The adipocyte-enriched secretory protein tetranectin exacerbates type 2 diabetes by inhibiting insulin secretion from ß cells.

Pancreatic ß cell failure is a hallmark of diabetes. However, the causes of ß cell failure remain incomplete. Here, we report the identification of tetranectin (TN), an adipose tissue-enriched secretory molecule, as a negative regulator of insulin secretion in ß cells in diabetes. TN expression is stimulated by high glucose in adipocytes via the p38 MAPK/TXNIP/thioredoxin/OCT4 signaling pathway, and elevated serum TN levels are associated with diabetes. TN treatment greatly exacerbates hyperglycemia in mice and suppresses glucose-stimulated insulin secretion in islets. Conversely, knockout of TN or neutralization of TN function notably improves insulin secretion and glucose tolerance in high-fat diet-fed mice. Mechanistically, TN binds with high selectivity to ß cells and inhibits insulin secretion by blocking L-type Ca2+ channels. Our study uncovers an adipocyte-ß cell cross-talk that contributes to ß cell dysfunction in diabetes and suggests that neutralization of TN levels may provide a new treatment strategy for type 2 diabetes.

Exogenous Tetranectin Alleviates Pre-formed-fibrils-induced Synucleinopathies in SH-SY5Y Cells by Activating the Plasminogen Activation System.

Parkinson's disease (PD) is a common neurodegenerative disease. Previously we identified tetranectin (TN) as a differentially expressed protein in the cerebrospinal fluid of PD patients, and we were surprised to find that TN knockout mice developed PD features. However, the specific role of TN in PD has not been clarified. In this study, we aimed to determine the effect of exogenous TN on cellular PD models and elucidate the underlying mechanisms. We found that exogenous TN could alleviate pre-formed-fibrils (PFFs)-induced synucleinopathies in SH-SY5Y cells and reduce the cell-to-cell transmission of α-synuclein (SYN). We also found that TN can promote the degradation of SYN by plasmin, which may account for its effect on cellular PD models. Moreover, administration of SYN/PFFs decreased the expression of TN and increased the expression of plasminogen activator inhibitor-1 (PAI-1) in SH-SY5Y cells, thereby reducing plasmin activity. Our findings depict a possible SYN-TN-plasmin interaction in which elevated levels of extracellular SYN monomers and aggregates in PD diminish the production of TN and PAI-1. Such changes lead to a reduced plasmin activity, which in turn reduces the degradation of extracellular SYN, thus forming a vicious cycle.

BNP and NT-proBNP Concentrations in Paired cerebrospinal Fluid and Plasma Samples of Patients with Traumatic Brain Injury.

BACKGROUND: The aim of this study was to investigate the secretion patterns of brain natriuretic peptide (BNP) and N-terminal-proBNP (NT-proBNP) after traumatic brain injury (TBI) and to analyze the source of them in cerebrospinal fluid (CSF). MATERIALS AND METHODS: We synchronously measured BNP and NT-proBNP concentrations in paired CSF and plasma samples from 22 moderate to severe TBI patients and 40 healthy control patients. The CSF and/or plasma ratio of albumin (QAlbumin) was calculated daily. The BNP and NT-proBNP levels of CSF and plasma were compared between TBI patients and control patients. RESULTS: CSF BNP and NT-proBNP levels peaked on day 3 after injury, as did the plasma BNP and NT-proBNP levels. The CSF BNP and NT-proBNP levels in TBI patients were elevated from day 1, which was significantly higher than control group (P < 0.05 and P < 0.01, respectively). However, in plasma, only NT-proBNP levels were significantly higher than in the control group from day 2 (P < 0.05). In addition, QBNP, defined as CSF BNP concentration and/or plasma BNP concentration, was significantly higher in TBI patients than in the control group (P < 0.01). However, QAlbumin remained within ranges of a mild to moderate dysfunction of blood-brain-barrier in TBI patients. CONCLUSIONS: CSF BNP concentrations are elevated and peak on day 3 after moderate to severe TBI. CSF BNP may originate from the brain and may be a potential biomarker of TBI.

