Double-chambered left ventricle (DCLV) is an extremely rare congenital heart disease. In this condition, the left ventricle (LV) is divided into the main left ventricular chamber (MLVC) and the accessory chamber (AC) by a septum or muscle fiber with abnormal proliferation. The MLVC and AC chambers are connected to each other and can be classified into different types on the basis of their positions. Many researchers have different opinions regarding this disease. 1 | C A S E PRE S ENTATI ONA boy was diagnosed with DCLV at our hospital. The pathological type, diagnostic points, and therapeutic schemes of this condition were considered in the context of current and relevant local and international studies and reports on DCLV. The 9-year-old boy was admitted with the major complaint of 8 years of cardiac murmur, which was originally diagnosed through physical examination when the boy was 9 months old, and 5 years of palpitations and shortness of breath. Echocardiographic examination showed that the boy has congenital heart disease and an atrial septal defect (ASD) with a length of 4 mm. The patient is always being followed up because of his slight ASD. Over the past 5 years, the patient has often experienced palpitations and shortness of breath when participating in strenuous activities. The patient's uncomfortable symptoms intensified 10 days before hospital admission.Admission examination revealed that the boy had a blood pressure of 100/62 mm Hg and heart rate of 74 times/min. The patient also exhibited nonpalpable tremors, slightly enlarged heart borders, regular cardiac rhythm, loud heart sound, and murmur in the left 3-4 sternum during the systolic period (II/III level).Coarse breathing sounds were heard in both lungs. Cyanosis and precordium abnormal uplift were not observed. The boy's liver, spleen, and subcostal areas were intangible, and his lower limbs were not edemic. The results of 12-lead electrocardiogram (ECG) and Holter monitoring obtained through aided examination indicated sinus arrhythmia with left axis deviation (Figure 1). Chest X-ray revealed an abnormal cardiac shape, as well as the localized protrusion of the left anterior margin of the heart (Figure 2).Echocardiography taken along the left ventricular long axis with an apical four-chamber view showed that the left chamber was obliquely separated into left and right chambers by abnormal muscle bundles. In the parasternal long-axis view, the size of the MLVC was 4.2 × 3.9 cm and that of the AC was 2.1 × 1.8 cm. A wide access hole with the diameter of 1.9 cm during the systolic period was found between the MLVC and AC. The flow rate from the How to cite this article: Zhang W-M, Chang D-Q, Huang J-J, et al. Double-chambered left ventricle: A rare case in a child.

Stress is a pivotal factor for inflammation, reactive oxygen species (ROS) production and formation of visceral hypersensitivity (VH) in the process of gastroesophageal reflux disease (GERD). In the present study, the effects of stress on esophageal inflammation, oxidative stress and VH were investigated in a chronic restraint stress mouse model. c57Bl/6J male mice were subjected to 2 weeks of intermittent restraint stress, and histopathological analysis revealed that stress induced esophageal inflammation and fibrosis, while no distinct changes were detected in non-stressed control mice. In addition, increased NADPH oxidase 4 expression was observed in the plasma and esophagus of stressed mice, indicating accumulation of ROS. The expression levels of antioxidants, including Mn-superoxide dismutase (MnSOD), cu/Zn-Sod, catalase and glutathione peroxidase, were also analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, transient receptor potential vanilloid 1 (TrPV-1) and protease-activated receptor 2 (Par-2), which are crucial receptors for VH, were measured by immunohistochemistry and RT-qPCR. The results demonstrated that stress markedly reduced antioxidant expression, while it significantly upregulated TRPV-1 and PAR-2 expression levels in the mouse esophagus. Finally, 2 weeks of restraint stress significantly increased the esophageal and plasma levels of inflammatory cytokines, including interleukin (IL)-6, IL-8, interferon-γ and tumor necrosis factor-α. Taken together, the present study results indicated that stress-induced esophageal inflammation and ROS generation involves VH.

Although the underlying mechanism of stress remains unknown, it has been associated with the pathophysiology of gastroesophageal reflux diseases, the development of which appear to be accelerated by oxidative stress and fibrosis. The aim of the current study was to investigate the effect of chronic restraint stress on esophageal oxidative stress and fibrosis, as well as the impact of oxidative stress in a murine model whereby 8-week old C57BL/6J male mice were subjected to intermittent chronic restraint stress for a two-week period. The current study demonstrated that chronic restraint stress significantly reduced the body weight of mice compared with the control group. Although chronic restraint stress did not significantly alter the levels of triglycerides or cholesterol, free fatty acid concentration was significantly increased compared with the control group. Furthermore, chronic restraint stress significantly upregulated the expression levels of several fibrotic biomarkers including collagen type I, transforming growth factor β-1, α-smooth muscle actin and SMAD-3 compared with the control group. In addition, the expression levels of the reactive oxygen species (ROS) NADPH oxidase-4 and malondialdehyde were significantly increased, while the expression levels of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 were significantly decreased in esophageal tissue from mice in the chronic restraint stress group compared with the control group. In conclusion, chronic restraint stress may induce esophageal fibrosis by accumulating ROS and increasing fibrotic gene expression in a murine model.

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Background: Primary cardiac tumors are rare, but few studies have examined the relationship between risk factors and the prognosis. The aim of this study was to provide a survival analysis and risk factors for mortality in patients with primary cardiac tumors. Methods: We retrospectively enrolled 71 patients diagnosed with primary cardiac tumors from June 2006 to November 2017 in our hospital. Patients’ population characteristics, treatment information, pathology, and follow-up data were obtained and analyzed. Results: Of the 71 patients, 60 cases were benign, and 11 cases were malignant. Sex, age, New York Heart Association classification, the percentage of peripheral embolism, and surgery had no significant difference between benign and malignant groups (P >.05), but the percentage of arrhythmia, leg edema, and mortality rate was higher in the malignant tumor group than in the benign tumor group (P <.05). Compared with the benign tumor group, the percentage of biatrial lesions in the malignant tumor group was significantly higher (P <.05). Moreover, Independent risk factors included the treatment choice, pathology type, and number of tumor lesions (P <.05). Conclusion: Our study suggests that conservative therapy, malignant cardiac tumor, and biatrial tumor lesion are independent risk factors for poor prognosis.