Anzhen Risk Evaluation System for Acute Aortic Syndrome (AZSCORE-AAS): protocol for a multicentre prospective cohort study in northern China.

INTRODUCTION: Acute aortic syndrome (AAS) is a group of acute and critical conditions, including acute aortic dissection (AAD), acute intramural haematoma and penetrating aortic ulcer. High mortality and morbidity rates result in a poor patient prognosis. Prompt diagnoses and timely interventions are paramount for saving patients' lives. In recent years, risk models for AAD have been established worldwide; however, a risk evaluation system for AAS is still lacking in China. Therefore, this study aims to develop an early warning and risk scoring system in combination with the novel potential biomarker soluble ST2 (sST2) for AAS. METHODS AND ANALYSIS: This multicentre, prospective, observational study will recruit patients diagnosed with AAS at three tertiary referral centres from 1 January 2020 to 31 December 2023. We will analyse the discrepancies in sST2 levels in patients with different AAS types and explore the accuracy of sST2 in distinguishing between them. We will also incorporate potential risk factors and sST2 into a logistic regression model to establish a logistic risk scoring system for predicting postoperative death and prolonged intensive care unit stay in patients with AAS. ETHICS AND DISSEMINATION: This study was registered on the Chinese Clinical Trial Registry website (http://www. chictr. org. cn/). Ethical approval was obtained from the human research ethics committees of Beijing Anzhen Hospital (KS2019016). The ethics review board of each participating hospital agreed to participate. The final risk prediction model will be published in an appropriate journal and disseminated as a mobile application for clinical use. Approval and anonymised data will be shared. TRIAL REGISTRATION NUMBER: ChiCTR1900027763.

[Mid-term outcome of endoscopic greater saphenous vein harvesting in coronary artery bypass grafting].

OBJECTIVE: To evaluate the mid-term clinical outcome of endoscopic greater saphenous vein harvesting (EVH) in coronary artery bypass grafting (CABG). Method A total of 205 patients receiving off-pump CABG between July, 2012 and April, 2013 at our department were enrolled in this study, including 66 patients (35 male and 31 female patients with a mean age of 60.3±7.92 years) undergoing EVH and 139 patients (109 male and 30 female patients with a mean age of 59.20±8.37 years) undergoing open greater saphenous vein harvesting (OVH). RESULTS: The surgical procedures were completed smoothly in all the cases. The perioperative mortality rates was 3.03% (2/66) in EVH group, as compared with 3.60% (5/139) in OVH group (P=1.00). Acute myocardial infarction (AMI) occurred during the perioperative period in 3 (2.16%) patients in OVH group and in 1 (1.52%) patient in EVH group. Perioperative low cardiac output syndrome was diagnosed in 4 (2.88%) patients in OVH group and in 2 (3.03%) in EVH group (P>0.05). During the follow-up, 8 (8.80%) patients in OVH group and 5 (8.06%) in EVH group had recurrent angina (P=0.93). No patients experienced AMI during the follow-up. The 2-year patency rate of the venous grafts was 83.59% in OVH group and 82.22% in EVH group (P=0.73). CONCLUSION: EVH has significant advantage in reducing the complications of the incision in the lower limbs. The mid-term patency rates of venous grafts are similar between OVH and EVH, but the long-term patency rate needs further evaluation.

A novel, recovery, and reproducible minimally invasive cardiopulmonary bypass model with lung injury in rats.

BACKGROUND: Cardiopulmonary bypass (CPB) has been shown to be associated with a systemic inflammatory response leading to postoperative organ dysfunction. Elucidating the underlying mechanisms and developing protective strategies for the pathophysiological consequences of CPB have been hampered due to the absence of a satisfactory recovery animal model. The purpose of this study was to establish a good rat model of CPB to study the pathophysiology of potential complications. METHODS: Twenty adult male Sprague-Dawley rats weighing 450-560 g were randomly divided into a CPB group (n = 10) and a control group (n = 10). All rats were anaesthetized and mechanically ventilated. The carotid artery and jugular vein were cannulated. The blood was drained from the right atrium via the right jugular and transferred by a miniaturized roller pump to a hollow fiber oxygenator and back to the rat via the left carotid artery. Priming consisted of 8 ml of homologous blood and 8 ml of colloid. The surface of the hollow fiber oxygenator was 0.075 m(2). CPB was conducted for 60 minutes at a flow rate of 100-120 ml× kg(-1)×min(-1) in the CPB group. Oxygen flow/perfusion flow was 0.8 to 1.0, and the mean arterial pressure remained 60-80 mmHg. Blood gas analysis, hemodynamic investigations, and lung histology were subsequently examined. RESULTS: All CPB rats recovered from the operative process without incident. Normal cardiac function after successful weaning was confirmed by electrocardiography and blood pressure measurements. Mean arterial pressure remained stable. The results of blood gas analysis at different times were within the normal range. Levels of IL-1ß and TNF-α were higher in the lung tissue in the CPB group (P < 0.005). Histological examination revealed marked increases in interstitial congestion, edema, and inflammation in the CPB group. CONCLUSION: This novel, recovery, and reproducible minimally invasive CPB model may open the field for various studies on the pathophysiological process of CPB and systemic ischemia-reperfusion injury in vivo.

