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ABSTRACT: Ghrelin has been reported to protect the cardiovascular system; however, the cardioprotective effect of ghrelin against cardiopulmonary bypass (CPB) induced myocardial injury are unclear. In this study, the protective effect of ghrelin on CPB induced myocardial injury and the underlying mechanisms were investigated.
Adult male rats were subjected to CPB and randomly to receive vehicle (n = 8), ghrelin (n = 8), ghrelin plus [D-Lys3]-GHRP-6, a GHSR-1a inhibitor (n = 8), or ghrelin plus wortmannin, a phosphoinositide 3'-kinase (PI3K) inhibitor (n = 8). In vitro study was performed on cultured cardiomyocytes subjected to simulated cardiopulmonary bypass (SCPB). Ghrelin attenuated the inflammatory response, as evidenced by reduced induction of TNF-α, IL-6 and myocardial myeloperoxidase activity and concurrent reduction in apoptosis, oxidative stress, and levels of myocardial injury markers following CPB. Moreover, ghrelin significantly increased cardiac function after CPB. In cultured cardiomyocytes subjected to simulated CPB, ghrelin increased cell viability and decreased the percentage of apoptotic myocytes. Inhibition of ghrelin downstream signaling blocked the cardioprotective effects both in vivo and vitro.
Ghrelin could provide an effective approach to the attenuation of CPB induced myocardial injury. The cardioprotective effects elicited by ghrelin may contribute to the inhibition of inflammatory response through the Akt-activated pathway.
PLoS ONE 01/2013; 8(1):e55021. · 4.09 Impact Factor
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Weixun Duan,
Yang Yang,
Wei Yi,
Juanjuan Yan,
Zhenxin Liang,
Ning Wang,
Yue Li,
Wensheng Chen, Shiqiang Yu,
Zhenxiao Jin,
Dinghua Yi
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ABSTRACT: Previous studies have shown that the JAK2/STAT3 signaling pathway plays a regulatory role in cellular oxidative stress injury (OSI). In this study, we explored the role of the JAK2/STAT3 signaling pathway in hydrogen peroxide (H2O2)-induced OSI and the protective effect of melatonin against (H2O2)-induced injury in human umbilical vein endothelial cells (HUVECs). AG490 (a specific inhibitor of the JAK2/STAT3 signaling pathway) and JAK2 siRNA were used to manipulate JAK2/STAT3 activity, and the results showed that AG490 and JAK2 siRNA inhibited OSI and the levels of p-JAK2 and p-STAT3. HUVECs were then subjected to H2O2 in the absence or presence of melatonin, the main secretory product of the pineal gland. Melatonin conferred a protective effect against H2O2, which was evidenced by improvements in cell viability, adhesive ability and migratory ability, decreases in the apoptotic index and reactive oxygen species (ROS) production and several biochemical parameters in HUVECs. Immunofluorescence and Western blotting showed that H2O2 treatment increased the levels of p-JAK2, p-STAT3, Cytochrome c, Bax and Caspase3 and decreased the levels of Bcl2, whereas melatonin treatment partially reversed these effects. We, for the first time, demonstrate that the inhibition of the JAK2/STAT3 signaling pathway results in a protective effect against endothelial OSI. The protective effects of melatonin against OSI, at least partially, depend upon JAK2/STAT3 inhibition.
