Objective To analyze and explore the risk factors of secondary tricuspid regurgitation (TR) after left-sided valve surgery (left cardiac valve replacement or valvuloplasty) using meta-analysis, so as to provide evidence for clinical diagnosis and treatment of secondary TR. Methods We electronically searched databases including PubMed, MEDLINE, CBM, CNKI, VIP, for literature on the risk factors of secondary TR after left-sided valve surgery from 1995 to 2012. According to the inclusion and exclusion criteria, we screened literature, extracted data, and assessed methodological quality. Then, meta-analysis was performed using RevMan 5.0 software. Results A total of 6 case-control studies were included, involving 437 patients and 2 102 controls. The results of meta-analysis showed that, the risk factors of progressive exacerbation of secondary TR after left-sided valve surgery included preoperative atrial fibrillation (OR=3.90, 95%CI 3.00 to 5.07; adjusted OR=3.04, 95%CI 2.21 to 4.16), age (MD=5.36, 95%CI 3.49 to 7.23), huge left atrium (OR=5.17, 95%CI 3.12 to 8.57; adjusted OR=1.91, 95%CI 1.49 to 2.44) or left atrium diameter (MD=4.85, 95%CI 3.18 to 6.53), degradation of left heart function (OR=2.97, 95%CI 1.73 to 5.08), rheumatic pathological change (OR=3.06, 95%CI 1.66 to 4.68), preoperative TR no less than 2+ (OR=3.52, 95%CI 1.26 to 9.89), and mitral valve replacement (MVR) (OR=2.35, 95%CI 1.68 to 3.30). Sex (OR=1.54, 95%CI 0.94 to 2.52) and preoperative pulmonary arterial hypertension (OR=1.28, 95%CI 0.77 to 2.12) were not associated with secondary TR after left-sided valve surgery. Conclusion The risk factors of progressive exacerbation of secondary TR after left-sided valve surgery include preoperative atrial fibrillation, age, huge left atrium or left atrium diameter, degradation of left heart function, rheumatic pathological change, preoperative TR no less than 2+, and MVR. Understanding these risk factors helps us to improve the long-time effectiveness of preventing and treating TR after left-sided valve surgery.
Objective To develop a tissue engineering scaffold by using 4arm branched polyethylene glycol-VS (PEG-VS) crosslinked with decellularized valved conduits (DVC), and to research on its mechanical and biological functions. Methods The valved aortic conduits of rabbits were taken and decellularized by trypsin method and then were crosslinked with 4arm branched PEG-VS to construct the composite scaffolds (CS). The functions of decellularized valved conduits and the composite scaffolds were tested by mechanics test system. Thirty New Zealand white rabbits were equally and randomly assigned to one of the three groups: the control group, the DVC group, and the CS group. Valved aortic conduits, decellularized valved conduits and composite scaffoldswere transplanted into the common carotid artery of the abovementioned three groups of rabbits respectively. Twentyeight days after the operation, patency of the transplants was tested by Color Doppler ultrasound; micromorphology and inflammatory infiltration were observed by hematoxylin eosin（HE） staining andscanning electron microscope (SEM)，and endothelialization of composite scaffolds was detected by immunofluorescent staining. Results A series of biomechanical analyses revealed that the composite scaffolds had highly similar mechanical properties as fresh tissue, and had superior elastic modulus (P=3.1×10-9) and tensile strength (P=1.1×10-6) compared with decellularized valved conduits. Color Doppler ultrasound revealed that the graft patency for the CS group was better than the control group (P=0.054) and the DVC group (P=0.019), and the intraaortic thrombosis rate and distortion rate decreased significantly. HE staining and SEM showed that the endothelialization of composite scaffolds in the CS group was significantly higher than the other two groups with the endothelial cells evenly distributed on the scaffolds. The [CM(159mm]immunofluorescent staining indicated that the positive rate of the endothelial cell marker CD34 was higher than the other two groups. Conclusion The composite scaffolds using 4arm branched PEGVS crosslinked with DVC have great mechanical and biological properties.
