A ubiquitous tire rubber additive induced serious eye injury in zebrafish (Danio rerio).

Previous studies have indicated that tire wear particles (TWPs) leachate exposure induced serious eye injury in fish through inhibiting the thyroid peroxidase (TPO) enzyme activity. However, the main TPO inhibitors in the leachate were still unknown. In this study, we identified 2-Mercaptobenzothiazole (MBT) as the potential TPO inhibitor in the TWPs leachate through references search, model prediction based on Danish QSAR and ToxCast database, molecular docking, and in vivo assay. We further explored the toxic mechanism of MBT under environmentally relevant concentrations. The decreased eye size of zebrafish larvae was mainly caused by the decreased lens diameter and cell density in the inner nuclear layer (INL) and outer nuclear layer (ONL) of the retina. Transcriptomics analysis demonstrated that the eye phototransduction function was significantly suppressed by inhibiting the photoreceptor cell proliferation process after MBT exposure. The altered opsin gene expression and decreased opsin protein levels were induced by weakening thyroid hormone signaling after MBT treatment. These results were comparable to those obtained from a known TPO inhibitor, methimazole. This study has identified MBT as the primary TPO inhibitor responsible for inducing eye impairment in zebrafish larvae exposed to TWPs leachate. It is crucial for reducing the toxicity of TWPs leachate in fish.

Mechanistic insight into the adverse outcome of tire wear and road particle leachate exposure in zebrafish (Danio rerio) larvae.

Tire wear particles (TWP) have become the major microplastic pollution in China. Road runoff containing TWP leachate can decrease the eye size and even induced mortality in the aquatic organisms. However, the toxic mechanism of TWP and road particles (RP) leachate on aquatic organisms is still unclear. In this study, the zebrafish embryos were exposed to TWP or RP leachate for 5 days at both environmental relevant and high concentrations. The adverse outcome pathways (AOPs) were screened from individual to molecular levels. The morphological and behavioral analysis demonstrated that the leachate exposure mainly impaired the eye development of zebrafish larvae and inhibited the larval swim behavior and phototactic response, which are the adverse outcomes. The phototransduction modulated by zebrafish retina was significantly down-regulated through transcriptomics and metabolomics analysis. The eye histopathological analysis showed that the decreased thickness of the retinal outer nuclear layer (ONL) and retinal pigmented epithelium (RPE) after leachate exposure were caused by the decreased photoreceptor cells. Moreover, the expression of NR2E3 and TPO genes showed concentration-dependent down-regulation after leachate exposure. The inhibition of photoreceptor cell proliferation was identified as the main reason for photoreceptor cell decrease in zebrafish larval eye. This study, for the first time, uncovered the underlying toxic mechanism of TWP and RP on zebrafish larval eyes.

Shear Wave Elastography in the Diagnosis of Peripheral Neuropathy in Patients With Chronic Kidney Disease Stage 5.

Objective: To observe the feasibility of shear wave elastography (SWE) in the diagnosis of peripheral neuropathy in patients undergoing hemodialysis [chronic kidney disease stage 5 dialysis (CKD5D)]. Methods: Forty patients with CKD5D were divided into a uremic peripheral neuropathy (UPN) group (n = 25) and a non-UPN group (n = 15) according to the results of a neuro-electrophysiological examination. Sixteen healthy control subjects were also enrolled in this study. Two-dimensional ultrasound examination was conducted, and SWE was then performed to measure Young's modulus of the tibial nerve. The left and right diameters (D1), anterior and posterior diameters (D2), perimeter (C), cross-sectional area (CSA), and Young's modulus (E) were measured three times at the same non-entrapment site. The average values were recorded and calculated. The following evaluation indices were also analyzed: sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and area under the receiver operating characteristic curve (AUC). Results: D1, D2, C, and CSA were not significantly different among the three groups (P > 0.05). However, the difference in the E value among the three groups was statistically significant (P < 0.05). The AUC was 0.889 based on the E value. Using a tibial nerve E value of 48.35 kPa as the cutoff value, the sensitivity, specificity, PPV, and NPV were 86.0%, 84.0%, 81.1%, and 88.1%, respectively. Conclusions: SWE is useful for the diagnosis of peripheral neuropathy in patients with CKD5D. Young's modulus of 48.35 kPa for the tibial nerve is the optimal cutoff value and has the best diagnostic efficiency for peripheral neuropathy in CKD5D patients.