Optic Nerve Sheath Measurements by Computed Tomography to Predict Intracranial Pressure and Guide Surgery in Patients with Traumatic Brain Injury.

BACKGROUND: Research has shown that the optic nerve sheath diameter (ONSD) is a good predictor of intracranial pressure (ICP) and may predict the need for surgery in patients with head injury. The objective was to test the value of ONSD in predicting the requirement for surgery in patients with traumatic brain injury (TBI). METHODS: In this retrospective cohort study, we first verified the correlation between ICP and ONSD using data from 62 patients with TBI who had undergone ICP monitoring. Second, we analyzed head computed tomography images from patients with TBI who were admitted to the emergency department where patients had been divided into surgery or conservative treatment groups, dependent on the assessment of a neurosurgeon. The correlation between ICP and ONSD was measured using linear regression analysis. Biologistic and receiver operating characteristic curve analyses were used to test the diagnostic value of ONSD to predict surgery. RESULTS: ONSD was significantly correlated with ICP (r = 0.606; P < 0.01), and there was a significant linear regression equation (y = 0.071 × ICP + 3.533; P < 0.01), with ONSD predicting the requirement for surgery in patients with TBI (area under the curve, 0.920; P < 0.01; 95% confidence interval, 0.877-0.962). CONCLUSIONS: ONSD measured via head computed tomography correlates with ICP and can predict the requirement for surgery in patients with TBI following admission to the emergency department.

Exogenous Tetranectin Protects Against 1-Methyl-4-Phenylpyridine-Induced Neurotoxicity by Inhibiting Apoptosis and Autophagy Through Ribosomal Protein S6 Kinase Beta-1.

BACKGROUND: Tetranectin is a secreted homotrimeric protein belonging to the C-type lectin family. Our previous studies found that tetranectin was not only related to, but also played a protective role in, Parkinson disease. In this study, we aim to illustrate the molecular mechanism of the secreted tetranectin. METHODS: We used exogenous tetranectin to investigate the function and molecular mechanism of secreted tetranectin in a 1-methyl-4-phenylpyridine (MPP+)-induced SH-SY5Y cell model. Cell viability and reactive oxygen species were measured to assess the protective effects of tetranectin against MPP+. Apoptosis was measured in several aspects, including Bcl-2/Bax expression, caspase-3/7 activity, annexin V staining, and nuclear morphology. Autophagy was measured as LC3 expression and autophagy flux. Moreover, we used cell immunofluorescence to detect the transport of tetranectin. Western blotting was performed to measure the phosphorylation level of ribosomal protein S6 kinase beta-1 (p70S6K1), and co-immunoprecipitation was applied to confirm the interaction between tetranectin and p70S6K1. RESULTS: The data showed exogenous tetranectin alleviated MPP+-induced toxicity, high reactive oxygen species levels, apoptosis, and autophagy and changed the phosphorylation level of p70S6K1. Immunofluorescence images suggested exogenous tetranectin could be taken into SH-SY5Y cells, and the co-immunoprecipitation experiment indicated tetranectin interacted with p70S6K1. CONCLUSIONS: Exogenous tetranectin protects against MPP+-induced neurotoxicity by promoting p70S6K1 phosphorylation once taken into SH-SY5Y cells.

Neuroprotective effect of docosahexaenoic acid in rat traumatic brain injury model via regulation of TLR4/NF-Kappa B signaling pathway.

OBJECTIVE: The experiments were conducted to prove that docosahexaenoic acid (DHA) alleviates traumatic brain injury (TBI) through regulating TLR4/NF-Kappa B signaling pathway. METHODS: Bioinformatic analysis was performed using published data from Gene Expression Omnibus (GEO) database to investigate differentially expressed genes and signaling pathways. Controlled cortical impact (CCI) injury rat model was built, and DHA (16 mg/kg in DMSO, once each day) was used to treat TBI rats. Neurological severity score (NSS) and beam walking test and rotarod test were used to confirm whether DHA is neuron-protective against TBI. The expression of TLR4, NF-Kappa B p65, (TNF)-α and IL-1ß were examined by qRT-PCR and western blot. The impact of DHA on neurocyte apoptosis was validated by TdT-mediated dUTP Nick-End Labeling (TUNEL) staining. The influence of DHA on CD11b and GFAP expression in the hippocampus was determined through immunohistochemical analysis. RESULTS: TLR4/NF Kappa B pathway was suggested to be closely correlated with TBI by bioinformatic analysis. DHA could improve the neurological function and learning and memory ability of rats after TBI as well as promote neurocytes from apoptosis. TLR4 expression and the expression of inflammatory mediator NF-Kappa B were also repressed by DHA treatment. CONCLUSIONS: DHA exerted a neuron-protective influence in a rat model of TBI via repressing TLR4/NF-Kappa B pathway.