Abstract: Objective To induce calcification in aortic valvular interstitial cells (VICs) in vitro and observe the shift of cellular phenotype during the process. Methods Porcine aortic VICs were isolated and expanded by collagenase methods. Fluorescent staining was performed to identify the interstitial cells. VICs at 48 passages were used for experiments. The cells were divided into two groups: the experimental group in which cells were cultured in osteogenic media supplemented with βglycerophosphate, vitamin C and dexamethasone, and the control group in which cells were cultured in normal media. After 2 weeks, calcified nodules were quantified. Calcium deposit was stained and measured by Alizarin Red S staining and assay. Real time reverse transcription polymerase chain reaction (RTPCR) was performed to measure expression of alpha smooth muscle actin (α-SMA) and calcification related factors such as osteocalcin, osteopontin and Corebinding factor α1/Runx2 (Cbfα1/Runx2). Results VICs were successfully harvested from porcine aortic valves, identified by positive staining of α-SMA, vimentin and negative staining of Von Willebrand factor (vWF). VICs could calcify after 2 weeks of osteogenic induction with calcified nodules formed. Quantification of calcified nodules and calcification deposit were significantly higher (Plt;0.05) in the experimental group than those in the control group (156.25±17.38 vs. 2.50±1.29, 17.52±2.04 vs. 1.00±0.22). Real Time RT-PCR indicated that expression of α-SMA, as well as calcification related markers like osteocalcin, osteopontin and Cbfα1/Runx2 was much higher in the experimental group than those in the control group (Plt;0.05). Conclusion VICs are activated during the progress of calcification with phenotype shifting to contraction and ossification, which might be the pathological basis of valvular calcification.
Abstract: Objective Using Amplex red fluorometric assay to detect the lysyl oxidase (LOX) enzyme activity in tissue engineered heart valve (TEHV). Methods Porcine aortic valves were decellularized with trypsin+ethylene diaminetetraacetic acid(EDTA), TritonX-100, and RNaseⅠ＋DNaseⅠ, then they were seeded by myo-fibroblasts that harvested from rats. Then they were fed with Dulbecco’s modified Eagle medium (DMEM) which contained high glucose for 27 days, they were fed with phenol red-free and serumfree DMEM for 24 hours, and the medium was harvested and used for LOX enzyme activity assays with the Amplex red fluorometric assay. And reverse transcription-polymerase chain reaction (RT-PCR) technique was used to analyze the expression of LOXmRNA in TEHV. Results All the samples produced measurable amounts of active LOX enzyme. The fluorescence units were 45.60±1.66, and the corresponding concentration of LOX enzyme were 0.123±0.003μg/ml. At the same time, all the samples expressed LOXmRNA. The expression of LOXmRNA was corresponding to the results of the Amplex red fluorometric assay. Conclusion It is feasible to detect the LOX enzyme activity in TEHV with the Amplex red fluorometric assay. And this assay gives a way to reflect that LOX plays an important role in collagen cross-linking of extracellar matrix in TEHV.
Objective To observe whether Cyclo-RGDfK (Arg-Gly-Asp-D-Phe-Lys) could enhance the adhesion of myofibroblast to decellularized scaffolds and upregulate the expression of Integrin αVβ3 gene. Methods Myofibroblast from the rat thoracic aorta was acquired by primary cell culture. The expression of Vimentin and α-smooth muscle actin(α-SMA) has been detected by immunoflurescent labeling. Decellularized valves have been randomly divided into three groups (each n=7). Group A (blank control): valves do not receive any pretreatment; Group B: valves reacted with linking agent NEthylN(3dimethylaminopropyl)carbodiimide hydrochloride (EDC) for 36 hours before being seeded; Experimental group: Cyclo-RGD peptide has been covalently immobilized onto the surface of scaffolds by linking agent EDC. The fifth generation of myofibroblast has been planted on the scaffolds of each group. The adhesion of myofibroblast to the scaffolds was evaluated by HE staining and electron scanning microscope. The expression of Integrin αVβ3 was quantified by halfquantitative reverse transcriptionpolymerase china reaction (RT-PCR). Results We can see that myofibroblast has exhibited b positive staining for Vimentin and α-SMA. Besides, it has been shown that the expression of Integrin αVβ3 was much higher in the experimental group than that of the group A and group B(Plt;0.05). There was no statistically difference in group A and group B (P=0.900). Conclusion RGD pretreatment does enhance the adhesive efficiency of seeding cells to the scaffolds and this effect may be related to the upregulation of Integrin αVβ3.