PLoS ONE 01/2013; 8(3):e57941. · 4.09 Impact Factor
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Yang Yang,
Xiaolong Yan,
Weixun Duan,
Juanjuan Yan,
Wei Yi,
Zhenxin Liang,
Ning Wang,
Yue Li,
Wensheng Chen, Shiqiang Yu,
Zhenxiao Jin,
Dinghua Yi
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ABSTRACT: Although pterostilbene (PTE) has been shown to have potent antitumor activities against various cancer types, the molecular mechanisms of these activities remain unclear. In this study, we investigated the antitumor activity of PTE against human lung adenocarcinoma in vitro and in vivo and explored the role of the Notch1 signaling pathway in this process. PTE treatment resulted in a dose- and time-dependent decrease in the viability of A549 cells. Additionally, PTE exhibited strong antitumor activity, as evidenced not only by a reduced mitochondrial membrane potential (MMP) and a decreased intracellular glutathione content but also by increases in the apoptotic index and the level of reactive oxygen species (ROS). Furthermore, PTE treatment induced the activation of the Notch1 Intracellular Domain (NICD) protein and activated Hes1. DAPT (a gamma secretase inhibitor) and Notch1 siRNA prevented the induction of NICD and Hes1 activation by PTE treatment and sensitized the cells to PTE treatment. The down-regulation of Notch signaling also prevented the activation of pro-survival pathways (most notably the PI3K/Akt pathway) after PTE treatment. In summary, lung adenocarcinoma cells may enhance Notch1 activation as a protective mechanism in response to PTE treatment. Combining a gamma secretase inhibitor with PTE treatment may represent a novel approach for treating lung adenocarcinoma by inhibiting the survival pathways of cancer cells.
PLoS ONE 01/2013; 8(5):e62652. · 4.09 Impact Factor
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Yang Yang,
Weixun Duan,
Zhenxin Liang,
Wei Yi,
Juanjuan Yan,
Ning Wang,
Yue Li,
Wensheng Chen, Shiqiang Yu,
Zhenxiao Jin,
Dinghua Yi
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ABSTRACT: Previous studies have demonstrated that Notch signaling pathway plays a regulatory role in cellular oxidative stress injury (OSI). In this study, our aim was to explore the role of the Notch signaling pathway in hydrogen peroxide (H(2)O(2))-induced OSI and the protective effect of curcumin during (H(2)O(2))-induced injury in human umbilical vein endothelial cells (HUVECs). DAPT, a specific inhibitor of the Notch signaling pathway, and Notch1 siRNA were used to study Notch activity. Further, HUVECs were exposed to H(2)O(2) in the absence or presence of curcumin. DAPT and Notch1 siRNA significantly inhibited OSI and the expression of Notch1 and Hes1. Curcumin conferred a protective effect on the HUVECs against H(2)O(2), which was evidenced by improved cell viability, adhesive ability and migratory ability and a decreased apoptotic index, decreased production of reactive oxygen species (ROS) and a reduction in several biochemical parameters. Immunofluorescence and Western blotting analyses demonstrated that H(2)O(2) treatment up-regulated the expression of Notch1, Hes1, Caspase3, Bax and Cytochrome c down-regulated the expression of Bcl2, and treatment with curcumin reversed these effects. We demonstrated for the first time that the inhibition of Notch signaling pathway imparts a protective effect against endothelial OSI. The protective effects of curcumin against OSI are at least in part dependent on Notch1 inhibition.
Cellular signalling 12/2012; · 4.09 Impact Factor
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ABSTRACT: The clinical profiles and outcomes of acute aortic dissection (AAD) have not been evaluated in China. We retrospectively analyzed, from January 1, 2008 to December 31, 2011, the data from 1,812 patients (mean age 51.1 ± 10.9 years; 77.5% men) with AAD (726 with type A and 1,086 with type B) from 19 large hospitals. Most patients had hypertension and presented with an abrupt onset of chest and/or back pain. Patients with type A AAD were more likely to present with typical symptoms and signs. Computed tomography was the most common initial imaging modality, used in 76.3% of patients with an AAD. The overall in-hospital mortality rate was 17.7%, with most of the deaths occurring within the first week. Surgery was used in 75.3% of patients with type A AAD. The mortality in this cohort was 33.8%. Endovascular treatment was performed in 76.1% of patients with type B AAD. The mortality rate was 2.2%. Multivariate analysis showed that hypertension (odds ratio 2.80, p <0.001), Marfan syndrome (odds ratio 1.76, p = 0.017), anterior chest pain (odds ratio 1.62, p = 0.004), abdominal pain (odds ratio 1.51, p = 0.041), migrating pain (odds ratio 1.56, p = 0.04), and arch vessel involvement (odds ratio 1.70, p <0.001) were predictive factors for increased in-hospital mortality in patients with an AAD. In conclusion, our study has provided insight into the current profiles and outcomes of AAD in China. This knowledge might be useful for clinicians when diagnosing and treating these patients.