Mortality and Outcome Comparison Between Brain Tissue Oxygen Combined with Intracranial Pressure/Cerebral Perfusion Pressure-Guided Therapy and Intracranial Pressure/Cerebral Perfusion Pressure-Guided Therapy in Traumatic Brain Injury: A Meta-Analysis.

BACKGROUND: The combination of brain tissue oxygen and standard intracranial pressure (ICP)/cerebral perfusion pressure (CPP)-guided therapy is thought to improve traumatic brain injury (TBI) prognosis compared with standard ICP/CPP-guided therapy. However, related results of previous observational studies and recently published cohort studies and randomized controlled trials (RCTs) remain controversial. The objective of this study was to compare the effect of the combined therapy with that of standard ICP/CPP-guided therapy on mortality rate, favorable outcome, ICP/CPP, and length of stay (LOS). METHODS: We systematically searched PubMed, Embase, Cochrane Library, ClinicalTrials.gov, and Web of Science in July 2016 for studies comparing the combined therapy and standard ICP/CPP-guided therapy. Random-effect and fixed-effect models were used for pooled analyses. RESULTS: After screening 362 studies, 8 cohort studies and 1 RCT were included. Primary outcomes were mortality and favorable outcome. The overall mortality risk ratio showed no obvious advantages between the 2 groups (risk ratio [RR], 0.76; 95% confidence interval [CI], 0.54-1.06) and discharge mortality (RR, 1.01; 95% CI, 0.80-1.26) and 3-month mortality (RR, 0.77; 95% CI, 0.53-1.12). Compared with the ICP/CPP group, the combined group was more likely to achieve better outcome during the 6 months after TBI (RR, 1.26; 95% CI, 1.04-1.52) or exactly at 6 months (RR, 1.34; 95% CI, 1.07-1.68), whereas ICP (standardized mean difference [SMD], -0.19; 95% CI, -0.43 to 0.05), CPP (SMD, 0.13; 95% CI, -0.09 to 0.35), and LOS (SMD, 0.13; 95% CI, -0.11 to 0.37) showed no obvious differences. CONCLUSIONS: Compared with standard ICP/CPP-guided therapy, brain tissue oxygen combined with ICP/CPP-guided therapy improved long-term outcomes without any effects on mortality, ICP/CPP, or LOS.

KLF8 Promotes Temozolomide Resistance in Glioma Cells via ß-Catenin Activation.

BACKGROUND/AIMS: The transcription factor Krüppel-like factor (KLF) 8 plays important roles in tumorigenesis and tumor metastasis. However, the relationship between KLF8 and glioma cell chemoresistance is not known. METHODS: The effects of KLF8 on glioma cell proliferation, apoptosis and chemosensitivity to temozolomide (TMZ) were analyzed by Cell Counting Kit 8 assay and flow cytometry assay. A xenograft model was used to study the effect of KLF8 on tumor growth and sensitivity to TMZ. RESULTS: We found that in the absence of KLF8, glioma cells showed greater sensitivity to TMZ, resulting in the inhibition of cell growth and enhanced apoptosis. KLF8 overexpression had the opposite effect; that is, cell resistance to TMZ was increased, which was associated with ß-catenin activation. CONCLUSION: Taken together, these data suggest that KLF8 modulates glioma cell resistance to TMZ via activation of ß-catenin; therefore, therapies that inhibit KLF8 levels in glioma can enhance the efficacy of TMZ treatment.