Inhibition of miRNA-27b enhances neurogenesis via AMPK activation in a mouse ischemic stroke model.

Stroke is a leading cause of death and disability, but treatment options remain limited. Recent studies have suggested that cerebral ischemia-induced neurogenesis plays a vital role in post-stroke repair. Overactivation of AMP-activated protein kinase (AMPK), a master sensor of energy balance, has been reported to exacerbate neuron apoptosis, but the role of chronic AMPK stimulus in post-stroke recovery remains unclear. MicroRNAs have emerged as regulators of neurogenesis and have been reported to be involved in neurological function. In this study, we verified that miR-27b directly targets AMPK and inhibits AMPK expression. In cultured neural stem cells, miR-27b inhibitor improved proliferation and differentiation via the AMPK signaling pathway, but did not have an obvious effect on cell viability under oxygen and glucose deprivation conditions. In a mouse middle cerebral artery occlusion model, administration of miR-27b inhibitor significantly enhanced behavioral function recovery and spatial memory. Up-regulation of neurogenesis was observed both in the subventricular zone and in the hippocampal dentate gyrus. Collectively, our data suggest that miR-27b inhibition promotes recovery after ischemic stroke by regulating AMPK activity. These findings may facilitate the development of novel therapeutic strategies for stroke.

MiRNA-27b Regulates Angiogenesis by Targeting AMPK in Mouse Ischemic Stroke Model.

Stroke is a leading cause of mortality and serious disability worldwide with limited treatment options. Angiogenesis has been reported to be involved in post-stroke recovery. Although the molecular mechanisms that regulate angiogenesis remain ambiguous, microRNAs have emerged as effective regulators of angiogenesis, involved in neurological function outcome. The present study aims to investigate the regulatory effects of miRNA-27b on post-stroke angiogenesis. In primary cultured brain microvascular endothelial cells (BMECs), the inhibition of miRNA-27b induced the activation of adenosine monophosphate-activated protein kinase (AMPK), which increased tube formation and migration. This action was attenuated when AMPKα2 was knocked down. Mice were subjected to middle cerebral artery occlusion (MCAo) surgery and administrated with Lentivirus miR-27b inhibitor. Enhanced angiogenesis in ischemic boundary zone (IBZ) was observed, and the neurological outcome during the entire study period was improved. The number of phosphate-AMPKα2+ cells that co-expressed endothelial cell marker CD31 was significantly increased. Taken together, the present study demonstrated that downregulated miRNA-27b promoted recovery after ischemic stroke via AMPK stimulus.

Lipocalin-2 protects against renal ischemia/reperfusion injury in mice through autophagy activation mediated by HIF1α and NF-κb crosstalk.

Renal ischemia/reperfusion injury is a main cause of acute kidney injury (AKI) triggering an inflammatory response associated with infiltrating macrophages. Lipocalin-2 (Lcn2) levels correlate positively and protect against renal ischemia/reperfusion injury. However, the mechanisms remain unclear. The aim of study was to investigate the protective mechanisms of Lcn2 on renal ischemia/reperfusion injury. We found that Lcn2 deficiency significantly aggravated renal injury as evidenced by higher serum creatinine, more severe morphological injury, and increased tubular epithelial cell death in mice. We also observed that attenuated autophagy in Lcn2-/- mice, as autophagy markers LC3 II level was significantly decreased and p62 was increased in the Lcn2-/- mice after I/R, compared with that of wild type. Mechanistically, we found that recombinant Lcn2 attenuated hypoxia-induced apoptosis in proximal tubule epithelial cells in vitro, and downregulation of HIF-1α blunted Lcn2-induced autophagy and enhanced apoptosis. In addition, the Lcn2 attenuated NF-κb subunit p65 activation under hypoxia conditions. Thus, our findings provide a better understanding of the protective role of Lcn2 in kidney ischemia/reperfusion injury and suggest that Lcn2 may be a promising therapeutic target for treating patients with AKI.