The American journal of cardiology 07/2012; 110(7):1056-61. · 3.58 Impact Factor
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ABSTRACT: We performed the first quadruple valve replacement with mechanical valves, combined with the correction of complex congenital heart disease on November 17, 1999. We report here the 11-year follow-up study.
A 47-year-old man with subacute rheumatic endocarditis, a ventricular septal defect, and an obstruction of the right ventricular outflow tract required replacement of the aortic, mitral, tricuspid, and pulmonary valves; repair of the ventricular septal defect; and relief of the obstruction of the right ventricular outflow tract. The surgery was done on November 17, 1999, after careful systemic preparation of the patient. Warfarin therapy with a target international normalized ratio (INR) range of 1.5 to 2.0 was used. Follow-up included monitoring the INR, recording the incidences of thromboembolic and bleeding events, electrocardiography, radiography, and echocardiography evaluations.
The patient's INR was maintained between 1.5 and 2.0. All 4 mechanical prosthetic heart valves worked well. He is in generally good health without any thromboembolic or bleeding complications.
Long-term management is challenging for patients who have experienced quadruple valve replacement with mechanical valves; however, promising results could mean that replacement of all 4 heart valves in 1 operation is feasible in patients with quadruple valve disease, and an INR of 1.5 to 2.0 could be appropriate for Chinese patients with undergoing valve replacement with mechanical valves.
Heart Surgery Forum 06/2012; 15(3):E145-9. · 0.63 Impact Factor
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Lei Wang,
Sancheng Cao,
Jun Li,
Lifang Yang,
Yin Liu,
Jun Ren,
Qiaomei Ma,
Haijian Xing,
Dan Li,
Danqiu Tian,
Yi Wan, Shiqiang Yu,
Tao Chen,
Xiuling Yang,
Jian Yang
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ABSTRACT: Perimembranous ventricular septal defects (pmVSDs) are one of the most common forms of congenital cardiac malformation in children. Results of transcatheter pmVSD closure remain debatable, prompting the need for further evaluation with regard to the safety and efficacy of this procedure. The aim of the study was to analyze the safety, efficacy, and long-term follow-up data associated with transcatheter closure of pmVSDs in children using symmetric occluders.
From December 2002 to October 2011, 525 children with pmVSDs between 2 and 12 years of age underwent transcatheter closure at three major heart centers in northwest China with symmetric pmVSD occluders. All patients were followed up until October 2011 with electrocardiogram and transthoracic echocardiography. Adverse events were recorded and evaluated.
There were 252 male and 273 female patients with an average weight of 21.5 kg. The mean age at the time of transcatheter closure was 5.6 years, and the average ratio of pulmonic to systemic blood flow was 2.5. Transcatheter intervention was successfully performed in 502 patients (95.6%). The median device size implanted was 6.5 mm (range, 4 to 18 mm). During a median 45-month follow-up period, no mortality occurred. A total of three major adverse events (0.6%) were reported; two were valve-related. Meanwhile, 104 minor adverse events were detected during the entire follow-up period. All individuals experiencing major adverse events were younger than 3 years of age. The incidence of major adverse events in patients younger than 3 years old was significantly higher than that of patients older than 3 years old (3.75% versus 0.00%; Fisher's exact test p=0.004).
Data from the current study suggest that transcatheter pmVSD closure using symmetric occluders displayed an excellent success rate and long-term follow-up results. The transcatheter approach provides a less-invasive alternative to open surgery and displays some promise in the treatment of pmVSDs in certain patient populations.
