Despite increasing global attention, significant knowledge gaps remain regarding the incidence of adverse outcomes associated with mpox. To support the development of World Health Organization (WHO) mpox guidelines, this systematic review and meta-analysis evaluated the incidence of complications among patients with mpox.

Myocarditis is a condition characterized by heterogeneous etiologies, clinical manifestations, and natural history. Its diagnosis remains challenging and requires a multidisciplinary approach that integrates clinical evaluation, biomarkers, electrocardiography, echocardiography, and advanced imaging modalities. Cardiac magnetic resonance has emerged as the non-invasive gold-standard test, that together with endomyocardial biopsy, constitutes the foundation of the current diagnostic classification. Myocarditis is also a frequent acquired cause of sudden cardiac death in young individuals, including athletes. In this setting, the evaluation of return-to-play eligibility in athletes after acute myocarditis is complex and often limited by scarce evidence-based data. Accurate risk stratification, guided by a comprehensive multiparametric evaluation and a shared decision-making process that considers the potential risks of resuming competitive sport, is fundamental to ensuring athlete safety. This review aims to discuss the management of athletes with myocarditis and to address the challenges associated with return-to-play decisions.

Cardiac magnetic resonance imaging (MRI) is a gold standard to assess functional and anatomical properties of the living heart. Inflammation changes the myocardial tissue and, furthermore, MR relaxation properties. Continuous-wave (CW) longitudinal rotating frame relaxation time (T1ρ) mapping has been used to assess myocardial fibrosis and inflammation. Conventional T2 relaxation time is a known marker of edema in the myocardium. In this study, we assessed myocardial inflammation after viral infection in a mouse heart using CW-T1ρ and T2 relaxation times. Adenoviral human vascular endothelial growth factor-A165 (AdVEGF-A165) and empty control adenoviral vector with cytomegalovirus promoter (AdCMV) gene transfers were used to induce inflammation in the mouse myocardium. In vivo CW-T1ρ and T2 relaxation time measurements were performed in both groups (AdVEGF-A165 and AdCMV) after -1-, 1-, 3-, 7-, 14-, 21-, and 28-day post-injection. The inflammation associated with gene transfer was verified by hematoxylin and eosin staining after 14-day post-injection. One day after AdVEGF-A165 and AdCMV injections and inflammatory reactions, CW-T1ρ showed a significant increase, which stayed increased as a function of time. T2 also increased significantly after both injections and inflammatory reactions as compared to before injections. Contrast difference between inflammation and remote areas was visually observed in both groups in CW-T1ρ and T2 maps. Hematoxylin and eosin staining revealed the area of inflammation after Ad injection in both groups after 14-day post-injection. This study showed that both acute and chronic phases of the inflammatory reaction in mouse myocardium caused by myocardial adenoviral injections were associated with increased CW-T1ρ and T2 relaxation time constants. Furthermore, the inflammatory reaction can be followed up with rotating frame and conventional relaxation time mappings.

Recent research has indicated that cardiac lymphatic vessels (CLVs) serve as a direct drainage route into the mediastinal lymph nodes for inflammation resolution. However, the role of CLVs in coxsackievirus B3-induced acute viral myocarditis (AVMC) remains unknown. In this study, we found that AVMC in mice promoted pathological cardiac lymphangiogenesis while impairing CLV-mediated drainage, leading to heart inflammation and dysfunction. Overexpression of apelin in cardiomyocytes improved CLV integrity and promoted effective lymph drainage to decrease inflammatory responses and enhance cardiac function. In vitro studies revealed that apelin stabilizes lymphatic endothelial cadherin and zonula occludens 1 to enhance lymphatic function via the AKT signaling pathway. Moreover, pre-existing lymphatic defects induced by blocking vascular endothelial growth factor receptor 3 partially diminished the benefits of cardiomyocyte-derived apelin overexpression in AVMC. Taken together, these data indicate that functional CLVs restored by cardiomyocyte-derived apelin facilitate inflammation resolution and improve heart dysfunction in AVMC. Thus, CLV-based therapeutic strategies may serve as a novel approach for alleviating AVMC heart damage.

Background: Coxsackievirus B2 (CVB2) causes a range of diseases, including hand, foot, and mouth disease; myocarditis; acute flaccid paralysis; meningitis; and encephalitis. However, no specific antiviral drugs or vaccines are currently available for CVB2. Methods: We used plaque purification, virus titre determination, and serial passaging to screen and identify an inactivated CVB2 vaccine candidate strain, KM31-C05, which exhibited high viral titres and good genetic stability. Comprehensive biological characterization of this candidate strain was performed, including phylogenetic analysis, virulence assessment in BALB/c mice, one-step growth curve analysis, optimization of the multiplicity of infection, as well as determination of viral load, pathological evaluation, and immunohistochemical analysis in tissues of BALB/c suckling mice post-challenge. An experimental inactivated vaccine was prepared using KM31-C05 to evaluate its immunogenicity and protective efficacy. Results: The viral titres of KM31-C05 reached 10[8] CCID50/mL. After 20 serial passages, only three amino acid mutations were identified (VP3-G165V, VP1-N84K, and VP1-D129N). Although the two VP1 mutations were located in surface-exposed loops, the strain maintained high neutralizing titres across passages, indicating good genetic stability. However, whether these sites affect virulence and replication requires further investigation. Phylogenetic analysis revealed that this strain belonged to genotype C, which is consistent with the strains circulating in mainland China in recent years. The experimental inactivated vaccine prepared from KM31-C05 induced effective neutralizing antibodies (1:128-1:256) in BALB/c mice and provided complete protection to suckling mice against lethal challenge with this CVB2 strain in maternal antibody protection experiments. Conclusions: KM31-C05 demonstrates potential as a CVB2 vaccine candidate in China and provides a theoretical basis for the development of a CVB2 vaccine.

Clozapine is the most effective antipsychotic medication for treatment-resistant schizophrenia but is associated with rare and potentially life-threatening myocarditis. Early clinical manifestations are often nonspecific and may delay diagnosis. We report a man in his 30s who developed fever and palpitations three weeks after initiation of clozapine therapy. Laboratory testing demonstrated a marked elevation in C-reactive protein that preceded the development of cardiac biomarker elevation and new left ventricular systolic dysfunction. Transthoracic echocardiography demonstrated an ejection fraction of 30% to 35%, consistent with acute heart failure with reduced ejection fraction. Clozapine was discontinued, and guideline-directed medical therapy was initiated, resulting in complete recovery of cardiac function on follow-up imaging. This case highlights the potential role of inflammatory markers as an early signal of evolving clozapine-associated myocarditis and emphasizes the importance of early recognition and prompt drug discontinuation.