Dynamic Contrast-Enhanced Magnetic Resonance Imaging of Advanced Cervical Carcinoma: The Advantage of Perfusion Parameters From the Peripheral Region in Predicting the Early Response to Radiotherapy.

OBJECTIVE: This study aimed to investigate the importance of perfusion parameters from the peripheral region in predicting the early response to radiotherapy for advanced cervical carcinoma by using dynamic contrast-enhanced (DCE) perfusion magnetic resonance imaging (MRI). METHODS: One hundred eight patients with advanced cervical carcinoma were enrolled into this study. Dynamic contrast-enhanced perfusion MR examinations were performed for all the patients before radiotherapy. Perfusion parameters were obtained from the central region and the peripheral region of tumor respectively. After radiotherapy, the patients were classified into responders and nonresponders according to tumor shrinkage on the basis of follow-up MRI examination. The mean follow-up time lasted 12 months. The perfusion parameters were compared between the 2 groups. The relationship between perfusion parameters from 2 different regions of tumor and treatment effect was analyzed. RESULTS: The mean value of volume transfer constant (K), rate constant (Kep) or extravascular extracellular volume fraction (Ve) from the peripheral region was higher than that from the central region of tumor, respectively (P = 0.01, 004, 0.03). Responders had higher Kperipheral (K from the peripheral region) and Kcentral (K from the central region) values than nonresponders (P = 0.04, 0.01). Responders had higher Kepperipheral (Kep from the peripheral region) than nonresponders (P = 0.03). Responders had lower Veperipheral (Ve from the peripheral region) than nonresponders (P = 0.04). At logistic regression analysis, the perfusion parameters that had predicting value were Kperipheral, Veperipheral, Kepperipheral and Kcentral according to diagnostic potency. CONCLUSIONS: Compared with perfusion parameters from the central region of tumor, perfusion parameters from the peripheral region are more valuable in predicting the early response to radiotherapy for advanced cervical carcinoma.

[Primary culture and multiple differentiation potency of mesenchymal stem cells from human umbilical cord].

OBJECTIVE: To establish a reliable method of isolation, culture and characterization of human umbilical cord-derived mesenchymal stem cells (hUCMSCs) and study its multiple differentiation potency. METHODS: HUCMSCs were isolated and cultured using Trypsin-type II collagen and hyaluronidase digestion method and tissue explant culture method, respectively. The cell growth of hUCMSCs was observed under an inverted microscope. Cell viability rate of the different passages was evaluated by trypan blue staining. The proliferation profile of hUCMSCs was analyzed by growth curve and MTT assay. Flow cytometry was used to study the cell cycle and immunophenotypage change. The differentiation potency of hUCMSCs towards the osteoblasts, adipocytes was assayed using the differentiation kits. The differentiation towards the cardiomyocytes and endothelial cells was tested by immunofluoresence staining with the specific markers. RESULTS: After 1-day culture of the enzyme digested cells, under the inverted microscope, the adherent cells were round, and 4 days later, they grew quickly and presented fusiform. Seven days later, the cells proliferated from the center to the peripheral and fused by 80% on day 10. With the tissue explant culture method, the cells started to proliferate gradually from the periphery of the tissue and grew quickly and arrayed closely in monolayer after 10 days. The cell viability in both isolation methods were more than 96% as tested by trypan blue staining. The growth curve of the third passage presented an "S" shape. MTT assay showed that the optimal cell proliferation occured on day 3 to 5. The ratios of G0/G1 phase and S+G2/M phase was 88.78% and 10.21% respectively by enzyme digestion, and 84.82% and 13.87% respectively by explant culture method. There was no significant difference in cell cycle. The positive rates of CD90, CD105, CD73 were more than 99% and the expressions of CD45, CD34, CD14, CD11b, CD79a, CD19, HLA-DR were lower than 1%. The hUCMSCs isolated by the two methods could efficiently differentiate towards the osteoblasts, lipocytes, cardiac myocytes and endothelial cells, and the positive rates were all above 90%. CONCLUSION: The hUCMSCs can be effectively isolated by both enzyme digestion and explant culture methods. The enzyme isolation method presents a better method regarding the cell number obtained. This study showed the enzyme isolation method may be an optimal method to isolate the hUCMSCs for the cellular therapy and stem cell bioengineering.