The Annals of thoracic surgery 05/2012; 94(2):592-8. · 3.74 Impact Factor
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ABSTRACT: In this study, we evaluated the effect of curcumin (Cur) post-treatment on isolated perfused rat hearts that had been subjected to a protocol of ischemia and reperfusion injury. We also examined whether the Janus kinase 2 and signal transducer and activator 3 of transcription (JAK2/STAT3) signaling pathway plays a role in the cardioprotective effects of Cur post-treatment. Isolated perfused rat hearts were subjected to 60 min of ischemia, followed by 60 min of reperfusion. The hearts were exposed to 1-μM Cur during the first 10 min of reperfusion in the absence or presence of the JAK kinase-specific inhibitor AG490 (AG, 1 μM). The Cur treatment conferred a cardioprotective effect, and the treated hearts demonstrated an improved post-ischemic cardiac functional recovery, a decreased myocardial infarct size and decreased lactate dehydrogenase release in the coronary flow, a reduced number of apoptotic cardiomyocytes, up-regulation of the anti-apoptotic protein Bcl2 and down-regulation of the pro-apoptotic protein Caspase3. AG blocked the Cur-mediated cardioprotection by inhibiting the JAK2/STAT3 signaling pathway, as reflected by the abrogation of the Cur-induced up-regulation of Bcl2 and down-regulation of Caspase3. The results suggest that Cur post-treatment can attenuate IR injury through the activation of the JAK2/STAT3 signaling pathway, which transmits a survival signal to the myocardium.
Archiv für Kreislaufforschung 05/2012; 107(3):263. · 7.35 Impact Factor
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Qijun Zheng,
Yuexing Yuan,
Wei Yi,
Wayne Bond Lau,
Yajing Wang,
Xiaoliang Wang,
Yang Sun,
Bernard L Lopez,
Theodore A Christopher,
Jonathan M Peterson,
G William Wong, Shiqiang Yu,
Dinghua Yi,
Xin-Liang Ma
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ABSTRACT: Reduced plasma adiponectin (APN) in diabetic patients is associated with endothelial dysfunction. However, APN knockout animals manifest modest systemic dysfunction unless metabolically challenged. The protein family CTRPs (C1q/TNF-related proteins) has recently been identified as APN paralogs and some CTRP members share APN's metabolic regulatory function. However, the vasoactive properties of CTRPs remain completely unknown.
The vasoactivity of currently identified murine CTRP members was assessed in aortic vascular rings and underlying molecular mechanisms was elucidated in human umbilical vein endothelial cells. Of 8 CTRPs, CTRPs 3, 5, and 9 caused significant vasorelaxation. The vasoactive potency of CTRP9 exceeded that of APN (3-fold) and is endothelium-dependent and nitric oxide (NO)-mediated. Mechanistically, CTRP9 increased AMPK/Akt/eNOS phosphorylation and increased NO production. AMPK knockdown completely blocked CTRP9-induced Akt/eNOS phosphorylation and NO production. Akt knockdown had no significant effect on CTRP9-induced AMPK phosphorylation, but blocked eNOS phosphorylation and NO production. Adiponectin receptor 1, but not receptor 2, knockdown blocked CTRP9-induced AMPK/Akt/eNOS phosphorylation and NO production. Finally, preincubating vascular rings with an AMPK-inhibitor abolished CTRP9-induced vasorelaxative effects.
We have provided the first evidence that CTRP9 is a novel vasorelaxative adipocytokine that may exert vasculoprotective effects via the adiponectin receptor 1/AMPK/eNOS dependent/NO mediated signaling pathway.
Arteriosclerosis Thrombosis and Vascular Biology 08/2011; 31(11):2616-23. · 6.37 Impact Factor
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ABSTRACT: Totally thoracoscopic cardiac surgery is an alternative to traditional cardiac surgery in adults, and in few cases, in small children. This study assesses totally thoracoscopic cardiac surgery and its advantages for application to small children with low body weight.
From March 2009 to October 2010, 28 patients, with a mean age of 5.8±2.1 years and mean weight of 15.0±4.65 kg (range, 13.5 to 22 kg), underwent totally thoracoscopic atrial septal defect closure. Three incisions 1.0 cm to 2.5 cm in length were made on the chest wall. Direct sutures were made in 20 patients, whereas Dacron patches were used in 8 patients. Mean follow-up was 6 months (range, 0 to 24 months).
