This study aims to explore computed tomography (CT) and magnetic resonance imaging (MRI) features of patients diagnosed with primary cardiac angiosarcoma. The study involved the analysis of 12 patients diagnosed with primary cardiac angiosarcoma who underwent non-contrast (8/12) or contrast-enhanced CT (10/12) or MRI (4/12). Imaging appearances, including the tumor location and adjacent infiltration, were analyzed. All 12 lesions were located in the right atrium with a broad base. Adjacent invasion including the tricuspid valve and right ventricle (2/12), inferior or superior vena cava (2/12), pericardium (10/12), and right coronary artery (7/12) was common. On unenhanced CT scans, tumors in two patients were homogeneous in density, whereas the others were inhomogeneous. Ten patients showed heterogeneous enhancement. The enhancement pattern showed no direct correlation with the differentiation degree of the tumor. Four lesions manifested as heterogeneous intensity, with hyperintense hemorrhage foci on both T1- and T2-weighted MRI. Three showed rim enhancement and one showed patchy enhancement. Primary cardiac angiosarcoma often involves the right side of the heart with infiltration of peripheral structures. CT features include typical inhomogeneous density on unenhanced scans and heterogeneous centripetal enhancement on enhanced scans. A cauliflower-like appearance on both T1- and T2-weighted MRI is common. The characteristic enhancement pattern of MRI remains to be determined.

Background: Primary cardiac angiosarcoma is a rare malignancy with high predilection to involve surrounding structures such as pulmonary metastases. We analysed the chest computed tomography (CT) imaging features of patients diagnosed with primary cardiac angiosarcoma with pulmonary metastases in this study. Methods: This study retrospectively reviewed 12 patients with confirmed primary cardiac angiosarcoma, out of which eight (all men) with pulmonary metastasis were included in the analysis. The patients’ age ranged from 17 to 74 (mean: 48) years. CT was performed in all patients with unenhanced, contrast-enhanced, and both scans were done in 1, 3 and 4 patients, respectively. Results: Nodular lesions were observed in 7 patients with multiple solid nodules observed in 6 out of 7 patients. A solitary solid nodule was found in the remaining patient in the upper lobe and apical segment of the right lung with a diameter of 11.7 mm. All solid nodules were distributed along with bronchovascular bundles in the lungs, and their maximum diameter ranged from 2.3 to 19.9 mm. Nodules larger than 10 mm in diameter were heterogeneously enhanced on contrast-enhanced CT images (5/8 patients), whereas those smaller than 10 mm were homogeneously enhanced (3/8 patients). Other imaging features, namely the tree-in-bud pattern, emphysema, pleural effusion, and mediastinal lymph node enlargement, were observed in 4, 3, 3, and 2 patients, respectively. Conclusion: CT enhancement features of pulmonary metastasis in patients with primary cardiac angiosarcoma depend on the size of pulmonary nodules, with larger ones being heterogeneous and smaller ones homogeneous. Other signs are less noticed.

The 2A protease (2A ^pro ) encoded by enterovirus 71 (EV71) serves as an accessory protein with significant involvement in the regulation of EV71 infection and viral replication. EV71-2A ^pro exhibits the ability to suppress various host factors, thereby disrupting the cellular antiviral immune response. However, whether host factors downregulate EV71-2A ^pro remains largely unknown. Here, we discovered that the speckle-type POZ protein (SPOP), functioning as a host E3 ubiquitin ligase, triggers ubiquitination modifications and subsequent degradation of EV71-2A ^pro . SPOP interacts with EV71-2A ^pro and exhibits a dose-dependent downregulation of EV71-2A ^pro levels. Conversely, knockdown of endogenous SPOP upregulated EV71-2A ^pro levels. Subsequent investigations revealed that the SPOP facilitates the lysosome-dependent degradation of EV71-2A ^pro by inducing K48-linked polyubiquitination of EV71-2A ^pro , which ultimately restricts EV71 replication. These findings shed light on the ubiquitination and lysosome-dependent regulation of the crucial EV71-encoded protease, offering a potential therapeutic target for the treatment of EV71 infection. IMPORTANCE: EV71 poses a significant health threat to children aged 5 and below. The process of EV71 infection and replication is predominantly influenced by ubiquitination modifications. Our previous findings indicate that EV71 prompts the activation of host deubiquitinating enzymes, thereby impeding the host interferon signaling pathway as a means of evading the immune response. Nevertheless, the precise mechanisms by which the host employs ubiquitination modifications to hinder EV71 infection remain unclear. The present study demonstrated that the nonstructural protein 2A ^pro , which is encoded by EV71, exhibits ubiquitination and degradation mediated by the host E3 ubiquitin ligase SPOP. In addition, it is the first report, to our knowledge, that SPOP is involved in the host antiviral response.

To assess the variation in left atrial (LA) and biventricular strain and its prognostic value in the course of suspected myocarditis, this retrospective study included 55 patients with clinically suspected myocarditis who underwent cardiac magnetic resonance (CMR) examinations at baseline and follow-up periods. Cine images were used for feature tracking analysis. Paired Student’s t test, McNemar’s test, and Cox proportional hazard regression were used for statistical analysis. The LA total emptying fraction was the only functional index that showed a statistically significant improvement. The initial LA peak’s late negative strain rate (SRa) was the only parameter with a significant predictive power of major adverse cardiac events under univariable (hazard ratio [HR] 2.396, 95% confidence interval [CI] 1.044–5.498, p = 0.039) and multivariable Cox survival analysis when adjusted by LA strain parameters (HR 5.072, 95% CI 1.478–17.404, p = 0.010), LA strain and functional parameters (HR 7.197, 95% CI 1.679–30.846, p = 0.008), and LA and biventricular strain and functional parameters (HR 10.389, 95% CI 2.250–47.977, p = 0.003). Thus, our findings indicate that CMR strain is useful for monitoring LA and ventricular function in suspected myocarditis, that LA function may recover preceding ventricular function changes, and that LA strain may serve as an incremental tool to predict adverse outcomes.