Expression of lymphocyte coding genes in peripheral blood and lymphocyte infiltration in cardiac tissues influenced by cyclosporin A in heterotopic heart transplantation model in rats.

UNLABELLED: To systematically compare the expression of coding genes with pathological changes of transplanted cardiac tissue and peripheral blood lymphocytes in an allo-heterotopic rat cardiac transplant model. Using SD rats as donors and Wistar rats as recipients, animals were divided into two groups, control and cyclosporine A intervention plus heart transplant groups. After transplant at 1, 3, 7, 10 and 12d, we assessed the ability of lymphocytes to infiltrate into cardiac tissues and levels of leukocyte coding genes in peripheral blood. Histopathological changes were monitored in cardiac tissue to determine the level of transplant rejection. RESULTS: (1) 24h after transplant peripheral blood lymphocytes' transcription and expression were temporarily reduced. (2) CD4(+) and CD8(+) lymphocytes infiltrate into cardiac tissue and Grade 1R pathological changes were observed 3d-7d after heart transplant. (3)Cyclosporine A was not able to completely block heart transplant rejection.(4) Although cyclosporine A was not able to effectively suppress CD4(+) T cell gene expression, it did suppress CD8(+) T cell gene transcription. (5) Cyclosporine A did not effectively reduce the rapid infiltration of CD4(+) or CD8(+) infiltration in 3d, but significantly reduced the degree of CD4(+) T cell infiltration in cardiac tissues between 3 and 7d. (6) Differential display (DD-PCR): Graft control group: there were differences in 2,3-bisphosphoglycerate, ribosomal protein S25, 12S ribosomal, gig18, MHC-III and ATPase H(+), which occurred 24h before CD4/CD8 surface protein expression. Cyclosporine A group: there were differences in thrombospondin-1, TCR, 2,3-bisphosphoglycerate, sodium channel beta-1, gig18 and TCR. In the cyclosporine A group 2,3-bisphosphoglycerate positive expression was observed 24h after the control group, which indicates that cyclosporine A slowed down the 2,3-bisphosphoglycerate transcription rate in peripheral lymphocytes and delayed its expression time. Cyclosporine A also suppressed gig18 transcription in peripheral lymphocytes. After 24h, sodium channel beta-1 was positively expressed in the cyclosporine A group. The relationship between molecular surface receptor expression and coding genes in cardiac tissue and peripheral blood after transplant indicates that early detection of acute rejection and anti-rejection drugs' curative effect can be assessed.

Expressional time phase of leukocyte molecules induced by allogenic cardiac antigen and cyclosporin A in rats' in vitro model.