Cardiopulmonary bypass time was 56 to 126 minutes, and the aortic cross-clamp time was 36 to 65 minutes. A total of 28 cases were classified as New York Heart Association functional class I. No patient required further operation.
Totally thoracoscopic surgical atrial septal defect closure in small children is feasible, minimally invasive, safe, and has good cosmesis.
The Annals of thoracic surgery 07/2011; 92(1):200-3. · 3.74 Impact Factor
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ABSTRACT: Patients with diabetes show enhanced susceptibility to myocardial ischemia/reperfusion (MI/R) injury. Epidemiological studies indicated that consumption of α-linolenic acid (ALA) significantly reduces the risk of cardiac events in post-acute myocardial infarction patients. The present study attempted to investigate the effects of ALA intake on MI/R injury in normal and diabetic rats and its mechanisms.
The high-fat diet-fed streptozotocin (HFD-STZ) rat model was developed. Age-matched normal and HFD-STZ rats were randomly assigned to receive normal diet or ALA (oral gavage, 500 μg/kg per day). After 4 weeks of feeding, animals were subjected to 30 min of myocardial ischemia and 4 or 6 h of reperfusion.
Compared with the normal control, HFD-STZ rats showed more severe myocardial functional impairment and injury. Although ALA intake for 4 weeks did not change myocardial function and injury in normal rats, it significantly improved the instantaneous first derivation of left ventricle pressure, reduced infarct size, plasma creatine kinase and lactate dehydrogenase activities, and apotosis at the end of reperfusion in HFD-STZ diabetic rats. Moreover, ALA intake not only significantly reduced tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) concentrations but reduced the increase in superoxide production and malonaldialdehyde formation and simultaneously enhanced the antioxidant capacity in the diabetic hearts. Myocardial PI3K expression and Akt phosphorylation were increased by ALA intake in diabetic but not normal rats.
Chronic ALA intake confers cardioprotection in MI/R by exerting anti-inflammatory and anti-oxidative stress effects in diabetic but not normal rats, which is possibly through PI3K-Akt-dependent mechanism.
Archives of medical research 04/2011; 42(3):171-81. · 1.88 Impact Factor
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ABSTRACT: Adenosine pretreatment reduces injury caused by ischemia-reperfusion. To investigate the hypothesis that adenosine pretreatment would modulate injury induced by cardiopulmonary bypass (CPB) and myocardial ischemia/reperfusion, we conducted a randomized controlled trial on the effects of adenosine pretreatment in children undergoing surgery to repair congenital heart defects.
Children undergoing surgery to repair congenital heart defects were randomized to adenosine pretreatment or control treatment. Adenosine pretreatment was performed by infusing a total of 2.45 mg kg⁻¹ of adenosine over 10 min. Serum troponin I was measured pre- and postoperatively. Multiple clinical parameters, including postoperative use of inotropic medicine and duration in the intensive care unit (ICU), were recorded.
A total of 82 patients were enrolled in the study. There were 42 control patients and 40 patients in the adenosine pretreatment group. The mean age and weight of the two groups were not significantly different, nor were cardiopulmonary bypass and cross-clamp times. There were no deaths and severe complications in both groups. The adenosine pretreatment protocol caused significant hypotension but had no significant effect on heart rate. One patient had severe tachycardia shortly after the adenosine pretreatment protocol was completed, and adenosine infusion was continued until CPB was started. Postoperative levels of serum troponin I were greater in the control patients than in the adenosine pretreatment group, indicating that the control group suffered greater myocardial injury. Control group patients required more postoperative inotropic agents than those in the adenosine pretreatment group at 0, 1, and 3 h, indicating that the adenosine pretreatment group had a better cardiac function. The adenosine pretreatment group also required significantly less time in the ICU than the control group (3.2 ± 1.2 days vs 3.9 ± 1.2 days, p = 0.013).
This study demonstrates that adenosine pretreatment is protective of the myocardium during open-heart surgery in pediatric patients.