Is Intracranial Pressure Monitoring of Patients With Diffuse Traumatic Brain Injury Valuable? An Observational Multicenter Study.

BACKGROUND: Although intracranial pressure (ICP) monitoring of patients with severe traumatic brain injury (TBI) is recommended by the Brain Trauma Foundation, any benefits remain controversial. OBJECTIVE: To evaluate the effects of ICP monitoring on the mortality of and functional outcomes in patients with severe diffuse TBI. METHODS: Data were collected on patients with severe diffuse TBI (Glasgow Coma Scale [GCS] score on admission <9 and Marshall Class II-IV) treated from January 2012 to December 2013 in 24 hospitals (17 level I trauma centers and 7 level II trauma centers) in 9 Chinese provinces. We evaluated the impact of ICP monitoring on 6-month mortality and favorable outcome using propensity score-matched analysis after controlling for independent predictors of these outcomes. RESULTS: ICP monitors were inserted into 287 patients (59.5%). After propensity score matching, ICP monitoring significantly decreased 6-month mortality. ICP monitoring also had a greater impact on the most severely injured patients on the basis of head computed tomography data (Marshall computed tomography classification IV) and on patients with the lowest level of consciousness (GCS scores 3-5). After propensity score matching, monitoring remained nonassociated with a 6-month favorable outcome for the overall sample. However, monitoring had a significant impact on the 6-month favorable outcomes of patients with the lowest level of consciousness (GCS scores 3-5). CONCLUSION: ICP monitor placement was associated with a significant decrease in 6-month mortality after adjustment for the baseline risk profile and the monitoring propensity of patients with diffuse severe TBI, especially those with GCS scores of 3 to 5 or of Marshall computed tomography classification IV.

Tetranectin gene deletion induces Parkinson's disease by enhancing neuronal apoptosis.

Parkinson's disease (PD) is a chronic neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). We previously identified tetranectin (TET) as a potential biomarker for PD whose expression is downregulated in the cerebrospinal fluid of PD patients. In the present study, we investigate the role of TET in neurodegeneration in vitro and in vivo. Our results showed that siRNA knockdown of TET decreased cell viability and the number of tyrosine hydroxylase (TH) positive cells, whereas it increased caspase-3 activity and the Bax/Bcl-2 ratio in cultured primary dopaminergic neurons. Overexpression of TET protected dopaminergic neurons against neuronal apoptosis in 1-methyl-4-phenylpyridinium cell culture model in vitro. In TET knockdown mouse model of PD, TET gene deletion decreased the number of TH positive cells in the SNpc, induced apoptosis via the p53/Bax pathway, and significantly impaired the motor behavior of transgenic mice. The findings suggest that TET plays a neuroprotective role via reducing neuron apoptosis and could be a valuable biomarker or potential therapeutic target for the treatment of patients with PD.

BQ-869, a novel NMDA receptor antagonist, protects against excitotoxicity and attenuates cerebral ischemic injury in stroke.

Stroke is one of the three diseases that cause human death in current world, and it is the common, frequently occurring disease in the middle-old ages. NMDA receptors mediate glutamate-induced cell death when intensely or chronically activated, which is an important cause of neuronal cell death after acute injuries. Here, we demonstrated that BQ-869, a potent NMDA receptor antagonist, blocked NMDA receptor in concentration-dependent and dose-dependent manner, attenuated NMDA-induced Ca(2+) influx, inhabited NMDAR-mEPSC in hippocampal pyramidal neurons, improved athletic ability of rats with MACO, decreased infarction size in focal cerebral ischemia rats and reduced stroke mortality. Taken together, our data demonstrate the neuroprotective effect of BQ-869 might be through inhibiting NMDA-mediated excitotoxicity. These findings indicate that BQ-869 is the most potent antagonist of NMDA receptors, and provide new insights with potential therapeutic applications for the treatment of stroke.

Tetranectin knockout mice develop features of Parkinson disease.