UNLABELLED: The immunosuppressive agent cyclosporin A has been proven to reduce the rejection rate and prolong the survival time of transplanted hearts. But some reports showed that cyclosporine A did not completely suppress the rejection. We performed in vitro studies to model a time course to observe the effect of cyclosporin A. METHODS: The experiment was divided into a control group (group I), an antigen group (group II), a cyclosporin A group (group III) and an antigen + cyclosporin A group (group IV). After transplantation, at 2 h, 6 h, 12 h, 24 h, 48 h and 72 h, leukocyte molecules were monitored. RESULTS: The expression of IL-2R peaked at 12 h in group II and at 6 h in group III. There was a gradual decline in the expression of the P59 gene in group I, positive expression at 2 h and between 12 h and 24 h in group II, in group IV, there was a decrease at 48 h. The expression of the CD4 gene was lowest at 2 h in group I and at 6 h in group II. CD4 expression then quickly increased to a maximum at 48 h in group III, at 2 h in group IV. There was a minimal expression was reached at 12 h in group I and IV and at 6 h in group III in the expression of the CD8 gene. CONCLUSIONS: Alloantigen induced lymphocytes to release IL-2R and P59 and stimulated the induction of the CD4 gene' transcription for 6 h. Cyclosporin A stimulated the release of IL-2R for 2 h. These results provide an in vitro basis for describing the time phases of rejection inhibited by cyclosporin A.

[Molecular expression of peripheral lymphocytes of the patients after organ transplantation].

AIM: To investigate the time course of the gene expression after the organ transplantation, and try to identify the relationship of the gene and protein changes with the pathological progression and the immune rejection. METHODS: We systematically observed the gene expression of CD4, CD8, P56, P59 by real-time PCR. The time courses of gene expression were analyzed by Fluorescent Differential Display after the organ transplantation. At the same time points, the clinical outcomes of the patients were followed up so that we could identify the relationship of the gene expression and the immune rejection. RESULTS: Immunosuppressive drugs could not prevent the transplantation rejection completely. P59 gene and tyrosine phosphatase genes started to express positively within 24 h after organ transplantation. Between 24-48 h, PKC-theta and CD4 gene expression levels increased. The expressions of PKC-theta, MHC-II, serine/threonine kinase, tyrosine phosphatase, serine/threonine kinase 15, clotting factor VIII, interferon gamma-inducible protein 16 and HLA-DR-H increased by three times compared to pre-transplantation in patients with kidney and heart transplantations. The expression of P59 gene remained stable within 24 h after transplantation, and then decreased to the lowest level at day 10. P56 and CD8 levels were down-regulated within 72 h, and then up-regulated to the first peak at day 5. The expression of CD4 was also inhibited within 24 h, and then increased to the first peak at 48 h. CONCLUSION: The monitoring on the expressions of the proteins and genes on the peripheral lymphocytes may help to early find the clinical immune rejection after organ transplantation and judge the efficiency of the anti-rejection drugs.

Off-pump coronary artery bypass grafting with device closure of atrial septal defect.

Patients with coronary artery disease and atrial septal defect may have unique clinical characters. We describe an off-pump combined approach for intraoperative device closure of atrial septal defect during coronary artery bypass grafting.

Analysis of risk factors for valve replacements in 5,128 cases from a single heart center in China.