European journal of cardio-thoracic surgery: official journal of the European Association for Cardio-thoracic Surgery 02/2011; 39(5):e90-6. · 2.40 Impact Factor
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ABSTRACT: Transcatheter occlusion of secundum atrial septal defects is a safe and effective alternative to traditional surgical closure; however, it is associated with serious occasional complications and inapplicable to more than 20% of atrial septal defects. In 2000, transthoracic occlusion was pioneered at Xijing Hospital as a novel method of atrial septal defect closure. The purpose of this study is to report the early and mid-term results of the transthoracic occlusion procedure and to evaluate its safety and efficacy.
From April 2000 to April 2006, 268 patients with atrial septal defects were classified into 2 groups: group A (unsuitable for transcatheter occlusion, n = 126) and group B (n = 142). The transthoracic occlusion method used transesophageal echocardiographic-guided atrial septal defects occluder deployment via a right minithoracotomy without cardiopulmonary bypass or fluoroscopy.
Device implantation was successful in 265 patients (98.9%), including 9 elliptical devices in group A. The average size of circular occluders in group A was 38.2 ± 4.2 mm, which was larger than in group B (24.0 ± 4.5 mm) (P < .001). The average procedure time was 37.2 ± 9.2 minutes, the average intracardiac manipulation time was 5.8 ± 3.0 minutes, and the average inpatient stay was 3.2 ± 0.8 days. Twenty-five complications (9.3%) occurred in patients during the follow-up period. No large residual shunting, device embolization, or other severe complications resulted from transthoracic occlusion.
Transthoracic occlusion is a new safe and effective method for atrial septal defect treatment, even for patients with partial atrial septal defects unsuitable for transcatheter occlusion. This hybrid method broadens the indications of atrial septal defect treatment with device occlusion.
The Journal of thoracic and cardiovascular surgery 01/2011; 142(1):113-9. · 3.41 Impact Factor
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Guang Tong,
Zhongchan Sun,
Xufeng Wei,
Chunhu Gu,
Alan David Kaye,
Yuemin Wang,
Juan Li,
Quanyu Zhang,
Haitao Guo, Shiqiang Yu,
Dinghua Yi,
Jianming Pei
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ABSTRACT: Evidence has indicated U50,488H, a selective κ-opioid receptor (κ-OR) agonist, administered before ischemia attenuates apoptosis and infarction during ischemia and reperfusion (I/R). However, it remains unclear whether U50,488H postconditioning reduces apoptosis during I/R. This study was designed, therefore, to test the hypothesis that U50,488H administered at the onset of reperfusion inhibits cardiomyocyte apoptosis and to investigate the underlying mechanisms.
Male Sprague-Dawley rats were subjected to myocardial ischemia and reperfusion(MI/R) and were randomized to receive either vehicle, U50,488H, U50,488H plus Nor-BNI, a selective κ-OR antagonist, U50,488H plus wortmannin, a specific inhibitor of phosphoinositide 3'-kinase (PI3K), or U50,488H plus L-NAME, a nitric oxide synthase inhibitor (NOS inhibitor), immediately prior to reperfusion. In vitro study was performed on cultured neonatal cardiomyocytes subjected to simulated ischemia/reperfusion.
Treatment with U50,488H resulted in increases in Akt and endothelial nitric oxide synthase (eNOS) phosphorylation with secondary NO production both in vivo and in vitro and these effect were completely blocked by wortmannin and specific Akt inhibitor(AI). L-NAME treatment had no effect on Akt and eNOS phosphorylation; but, significantly reduced NO production. Moreover, treatment with U50,488H markedly reduced myocardial apoptotic death. Treatment with wortmannin and specific Akt inhibitor abolished the anti-apoptotic effect of U50,488H. L-NAME also significantly attenuated the anti-apoptotic effect of U50,488H.
These results demonstrate that U50,488H administered immediately prior to reperfusion increases Akt phosphorylation through a PI3-kinase-dependent mechanism and reduces postischemic myocardial apoptosis. Phosphorylation of eNOS with secondary NO production contribute significantly to the anti-apoptotic effect of U50,488H postconditioning.
