0.004). Median clinical follow-up was 20 months (IQR 11-38), with no documented arrhythmias, heart failure symptoms, cardiac-related rehospitalizations, or mortality. In pediatric myocarditis associated with COVID-19, most CMR abnormalities improve over time, with resolution of edema and substantial reduction in LGE and pericardial effusion. Persistent EGE remains common, although its clinical significance is uncertain. Medium-term clinical outcomes were favorable. Larger prospective studies are needed to define the long-term significance of persistent imaging abnormalities.