BACKGROUND: Numerous studies have developed a "severity score" or "risk index" for short-term mortality associated with coronary artery bypass grafting (CABG). Due to the different distribution of disease types, the number of valve surgeries in the US and Europe is relatively small. Thus, a risk-scoring system for valve surgeries was developed later and used less than that for the CABG surgery. We retrospectively reviewed 5128 cases of heart valve replacement, to quantitatively assess the risk factors for hospital mortality, and establish risk models for the hospital mortality of cardiac valve replacement patients. METHODS: A total of 1549 cases of aortic valve replacement, 2460 cases of mitral valve replacement, and 1119 cases of combined aortic valve and mitral valve replacement that were recorded from January 2005 to December 2009 in the cardiac surgery database at Beijing Anzhen Hospital were selected for this study. The cases were randomly assigned to a model group (n = 3657) and a validation group (n = 1471) with a ratio of 7:3. Thirty-two pre- and intra-operative clinical indicators were selected as possible influencing factors for hospital mortality. Single-factor analysis was performed to screen these factors, and then multi-factor analysis was used to determine the risk factors for hospital mortality in the three surgeries and to establish risk models. RESULTS: In the multi-factor analysis, age, body surface area, etiology, cardiopulmonary bypass time, preoperative cardiothoracic ratio, cardiac functional classification, and preoperative creatinine were risk factors for aortic valve replacement. Etiology, preoperative history of heart failure, cardiopulmonary bypass time, preoperative cardiothoracic ratio, and preoperative left ventricular end systolic diameter were risk factors for mitral valve replacement. Age, body mass index, cardiopulmonary bypass time, and cardiac function classification were risk factors for combined aortic valve and mitral valve replacement. The risk models showed good predictive ability (Hosmer-Lemeshow test: P = 0.981 in the model for aortic valve replacement, P = 0.503 in the model for mitral valve replacement, and P = 0.154 in the model for combined aortic valve and mitral valve replacement). The area under the ROC curve of the validation group was 0.958 (95%CI: 0.936 - 0.975) for the aortic valve replacement model, 0.876 (95%CI: 0.805 - 0.948) for the mitral valve replacement model, and 0.845 (95%CI: 0.753 - 0.939) for the combined aortic valve and mitral valve replacement, indicating that the risk models were good in predicting hospital mortality for surgeries. CONCLUSION: The three risk models can quantitatively assess the hospital mortality risk in the patients treated with cardiac valve replacement.

The unidirectional valve patch provides no benefits to early and long-term survival in patients with ventricular septal defect and severe pulmonary artery hypertension.

OBJECTIVE: Our aim was to test whether a unidirectional valve patch would provide benefit to early and long-term survival for patients with ventricular septal defect and severe pulmonary artery hypertension. METHODS: Eight hundred seventy-six cases of ventricular septal defect with severe pulmonary artery hypertension were closed with or without a unidirectional valve patch and were classified as the unidirectional valve patch (UVP) group (n = 195) and nonvalve patch (NVP) group (n = 681), respectively. Propensity scores of inclusion into the UVP group were used to match 138 pairs between the 2 groups. Kaplan-Meier survival curves were constructed to compare early and long-term survival. RESULTS: For the 138 propensity-matched pairs, there were 7 and 9 early deaths (in-hospital deaths) in the UVP and NVP groups, respectively. The difference in early mortality between the 2 groups did not reach statistical significance (chi(2) = 0.265, P = .6064). With a mean of 9.2 +/- 4.92 years' and 2511 patient-years' follow-up, there were 6 late deaths in the UVP group and 7 late deaths in the NVP group. The difference in actuarial survival at 5, 10, 15, and 18 years between the 2 groups was not significant (log-rank test, chi(2) = 0.565, P = .331). The difference in the late mortality between the groups with or without a patent patch at the time of discharge did not reach statistical significance (chi(2) = 1.140, P = .2856). There was no difference between the 2 groups in the 6-minute walk distance assessed at the last follow-up (525.9 +/- 88.0 meters for the UVP group and 536.5 +/- 95.8 meters for the NVP group, F = 1.550, P = .214). CONCLUSION: A unidirectional valve patch provides no benefits to early and long-term survival when it is used to deal with ventricular septal defect and severe pulmonary artery hypertension.

Evaluation of left ventricular diastolic function after edge-to-edge mitral valve plasty.

