Intraventricular Thrombosis and Pulmonary Embolism Post-Nuss Procedure: A Rare Case of Chronic Bar Displacement in a 16-Year-Old Patient.

This novel report presents the first known case, to our knowledge, of a 16-year-old male patient who experienced intraventricular thrombosis and pulmonary embolism after a Nuss procedure for pectus excavatum, attributed to chronic bar displacement. Two years after the operation, the patient experienced post-exercise cough and hemoptysis, which led to his admission. Imaging revealed pulmonary embolism, thrombosis in the right ventricular outflow tract, and lung infiltrative lesions. We hypothesize that the chronic bar displacement led to its embedment in the right ventricle, resulting in thrombus formation, which subsequently contributed to partial pulmonary embolism. Surgery revealed the bars' intrusion into the right ventricle and lung. This case highlights the risk of severe complications from bar displacement in the Nuss procedure, which necessitates long-term follow-up evaluation, caution against strenuous activities after surgery, and use of thoracoscopic guidance during bar implantation and removal. It underscores the importance of vigilant evaluation for late-stage complications in patients with respiratory distress or thrombosis after a Nuss procedure.

Circular RNA PVT1 silencing prevents ischemia-reperfusion injury in rat by targeting microRNA-125b and microRNA-200a.

Circular RNAs (circRNAs) are essential regulators associated with many cardiac conditions, including myocardial infarction (MI). This study aimed to explore circRNA expression during MI development in an animal model and in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Microarray and real-time quantitative PCR showed that the circRNA PVT1 (circPVT1) was expressed at high levels in MI tissues and H/R-triggered cardiomyocytes. Loss-of-function assays were utilized for examining the influence of circPVT1 on cardiac function and cardiomyocyte properties. Cardiac function was measured by echocardiography at 7 d after MI. Reduced circPVT1 expression significantly decreased MI-triggered myocardial infarct size by 60% and prevented MI-triggered reductions in fractional shortening (%FS) and ejection fraction (EF%). Results of LDH, CCK-8, EdU staining, colony formation assays, and flow cytometry showed that circPVT1 silencing restored cell viability and proliferation while decreased apoptosis. Mechanistic experiments indicated that microRNAs (miR)-125b and miR-200a associated with circPVT1. We demonstrated that circPVT1 functioned as a competitive endogenous RNA (ceRNA) to sponge both miR-125b and miR-200a. Gain-of-function assays showed that miR-125b and miR-200a upregulation partially eliminated the effects of circPVT1 on cardiomyocyte properties. In addition, we found that the previously reported p53/TRAF6, SIRT7, Keap1/Nrf2, and PDCD4 pathways were regulated by the circPVT1/miR-125b/miR-200a axis. In conclusion, our study suggests that circPVT1 protects the myocardium from MI and H/R injury by preventing miR-125b- and miR-200a-mediated apoptotic signaling.

Effect of different cardioprotective methods on extracorporeal circulation in fetal sheep: a randomized controlled trial.

BACKGROUND: Congenital heart disease is a leading cause of death in newborns and infants. The feasibility of fetal cardiac surgery is linked to extracorporeal circulation (ECC); therefore, cardioplegic solutions need to be effective and long-lasting. METHODS: Eighteen pregnant sheep were divided into an ECC-only group, St. Thomas' Hospital cardioplegic solution (STH1) group (STH group), and HTK preservation solution (Custodiol®) group (HTK group). Markers of myocardial injury including troponin I (cTnI), troponin T (cTnT) and creatine kinase myocardial band (CKMB) were measured at specific time points (T1: pre-ECC, T2: 30 min of ECC, T3: 60 min of ECC, T4: 60 min post-ECC, T5: 120 min post-ECC). Myocardial tissue was removed from the fetal sheep at T5, and apoptosis was detected by TUNEL staining. RESULTS: Changes in the serum cTnI, cTnT and CKMB concentrations were not significantly different among the three groups before and during the ECC(T1,T2,T3). At 60 min after ECC shutdown(T4), cTnI and cTnT concentrations were significantly higher in the STH group than before the start of ECC. The concentration of cTnI was higher in the STH group than in the HTK and ECC-only groups. The concentration of cTnT was higher in the STH group than in the ECC-only group. At 120 min after ECC shutdown(T5), cTnI and cTnT concentrations were significantly higher in the ECC and HTK groups than before the start of ECC, and CKMB concentration was significantly higher in STH and HTK groups. The concentrations of cTnT, cTnI and CKMB was higher in the STH group than in the HTK and ECC-only groups. The number of TUNEL-positive cells in the HTK and STH groups was higher than in the ECC-only group. The number of TUNEL-positive cells in the STH group was higher than in the HTK group. There was no statistically significant difference among the groups in the heart rate and mean arterial pressure after ECC. CONCLUSION: The HTK preservation solution was significantly better than STH1 in reducing the release of cardiomyocyte injury markers and the number of apoptotic cells in fetal sheep ECC. Fetal sheep receiving ECC-only had an advantage in all indicators, which suggests ECC-only fetal heart surgery is feasible.

Deficiency of Interleukin-36 Receptor Protected Cardiomyocytes from Ischemia-Reperfusion Injury in Cardiopulmonary Bypass.