Life sciences 10/2010; 88(1-2):31-8. · 2.56 Impact Factor
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Jian Yang,
Lifang Yang,
Yi Wan,
Jian Zuo,
Jun Zhang,
Wensheng Chen,
Jun Li,
Lijun Sun, Shiqiang Yu,
Jincheng Liu,
Tao Chen,
Weixun Duan,
Lize Xiong,
Dinghua Yi
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ABSTRACT: The aim of this study was to evaluate the safety and efficacy of transcatheter closure for perimembranous ventricular septal defect (pmVSD) and its long-term results. The most common congenital heart condition is pmVSD. Transcatheter closure of pmVSD is a recently described technique with limited results for mid- to long-term follow-up.
Between June 2002 and June 2008, 848 patients with pmVSD were enrolled in our study and treated percutaneously with pmVSD occluders. All patients were followed up until December 2008, an average of 37 months. According to colour Doppler transthoracic echocardiography before the intervention and ventriculography, the average end-diastolic pmVSD size was 5.1 and 5.4 mm, respectively. Placement of the device was successful in 832 patients (98.1%) and the median device size was 8.6 mm. During follow-up, 103 adverse events (12.4%) were reported. Most adverse events were categorized as minor and there were nine major adverse events (8.7%), including two complete atrioventricular block requiring pacemaker implantation. Kaplan-Meier estimates showed >85% freedom from major or minor adverse events during a maximal follow-up of 79 months.
In experienced hands, transcatheter pmVSD closure can be performed safely and successfully with low morbidity and mortality. Long-term prognostic results are favourable, and the transcatheter approach provides a less-invasive alternative that may become the first choice in selected pmVSD patients. This trial is registered with ClinicalTrials.gov, number NCT00890799.
European Heart Journal 09/2010; 31(18):2238-45. · 10.48 Impact Factor
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ABSTRACT: Myxomas are the most common type of primary cardiac tumors. We report our use of totally thoracoscopic surgery in resecting cardiac myxomas in 12 cases with 10 in the left atria and 2 in the right atria. Totally thoracoscopic surgical resection of myxoma was successfully performed in all cases through three minimal incisions, with the largest incision less than 3 cm. The cardiopulmonary bypass time was 96 to 126 minutes, and the aortic cross-clamp time was 46 to 63 minutes. Postoperative ventilation assistance was 3 to 11 hours. We show that the method is safe and achieves complete tumor resection.
The Annals of thoracic surgery 08/2010; 90(2):674-6. · 3.74 Impact Factor
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ABSTRACT: We report a case of total anomalous pulmonary venous connection in a 6-year-old boy who was successfully treated by thoracoscopic surgery. We believe this is the first report of the use of totally thoracoscopic surgery for the correction of a total anomalous pulmonary venous connection.
The Annals of thoracic surgery 07/2010; 90(1):272-3. · 3.74 Impact Factor
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Qiang Li,
Jinzhou Zhang,
Wen Wang,
Jincheng Liu,
Hailong Zhu,
Wensheng Chen,
Tao Chen, Shiqiang Yu,
Hongbing Wang,
Guocheng Sun,
Dinghua Yi
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ABSTRACT: The permeability of pulmonary microvessel endothelial cells increases markedly after acute lung injury via paracellular gap. Connexin40 is a primary component of pulmonary microvessel endothelial cells gap junction channel and mediates intercellular communication. However, the relationship between connexin40 and the permeability of pulmonary microvessel endothelial cells is still unknown. Therefore, we determined whether connexin40 affected rabbits' pulmonary microvessel endothelial cells permeability after acute lung injury induced by gunshot trauma.
We used an acute lung injury model in New Zealand rabbits following gunshot chest trauma and correlated connexin40 immunohistochemistry in gunshot lung tissue with Evans blue leak rate. Cultured pulmonary microvessel endothelial cells were divided into three groups, control (G control), injured serum (G serum), and blocker agent (G blocker). Gap junction channel function was assessed by scrape-loading and dye transfer techniques. Pulmonary microvessel endothelial cells permeability was measured by Evans blue-labeled albumin transfer.