BACKGROUND: Edge-to-edge mitral valve plasty technique has been widely used to treat bileaflet prolapse. This procedure anchors the correspondence leaflets to create a double-orifice mitral valve. The original mitral valve anatomy is changed, and the opening of mitral valve is restricted. Little is known whether this procedure affects the left ventricular diastolic function. METHODS: Thirty patients with mitral regurgitation were included in this study. Fifteen with posterior leaflet prolapse received quadrangular resection (group 1), 15 with anterior or bileaflet prolapse underwent edge-to-edge procedure (group 2). Acute hemodynamics was monitored with a Swan-Ganz catheter (Edwards Lifesciences LLC, Irvine, CA, USA). Left ventricular diastolic function was also evaluated with echocardiography in 28 patients with sinus rhythm. The ratio of peak E velocity and A velocity (E/A), the ratio of early diastolic peak flow velocity to early diastolic mitral annular movement velocity (E/Em), and the ratio of early diastolic mitral annular velocity to late diastolic mitral annular velocity (Em/Am) were measured before operation and one week after operation. RESULTS: Mitral valve area and mitral regurgitate grade decreased significantly after operation. There was no significant change in pulmonary artery wedge pressure between two groups and in each group before and after operation. Echocardiography evaluation showed there was no significant difference in E/A, E/Em, and Em/Am before and after operation between two groups and in each group. CONCLUSION: Edge-to-edge mitral valve plasty procedure has no significant impairment on left ventricular diastolic function. A double-orifice mitral valve has similar hemodynamic behavior with a physiological valve.

Utilization of the edge-to-edge valve plasty technique to correct severe tricuspid regurgitation in patients with congenital heart disease.

OBJECTIVE: Tricuspid regurgitation is often associated in patients with congenital heart disease. Significant morbidity and mortality are related to tricuspid valve replacement. Tricuspid valve plasty is still a preferred choice. This report deals with our surgical experience in using the edge-to-edge valve plasty technique to correct severe tricuspid regurgitation in patients with congenital heart disease. METHODS: From December 2002 to August 2007, severe tricuspid regurgitation was corrected with a flexible band annuloplasty and edge-to-edge valve plasty technique in nine patients with congenital heart disease. The age ranged from 7 to 62 years (average 24.4 years). Congenital cardiac anomalies included atrioventricular canal in five cases, secundum atrial septal defect in three cases, and cor triatriatum in one case. RESULTS: No hospital death or postoperative morbidity occurred. No or trivial tricuspid regurgitation was present in six cases and mild tricuspid regurgitation in three cases at discharge. The follow-up ranged from 12 months to 70 months (average 39.3 months). No tricuspid stenosis was found. No to mild tricuspid regurgitation was present in eight cases, and moderate tricuspid regurgitation in one case at the latest follow-up. CONCLUSIONS: Edge-to-edge valve plasty is an easy, effective, and acceptable additional procedure to correct severe tricuspid regurgitation in patients with congenital heart disease.

[Prognosis of patients with chronic thromboembolic pulmonary hypertension receiving conservative or operative treatments according to a new clinical classification scheme].

OBJECTIVE: To compare the efficacy of conservative or pulmonary thromboendarterectomy (PTE) therapy for chronic thromboembolic pulmonary hypertension (CTEPH) patients according to a new clinical classification scheme. METHODS: This retrospective study analyzed 63 cases of CTEPH admitted to our hospital from February 1995 to October 2007 and 45 cases were treated surgically (Group A) and 18 cases received conservative therapy (Group B). Results were analyzed using Fisher exact test and t test according to San Diego medical center quartering classification scheme and Anzhen Hospital modified bifurcate classification scheme. RESULTS: There were 6 operational deaths in Group A and 2 deaths during hospital stay in Group B. During follow-ups (mean 3.6 +/- 2.5 years), there were 4 deaths in Group A and 9 deaths in Group B. the totality survival rate is significantly higher in Group A than that in Group B (P < 0.05). For patients with San Diego Type I CTEPH, survival rate was significantly higher in Group A compared with Group B (P = 0.009) and was similar for patients with type II and III and IV CTEPH between the two groups (P = 0.338, 0.455, 0.800). Survival rate was significantly higher in Group A than that in Group B for patients with Anzhen central type CTEPH (P = 0.009), but was similar between the two groups for patients with Anzhen peripheral type CTEPH (P = 0.125). The Kaplan-Meier survival curve 5 years survival rate in the Group A was (91.7 +/- 8.0)% for Anzhen central type and (76.0 +/- 8.5)% for Anzhen peripheral type (P = 0.04), and the 5 years Kaplan-Meier survival rate in the Group B was (42.9 +/- 18.7)% for Anzhen central type and (56.2 +/- 10.8)% for Anzhen peripheral type (P = 0.851). CONCLUSION: Anzhen Hospital modified bifurcate classification scheme is a simple and effective classification to predict the prognosis and choose treatment method of CTEPH.