BACKGROUND/AIMS: Aggregation of insoluble α-synuclein to form Lewy bodies (LBs) may contribute to the selective loss of midbrain dopaminergic neurons in Parkinson disease (PD). Lack of robust animal models has impeded elucidation of the molecular mechanisms of LB formation and other critical aspects of PD pathogenesis. METHODS: We established a mouse model with targeted deletion of the plasminogen-binding protein tetranectin (TN) gene (TN(-/-)) and measured the behavioral and histopathological features of PD. RESULTS: Aged (15-to 20-month-old) TN(-/-) mice displayed motor deficits resembling PD symptoms, including limb rigidity and both slower ambulation (bradykinesia) and reduced rearing activity in the open field. In addition, these mice exhibited more numerous α-synuclein-positive LB-like inclusions within the substantia nigra pars compacta (SNc) and reduced numbers of SNc dopaminergic neurons than age-matched wild type (WT) mice. These pathological changes were also accompanied by loss of dopamine terminals in the dorsal striatum. CONCLUSION: The TN(-/-) mouse exhibits several key features of PD and so may be a valuable model for studying LB formation and testing candidate neuroprotective therapies for PD and other synucleinopathies.

Proteomic analysis of the cerebrospinal fluid of Parkinson's disease patients pre- and post-deep brain stimulation.

AIMS: To investigate alterations in protein expression associated with deep brain stimulation (DBS) in an attempt to elucidate possible mechanisms of action . METHODS: Cerebrospinal fluid (CSF), obtained from six Parkinson's disease (PD) patients (pre- and post-DBS) and from six normal healthy controls, was studied for differentially expressed proteins. 2-D DIGE, in combination with MALDI-TOF and TOF-TOF Mass Spectrometry (MS) or ESI-MS, was used to identify the changed proteins (3 PD patients and 3 controls). Selected proteins were further studied using western blotting (6 PD patients and 6 controls). RESULTS: Twenty-one proteins were identified after MS and protein database interrogation. Apart from apolipoprotein A-I (apoA-I), the expression levels of complement C4 (C4), IgA, tetranectin, and extracellular superoxide dismutase (EC-SOD), detected by western blotting, correlated well with the 2-D DIGE results. In the follow-up period, the expression levels of C4, apoA-I and IgA were stable whereas EC-SOD and tetranectin were significantly elevated. In addition, when DBS was ceased in one patient due to a suicide attempt, the levels of EC-SOD and tetranectin significantly decreased. CONCLUSION: Our preliminary results suggest that variations in the expression levels of EC-SOD and tetranectin in CSF is related to DBS.

Validating the incidence of coagulopathy and disseminated intravascular coagulation in patients with traumatic brain injury--analysis of 242 cases.

OBJECTIVES: To estimate the incidence of coagulopathy and disseminated intravascular coagulation (DIC) in patients with traumatic brain injury (TBI) and to investigate its relationship to patient outcome. DESIGN: A prospective observational study. MEASUREMENTS AND MAIN RESULTS: From January 2007 to June 2009, 242 consecutive adult patients with TBI seen in three independent hospitals were recruited. Glasgow Coma Score (GCS) on admission, platelet counts (PLT), prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FIB), D-dimer (D-DT) and DIC scores were recorded for each case on admission. Clinical outcome was measured according to the Glasgow Outcome Scale (GOS) at 3 months after injury. Statistical analysis was carried using Student's t-test, one-way analysis of variance (ANOVA), and Tudey test. Coagulation abnormalities were present in approximately 50% of patients with TBI. Prolonged PT and increased D-DT and FIB levels occurred in patients with more severe brain injury and poorer outcome, and these findings were statistically significant. CONCLUSIONS: Coagulation changes, particularly the incidence of DIC, may occur within 6 h after TBI and are more pronounced in patients with severe injuries and poor outcome. PT, D-DT levels and more comprehensively a DIC scores may be useful prognostic indicators in patients with TBI.

[Reoperative valve replacement in patients undergoing cardiac reoperation: a report of 104 cases].