BACKGROUND Interleukin-36 has been demonstrated to be involved in inflammatory responses. Inflammatory responses due to ischemia-reperfusion injury following cardiopulmonary bypass (CPB) can cause heart dysfunction or damage. MATERIAL AND METHODS The CPB models were constructed in IL-36R-/-, IL-36RN-/-, and wild-type SD rats. Ultrasonic cardiography and ELISA were used to evaluate the cardiac function and measuring myocardial biomarker levels in different groups. TUNEL assay was used to evaluate apoptosis. Western blot assays and RT-PCR were performed to measure the expression of chemokines and secondary inflammatory cytokines in the heart. Oxidative stress in tissue and cultured cells was assessed using a DCFH-DA fluorescence probe and quantification of superoxide dismutase activity. RESULTS Improved systolic function and decreased serum levels of myocardial damage biomarkers were found in IL-36R-/- rats compared to WT rats, while worse cardiac function and cardiomyocyte IR injury were observed in IL-36RN-/- rats compared to WT rats. TUNEL staining and Western blot analyses found that cardiomyocyte apoptosis and inflammation were significantly lower in the hearts of IL-36R-/- rats compared with that of WT rats. Oxidative stress was significantly lower in IL-36R-/- rats compared to WT rats. iNOS expression was significantly reduced, while eNOS expression was increased in the hearts of IL-36R-/- rats. Silencing of IL-36R expression in vitro activated SIRT1/FOXO1/p53 signaling in cardiomyocytes. CONCLUSIONS IL-36R deficiency in cardiomyocytes repressed infiltration of bone marrow-derived inflammatory cells and oxidative stress dependent on SIRT1-FOXO1 signaling, thus protecting cardiomyocytes and improving cardiac function in CPB model rats.

Histologic lung cancer subtype differentiates synchronous multiple primary lung adenocarcinomas from intrapulmonary metastases.

BACKGROUND: Distinguishing synchronous multiple primary lung cancers (SMPLCs) from intrapulmonary metastases is important. The objective of this study was to determine long-term survival in patients who underwent surgical resection for synchronous multiple lung cancers and identify additional criteria that may be useful to distinguish patients with SMPLCs from those with more advanced disease. METHODS: The medical records of patients with lung cancer who underwent planned resection for synchronous multiple lung cancers from 2007 to 2012 at our institutions were reviewed retrospectively. A comprehensive histologic assessment was used to determine whether the tumors were metastases or separate synchronous primary tumors. RESULTS: A total of 51 patients with synchronous multiple lung cancers underwent surgical resection. Twenty-nine patients had ipsilateral synchronous multiple lung cancers, and 22 had bilateral synchronous multiple lung cancers. No perioperative death occurred. The survival analysis of all 51 patients with synchronous multiple lung cancers who underwent planned resection of all lesions showed 3- and 5-year overall survival rates of 86% and 67%, respectively, The median overall survival was not reached. The comprehensive histologic assessment identified six patients with intrapulmonary metastasis and 45 patients with SMPLCs. Intrapulmonary metastases were associated with decreased survival. Among patients with SMPLCs, the epidermal growth factor receptor mutation distribution shown high concordant frequency rate of 35% (5/14). CONCLUSIONS: Survival after surgical resection of synchronous multiple lung cancers in different lobes was promising. A comprehensive histologic assessment was useful for differentiating SMPLCs from intrapulmonary metastases.

Malignant solitary fibrous tumor of pleura accompanied with first symptoms of chest pain and hemoptysis: a case report.

Solitary fibrous tumor of the pleura (SFTP) is a rare tumor especially presents malignant features. Such symptoms of hemoptysis and dyspnea were rarely seen and take 5% and 4% respectively in malignant SFTP. A 26-year-old Chinese man, presenting with hemoptysis in the emergency room, was hospitalized because of dyspnea. The X-ray examination revealed a tumor in the right chest cavity. The patient refused treatment, and the tumor grew rapidly, which complicated the symptoms of the patient. En-bloc excision of tumor plus the involved lung was performed. There was at least a 5000-ml mixture of blood and tumor tissue in the right chest cavity because of continuous bleeding, leading to a tumor capsule split. Histopathology and immunohistochemistry identified the tumor as malignant SFTP, but CD34 was negative. In this case, the tumor grew rapidly and aggressively in two months, indicating that close follow-up and active treatment are needed.

Palliative arterial switch for transposition of the great arteries, ventricular septal defect, and pulmonary vascular obstructive disease: midterm outcomes.

OBJECTIVE: Our objective was to evaluate the early and midterm outcomes of palliative arterial switch operation in which a ventricular septal defect was not closed or repaired with a fenestrated patch in patients with transposition of the great arteries, ventricular septal defect, and severe pulmonary vascular obstructive disease. METHODS: Between March 2000 and September 2009, the palliative arterial switch operation was performed in 21 patients with a mean age of 3.7 years (range, 0.5-15). Mean preoperative values for systolic pulmonary arterial pressure and systemic arterial oxygen saturation were 91 mm Hg and 69%, respectively. Eighty-one percent of the patients were in New York Heart Association functional class III or IV preoperatively. RESULTS: Early mortality was 14.3%. Mean follow-up was 4.0 years (maximum 9.5 years). Regression of pulmonary arterial pressure occurred in 8 patients (44% of the early survivors). Three of the 8 fenestrations were closed interventionally. Mean postoperative systemic arterial oxygen saturation increased significantly to 93% (P < .001). One late death occurred 3 months after surgery. All the long-term survivors (n = 17) were in New York Heart Association functional class I or II (P < .001). CONCLUSIONS: The palliative arterial switch operation significantly improved the quality of life and possibly life expectancy in patients with transposition of the great arteries, ventricular septal defect, and severe pulmonary vascular obstructive disease. Postoperative pulmonary vascular resistance might be reversible in some patients. Closing the ventricular septal defect with a fenestrated patch, which can be easily closed nonsurgically later on, might contribute to a safer postoperative recovery.