[The clinical analysis of 54 cases for the surgical treatment of pulmonary embolism].

OBJECTIVE: To evaluate the results of surgical procedures for pulmonary embolism. METHODS: Fifty-four patients of pulmonary embolism received surgical treatment from October 1994 to June 2007, of which 9 were acute pulmonary embolism underwent pulmonary embolectomy and 45 patients were chronic thromboembolic pulmonary hypertension (CTEPH) underwent pulmonary thromboendarterectomy. RESULTS: The mortality rate was 44.4% in acute pulmonary embolism group and 13.3% in CTEPH group (P < 0. 05). Thirteen patients had residual pulmonary hypertension and 23 patients had severe pulmonary reperfusion injury postoperatively. The pulmonary artery systolic pressure changed from (89.4 +/- 36.3) mm Hg (1 mm Hg =0.133 kPa) preoperative to (55.6 +/- 22.4) mm Hg postoperative. The pulmonary vascular resistance changed from (89. 7 +/- 56.7) kPa L(-1) S(-1) preoperative to (38.9 +/- 31.1) kPa L(-1) S(-1) postoperative. The arterial partial pressure of oxygen changed from (52. 3 +/- 6.7 ) mm Hg preoperative to (87.6 +/- 6.5) mm Hg postoperative. The arterial oxygen saturation changed from (88.9 +/- 4.5)% preoperative to (95.3 +/- 2.8 )% postoperative (P < 0.05). With the follow-up of (41.8 +/- 36.4) months, there were 4 patients died. According to NYHA, there were 28 patients for class I , 10 patients for class II and 2 patients for class III. According to Kaplan-Meier survival curve, the 3-year, 4-year, 5-year and 8-year survival rate were (97.1 +/- 2.8 )%, (94.0 +/- 4.1)%, (90.8 +/- 5.2)% and (85.0 +/- 7.3)% respectively. Linear rate of bleeding and thromboembolic related to anticoagulation were 0. 63% patient-years and 0. 62% patient-years respectively. CONCLUSIONS: The operational mortality of acute pulmonary embolism is significantly higher than CTEPH, and the mid-long term survival rate is agreeable and the complication rate related to anticoagulation is relatively low.

Concomitant irrigated monopolar radiofrequency ablation of atrial fibrillation in adults with congenital heart disease.

Atrial fibrillation is the most frequent form of atrial arrhythmias in adults with congenital heart disease. Some serious complications are related with the presence of atrial fibrillation after surgery. Because of the complexity and the risk of bleeding, the Maze III procedure has been largely replaced by alternative energy sources. Our experience in using irrigated monopolar radiofrequency ablation to treat atrial fibrillation in adults with congenital heart disease is reported. Seven patients with congenital heart disease and atrial fibrillation underwent irrigated monopolar radiofrequency ablation. All patients were confirmed in permanent fibrillation preoperatively. Six were adult atrial septal defect patients and one was an adult patent ductus arteriosus patient. All patients survived the procedure and discharged in sinus rhythm. There were no complications related to radiofrequency ablation. The time of ablation ranged from 17 to 22 min (average 19.5 min). Follow-up ranged from 3 to 48 months. One patient with mitral valve replacement (MVR) died of cerebral hemorrhage 13 months after surgery. The last electrocardiogram showed that six patients were in sinus rhythm and one patient in junctional rhythm. Irrigated monopolar radiofrequency ablation is an easy, effective, safe and economic concomitant operation to eliminate atrial fibrillation in adult patients with congenital heart defect and atrial fibrillation.