OBJECTIVE: To review the experience of reoperative valve replacement for 104 patients. METHODS: From January 2002 to December 2009, 104 patients underwent heart valve replacement in reoperations, accounting for 2.92% of the total patient population (3557 cases) who had valve replacement during this period. In this group, 53 male and 51 female patients were included with a median age of 46 years (ranged from 13 to 72 years). The reasons of reoperation included 28 cases suffered from another valve lesion after valve replacement, 10 cases suffered from valve lesion after mitral valvuloplasty, 19 cases suffered from perivalvular leakage after valve replacement, 18 cases suffered from valve lesion after previous correction of congenital heart defect, 7 cases suffered from bioprosthetic valve decline, 10 cases suffered from prosthetic valve endocarditis, 9 cases suffered from dysfunction of machine valve, and 3 cases suffered from other causes. The re-operations were mitral and aortic valve replacement in 2 cases, mitral valve replacement in 59 cases, aortic valve replacement in 24 cases, tricuspid valve replacement in 16 cases, and Bentall's operation in 3 cases. The interval from first operation to next operation was 1 month-19 years. RESULTS: There were 8 early deaths from heart failure, renal failure and multiple organ failure (early mortality 7.69%). Major complications were intraoperative hemorrhage in 2 cases, re-exploration for mediastinal bleeding in 2 cases and sternotomy surgical site infection in 1 case. Complete follow-up (3 months-7 years and 2 months) was available for all patients. Two patients died, one patient died of intracranial hemorrhage, and another cause was unknown. CONCLUSION: Satisfactory short-term and long-term results can be obtained in reoperative valve replacement with appropriate timing of operation control, satisfactory myocardial protection, accurate surgical procedure and suitable perioperative treatment.

Transcatheter closure of multi-hole perimembranous VSD with aneurysm: 3-year follow-up study.

The majority of ventricular septal defects (VSDs) are perimembranous, accounting for 75-80% of all VSDs. The objective of this study was to investigate occluder selection and transcatheter closure technique for multi-hole perimembranous VSD with aneurysm, and to evaluate clinical efficacy and safety. Patients with multi-hole VSDs and aneurysm (n = 64) were selected for the procedure using transthoracic echocardiography. Double-disc symmetrical, small-waist double-disc asymmetrical and zero eccentricity occluders were selected based on left ventricular angiography. The closure was successful in 63 of 64 patients (98%). The double-disc symmetrical occluder was used in 16 cases, the small-waist double-disc asymmetrical occluder in 42 cases, and the zero eccentricity occluder in 8 cases (2 occluder types were used in 2 cases). Fifteen minutes after the procedure, 52 cases had no residual shunt and 12 had a trace amount of residual shunt. The residual shunt disappeared in five cases 5-7 days post procedure, with a trace amount of shunt remaining in seven cases. Transient conduction abnormalities related to the procedure occurred in six patients; however, none required permanent pacemaker implantation. At the 1-month, 6-month, 1-year, 2-year, and 3-year follow-up visits, echocardiography indicated that the position of the occluders was fixed, and there were no complications including residual shunt, newly developed atrioventricular block, thromboembolism, or bacterial endocarditis. The study results indicate that left ventricular angiography is useful in selecting the most appropriate device for transcatheter closure of multi-hole perimembranous VSD with aneurysm. The transcatheter closure procedure is safe and effective with little residual shunt and no major complications for up to 3 years of follow-up.

[Experiences on surgical treatment of severe aortic valve stenosis: a report of 171 cases].