Total liquid ventilation reduces oleic acid-induced lung injury in piglets.

BACKGROUND: Pediatric patients are susceptible to lung injury that does not respond to traditional therapies. Total liquid ventilation has been developed as an alternative ventilatory strategy for severe lung injury. The aim of this study is to investigate the effect of total liquid ventilation on oleic acid (OA)-induced lung injury in piglets. METHODS: Twelve Chinese immature piglets were induced acute lung injury by OA. Twelve piglets were randomly treated with conventional gas ventilation (control group) or total liquid ventilation (study group) for 240 minutes. Samples for blood gas analysis were collected before, and at 60-minute intervals after OA-induced lung injury. The degree of lung injury was quantified by histologic examination. The inflammatory cells and the levels of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were analyzed. RESULTS: Neutrophil and macrophage counts in bronchoalveolar lavage were significantly decreased in the study group (P < 0.05). The total lung injury score was also reduced in the study group (P < 0.05). The concentrations of IL-1ß, IL-6, IL-10 and TNF-α in plasma, tissue and bronchoalveolar lavage were significantly reduced in the study group (P < 0.05). CONCLUSIONS: Total liquid ventilation reduces biochemical and histologic OA-induced lung injury in piglets.

Atrial natriuretic peptide attenuates inflammatory responses on oleic acid-induced acute lung injury model in rats.

BACKGROUND: An inflammatory response leading to organ dysfunction and failure continues to be a major problem after injury in many clinical conditions such as sepsis, severe burns, and trauma. It is increasingly recognized that atrial natriuretic peptide (ANP) possesses a broad range of biological activities, including effects on endothelial function and inflammation. A recent study has revealed that ANP exerts anti-inflammatory effects. In this study we tested the effects of human ANP (hANP) on lung injury in a model of oleic acid (OA)-induced acute lung injury (ALI) in rats. METHODS: Rats were randomly assigned to three groups (n = 6 in each group). Rats in the control group received a 0.9% solution of NaCl (1 ml × kg(-1) × h(-1)) by continuous intravenous infusion, after 30 minutes a 0.9% solution of NaCl (1 ml/kg) was injected intravenously, and then the 0.9% NaCl infusion was restarted. Rats in the ALI group received a 0.9% NaCl solution (1 ml × kg(-1) × h(-1)) intravenous infusion, after 30 minutes OA was injected intravenously (0.1 ml/kg), and then the 0.9% NaCl infusion was restarted. Rats in the hANP-treated ALI group received a hANP (0.1 µg × kg(-1) × min(-1)) infusion, after 30 minutes OA was injected intravenously (0.1 ml/kg), and then the hANP infusion was restarted. The anti-inflammation effects of hANP were evaluated by histological examination and determination of serum cytokine levels. RESULTS: Serum interleukin (IL)-1ß, IL-6, IL-10 and tumor necrosis factor (TNF) α were increased in the ALI group at six hours. The levels of all factors were significantly lower in the hANP treated rats (P < 0.005). Similarly, levels of IL-1ß, IL-6, IL-10 and TNF-α were higher in the lung tissue in the ALI group at six hours. hANP treatment significantly reduced the levels of these factors in the lungs (P < 0.005). Histological examination revealed marked reduction in interstitial congestion, edema, and inflammation. CONCLUSION: hANP can attenuate inflammation in an OA-induced lung injury in rat model.

A novel, stable and reproducible acute lung injury model induced by oleic acid in immature piglet.