Connexin40 expression decreased time dependently, whereas Evans blue leak rate increased. Connexin40 expression and Evans blue leak rate exhibited a strong inverse correlation (gamma = -0.934, p < 0.05). Injured serum decreased gap junction channel function, and the gap junction channel blocker aggravated this effect. Similarly, pulmonary microvessel endothelial cells permeability increased significantly in G serum and G blocker.
Connexin 40 expression in pulmonary microvasculature endothelial cells is downregulated after acute lung injury induced by gunshot trauma. This is associated with impaired gap junction channel function and increased pulmonary microvessel endothelial cells permeability.
The Journal of trauma 04/2010; 68(4):802-9. · 2.48 Impact Factor
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Jinzhou Zhang,
Wen Wang,
Jing Sun,
Qiang Li,
Jincheng Liu,
Hailong Zhu,
Tao Chen,
Hongbing Wang, Shiqiang Yu,
Guocheng Sun,
Wensheng Chen,
Dinghua Yi
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ABSTRACT: Increased pulmonary vascular permeability is a hallmark of acute lung injury (ALI). Gap junction channels (GJCs) connect adjacent cells and facilitate ion exchange. It remained unclear whether GJCs modulate pulmonary permeability in ALI through intracellular calcium. Objectives: This study aimed to verify if GJCs in pulmonary microvessel endothelial cells (PMVECs) modulate pulmonary vascular permeability in ALI via intracellular calcium.
Firstly, an animal model of ALI was studied using connexin 40 (Cx40) immunohistochemistry in the lung with Evans' blue (EB) leakage. Then cultured PMVECs were divided into three groups: G(control), G(serum) and G(blocker). Serum was obtained from animals with ALI following gunshot injury (injured serum). Initially, G(blocker) was treated with the blocker of GJCs, and then G(serum) and G(blocker) were stimulated with the injured serum, respectively. GJCs, the permeability of cell monolayers and intracellular Ca(2+) were assessed.
Cx40 time-dependently decreased, whereas EB leakage increased. Cx40 and EB leakage exhibited a strong inverse correlation (rho = -0.934, p < 0.05). Injured serum decreased GJCs and expression of Cx40, whereas the blocker aggravated this effect. Similarly, when PMVEC monolayer was treated with injured serum, both permeability and intracellular Ca(2+) increased. These effects were also aggravated with the blocker.
Depression of GJCs of PMVECs increased pulmonary vascular permeability in ALI; this effect may be mediated by the overload of intracellular calcium.
Respiration 01/2010; 80(3):236-45. · 2.26 Impact Factor
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ABSTRACT: Given the increasing popularity of percutaneous closure of ventricular septal defects (VSDs), a comparative analysis of the different treatments (surgical vs. percutaneous closure) for VSDs is needed.
This is a single center, retrospective clinical study. A total of 2,178 patients with VSDs were enrolled, including 852 patients treated with percutaneous closure (device group) and 1,326 patients underwent traditional surgical repair (surgical group). Several characteristics (e.g. procedure success rate, complications, blood transfusions) were compared between the 2 groups.
There were no differences (p > 0.05) between the device and surgical groups according to the success rates (99.8 vs. 100%) and occurrences of main complications (1.9 vs. 2.5%). The incidence of minor complications was significantly lower in the device group (0.6%, 5/852) than the surgical group (6.4%, 85/1,326) (p < 0.01). No blood transfusions were needed in the device group, while 136 patients (10.3%) required blood transfusions in the surgical group. The duration of hospital stay was shorter in the device group than in the surgical group (3.2 vs. 12.9 days, p < 0.01).
Percutaneous VSD closure is an effective method with fewer complications, shorter hospital stay and good cosmetic effect. It can serve as a reasonable alternative treatment for traditional open heart surgery.
Cardiology 09/2009; 114(4):238-43. · 1.71 Impact Factor