OBJECTIVE: To analyze the experiences on surgical treatment of severe aortic valve stenosis. METHODS: From December 1990 to December 2006, 171 patients with severe aortic valve stenosis underwent aortic valve replacement (AVR). There were 135 males and 36 females aged from 10 to 75 years old, with a mean of (45.8 +/- 15.6) years old. The intervals between the first episode of exertion dyspnea and administration to operation were 2 months to 52 years. The pathological lesions of the group were rheumatic aortic valve stenosis in 75 cases, calcified aortic stenosis in 66 cases, bicuspid aortic valve in 26 cases and other congenital aortic valve stenosis in 4 cases. One hundred and twenty-four patients underwent AVR, 7 AVR combined with replacement of the ascending aorta, 5 AVR with coronary artery bypass grafting, 19 AVR with mitral valve plasty (MVP), 8 AVR with plasty of the ascending aorta and 8 AVR with enlargement of the aortic root. RESULTS: The averaged operation time was (4.4 +/- 0.6) h. Cardiopulmonary bypass (CPB) time was (124.7 +/- 38.5) min and the aorta clamp time was (78.3 +/- 21.7) min. The averaged blood loss during operation was (754.5 +/- 518.4) ml. All the procedures were successfully performed and all patients were weaned off CPB uneventfully. The indication of early complications was 12.3% (21/171), including low cardiac output syndrome in 7 cases, multi-organ failure in 3 cases, endocarditis in 1 case, renal dysfunction in 4 cases, ventricular fibrillation in 1 case, excessive bleeding in 2 cases, III atrial-ventricular block in 2 cases, and mediastinal infection in 1 case. The total mortality was 5.8% (10/171) with the main causes as cardiac failure for 4 cases, arrhythmia for 1 case, multi-organ failure for 4 cases, and infectious endocarditis for 1 case. CONCLUSIONS: Successful management of severe aortic valve stenosis requires sophisticated surgical techniques and experienced peri-operative care. Satisfactory results can be achieved if valve replace surgery is performed adequately.

[Aortic valve replacement: the experiences of 1026 cases].

OBJECTIVE: To study the changes in pathogenic causes and the prognosis of aortic valve replacement (AVR). METHODS: The clinical data of 1026 patients undergoing AVR from December 1980 to December 2006 were analyzed retrospectively. The mortality, morbidity, changes in pathogenic causes and risk factors were analyzed. RESULTS: The postoperative mortality and complication morbidity were 4.3% and 10.6% respectively within 30 days followed operation. Main causes of operative death were heart failure, multi organ failure and endocarditis. The major risk factors for operative death were left ventricle ejection fraction less than 0.4, endocarditis, valve regurgitation and emergency operation before AVR. Late mortality was 0.54% patient-year (3.4%), most of whom died of heart failure, endocarditis and arrhythmias. Patients underwent reoperation 0.22% patient-year (1.4%), with the causes of endocarditis and perivalvular fistula. CONCLUSIONS: Morbidity of rheumatic damage in aortic valve has decreased, while valve degeneration has increased gradually in the recent years. Avoiding prosthesis-patient mismatch, good postoperatively guide and prevention of endocarditis can improve the prognosis of AVR.

[Diagnosis and surgical management of primary cardiac neoplasms].

OBJECTIVE: To review and summarize the experience in diagnosis and surgical management of primary cardiac neoplasms. METHODS: 112 patients with primary cardiac neoplasms were treated surgically from Jan. 1980 to Jan. 2005. Those tumors were grouped into three categories: myxomas (98), benign nonmyxomas (3), and malignant tumors (11). Five of 11 malignant tumor patients underwent biopsy or palliative operation, the other patients received complete excision. Mitral valve replacement were done simultaneously in 2 of these patients, mitral valve repair in 4 and tricuspid valvoplasty in 33. All patients' diagnosis was confirmed by echocardiography. RESULTS: 108 patients survived the operation and 4 patients died postoperatively. The hospital mortality was 3.6% (4/112). Two patients developed poor left ventricular function postoperatively and died at the third and the seventh postoperative day due to low cardiac output. One patient developed and died of progressive hepatic and renal function failure postoperatively. Another one patient died of severe arrhythmia. Mean follow-up of 76 myxoma patients who are still alive was 6.4 years (range, 3 month to 17 years). Fifty-five patients still had heart function in New York Heart Association class I and 21 in class II at the end of follow-up without any evidence of recurrance. The follow-up results of benign nonmyxomas were similar to those of myxomas. Mean follow-up of all survived malignant tumor patient was 6 months (range, 2 months to 12 months). Ten of them died of recurrence or metastasis within 1 year postoperatively except only one still alive. CONCLUSION: Surgical resection, whenever possible, is the first treatment choice for all kinds of primary cardiac tumors. Surgical resection of myxoma and benign nonmyxoma can give excellent long-term results which may lead to eventual cure of myxoma and benign nonmyxoma. For malignant tumor patient, surgical treatment is only palliative and to prolong the life of patients.