BACKGROUND: Young children are susceptible to pulmonary injury, and acute lung injury (ALI) often results in a high mortality and financial costs in pediatric patients. A good ALI model will help us to gain a better understanding of the real pathophysiological picture and to evaluate novel treatment approaches to acute respiratory distress syndrome (ARDS) more accurately and liberally. This study aimed to establish a hemodynamically stable and reproducible model with ALI in piglet induced by oleic acid. METHODS: Six Chinese mini-piglets were used to establish ALI models by oleic acid. Hemodynamic and pulmonary function data were measured. Histopathological assessment was performed. RESULTS: Mean blood pressure, heart rate (HR), cardiac output (CO), central venous pressure (CVP) and left atrial pressure (LAP) were sharply decreased after oleic acid given, while the mean pulmonary arterial pressure (MPAP) was increased in comparison with baseline (P < 0.05). pH, arterial partial pressure of O2 (PaO2), PaO2/inspired O2 fraction (FiO2) and lung compliance decreased, while PaCO2 and airway pressure increased in comparison with baseline (P < 0.05). The lung histology showed severe inflammation, hyaline membranes, intra-alveolar and interstitial hemorrhage. CONCLUSION: This experiment established a stable model which allows for a diversity of studies on early lung injury.

[Pretreatment of donor dendritic cells with NBD-peptide prolongs mouse cardiac allograft survival].

OBJECTIVE: To observe the effects of NBD-peptide pretreatment of the donor dendritic cells in immune tolerance induction in mouse allograft recipients and investigate the mechanisms. METHODS: BALB/c mouse DCs pretreated with NBD-peptide (NBD-Peptide-DC) were injected into the recipient C57BL/6 mice 7 days before transplantation. Cervical heterotopic heart transplantation model was established using the cuff technique and the cardiac allograft survival time was observed. Pathological analysis were performed to examine the graft injection and the responsiveness of the recipient spleen T cell to the donor alloantigen was determined by mixed lymphocyte reaction (MLR). The serum levels of cytokines were determined using ELISA. RESULTS: The cardiac allograft survival time in the NBD-Peptide-DC-treated group (21.83-/+3.54 days) was significantly longer than that in the Day9-DC group (13.33-/+2.58 days) and PBS-treated group (6.66-/+1.21 days) (P<0.01), with also significantly lower pathological grade for graft rejection (P<0.01). The donor-derived NBD-Peptide-DCs induced alloantigen-specific T-cell hyporesponsiveness. In the NBD-Peptide-DC-treated group, the serum levels of IL-12 and IFN-gamma decreased significantly (P<0.01), but the levels of IL-4 and IL-10 increased significantly (P<0.01). CONCLUSION: Injection of donor-derived NBD-Peptide-DCs can leads to donor-specific tolerance in the transplant recipients, and the induction of recipient T-cell hyporesponsiveness and polarization of Th2 response may play important roles in immune tolerance to cardiac allografts.

[Comparative study of right anterolateral minithoracotomy and median sternotomy in the repair of atrial septal defects].

OBJECTIVE: To compare the effect of right anterolateral minithoractomy and median sternotomy for atrial septal defect closure. METHODS: In this study, 82 patients, whose age ranged from 4 to 46 years with a mean of 15.7+/-8.6 years, underwent surgical repair of the atrial septal defects on the beating heart through right anterolateral minithoractomy. Ten of these cases were complicated by moderate to severe pulmonary hypertension, and 3 by partial anomalous pulmonary venous connection. Another 67 patients with an age range of 3 to 49 years (mean 17.0+/-12.5 years) underwent surgical repair of the atrial septal defects through full-length median sternotomy with the heart beat arrested, and complication of moderate to severe pulmonary hypertension was identified in 11 cases and partial anomalous venous connection in 5. Comparisons were performed between the 2 groups in terms of the length of skin incision, cardiopulmonary bypass (CPB) time, postoperative mechanical ventilation time, intensive care unit stay, postoperative hospital stay, and the volume of postoperative drainage. RESULTS: There was no operative mortality in either of the 2 groups. In the former group, the CPB time (35.2+/-14.1 min), postoperative mechanical ventilation time (6.5+/-2.5 h), postoperative drainage volume (237.6+/-172.5 ml), postoperative hospital stay (7.4+/-1.2 d) and skin incision length (6.5+/-0.9 cm) were all significantly less than those of the latter group of patients, whose CPB time was 42.7+/-11.8 min, postoperative mechanical ventilation time 7.9+/-3.8 h, postoperative drainage volume 304.3+/-192.4 ml, postoperative hospital stay 9.0+/-2.9 d and skin incision length 15.9+/-1.7 cm (P < 0.01). The intensive care unit stay did not differ significantly between the 2 groups (35.1+/-16.2 h vs 32.3+/-24.1 h, P > 0.05). CONCLUSION: A right anterolateral minithoracotomy for repairs of atrial septal defects is a safe, effective and simple technique to ensure minimal surgical invasion with shorter postoperative hospital stay. Minithoracotomy can be performed to replace median sternotomy in the correction of atrial septal defects, including those complicated by partial anomalous pulmonary venous connection.