ObjectiveTo investigate clinical outcomes and risk factors of patients with valvular heart disease (VHD) and giant left ventricle undergoing heart valve replacement (HVR). MethodsClinical data of 144 VHD patients with giant left ventricle who underwent HVR in Union Hospital of Tongji Medical College, Huazhong University of Science and Technology from January 2009 to December 2012 were retrospectively analyzed. There were 116 male and 28 female patients with their age of 15-69 (44.9±11.9) years and disease duration of 57.8±98.3 months (range, 1 month to 40 years). There were 92 patients with rheumatic VHD, 28 patients with degenerative VHD, 15 patients with congenital VHD, and 9 patients with infective endocarditis. A total of 137 patients who were discharged alive were followed up. Risk factors of postoperative mortality, morbidity and late death of VHD patients with giant left ventricle undergoing HVR were analyzed with t-test, chi-square test or Fisher's exact test, and logistic regression analysis. The life-table method was used to calculate long-term survival rate and draw the survival curve. ResultsMajor postoperative complications included low cardiac output syndrome (LCOS) in 19 patients (13.2%), ventricular arrhythmias in 56 patients (38.9%), prosthetic paravalvular leaks in 7 patients (4.9%), pleural effusion in 33 patients (22.9%), pericardial effusion in 8 patients (5.6%), liver failure in 23 patients (16.0%), and renal failure in 5 patients (3.5%). Seven patients (4.9%) died postoperatively. Logistic univariate analysis showed that advanced-age ( > 50 years), rheumatic VHD, higher preoperative NYHA class (Ⅲ or Ⅳ), long disease duration, poor preoperative left ventricular function[left ventricular ejection fraction (LVEF) < 40%], double valve replace-ment (DVR), other concomitant intracardiac procedures, prolonged cardiopulmonary bypass (CPB) time and aortic cross-clamping time, postoperative LCOS and ventricular arrhythmias were risk factors of early mortality of VHD patients with giant left ventricle undergoing HVR (P < 0.05). Logistic multivariate analysis showed that advanced age ( > 50 years), long disease duration, higher preoperative NYHA class (Ⅳ), poor preoperative left ventricular function (LVEF < 40%), DVR, prolonged CPB time were independent predictors of early mortality (P < 0.05). Logistic multivariate analysis showed that higher preoperative NYHA class (Ⅲ or Ⅳ), other concomitant intracardiac procedures, poor preoperative left ventricular function (LVEF < 50%) were independent predictors of postoperative LCOS (P < 0.05). Higher preoperative NYHA class (Ⅲ or Ⅳ) and preoperative non-sinus rhythm were independent predictors of postoperative ventricular arrhy-thmias (P < 0.05). Within 2 weeks after the operation, left ventricular end-diastolic dimension (LVEDD), left atrial diameter (LAD), LVEF and left ventricular fractional shortening (LVFS) were all significantly reduced compared with preoperative parameters (P < 0.05). Five patients died during follow-up. One-year, 2-year, 3-year and 4-year survival rates were 97.1%, 95.0%, 92.7% and 92.7% respectively. Preoperative LVEF, LVEDD and NYHA were significantly different between patients who died or survived during follow-up. ConclusionsHVR can produce low postoperative mortality, high long-term survival rates and satisfactory clinical outcomes for VHD patients with giant left ventricle. Advanced age ( > 50 years), long disease duration, higher preoperative NYHA class (Ⅳ), preoperative non-sinus rhythm, poor preoperative left ventricular function (LVEF < 40%), DVR and prolonged operation time may be risk factors of postoperative mortality and morbidity. Poor preoperative left ventricular function and significantly enlarged left ventricle may be risk factors of late death after HVR.
ObjectiveTo evaluate the changes of left ventricular morphology and contractile function of patients with mitral stenosis and small left ventricle after mitral valve replacement. MethodsStudies on the changes of left ventricular morphology and contractile function of patients with mitral stenosis and small left ventricle after mitral valve replacement were searched from the databases of Wangfang, VIP, CNKI, PubMed, Elsevier Science Direct, and Cochrane Library from establishment to January 2015. Quality of articles was evaluated. Relevant data were extracted from eligible studies to conduct meta-analysis. Mean differences (MD) of left ventricle end-diastolic volume index (LVEDVI), left ventricle end-diastolic diameter (LVEDD), left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) between the preoperative and the postoperative value from eligible studies were analyzed and pooled, and their 95% confidence intervals (CI) were calculated. R2.15.3 software was applied for statistical analysis. ResultsEight eligible studies involving 446 patients were analyzed in the study. The quality of included literature was high. The results of meta-analysis showed that LVEDVI and LVEDD increased by 14.51 ml/m2 with 95%CI -22.78 to -6.25 (P<0.01) and 4.88 mm with 95%CI -10.85 to 1.09 (P=0.11) respectively at 2 weeks postoperatively compared with preoperative value. LVEF decreased by 3.05% with 95%CI -3.02% to 9.12% (P=0.32) while LVFS increased by 1.16% with 95%CI -4.83% to 2.50% (P=0.53) at 2 weeks postoperatively. Compared with preoperative value, LVEDVI and LVEDD markedly increased by 16.11 ml/m2 with 95%CI -20.32 to -11.90 (P<0.01) and 10.56 mm with 95%CI -11.52 to -9.60 (P<0.01) respectively at 6 months postoperatively. LVEF and LVFS increased by 7.69% with 95%CI -17.18% to 1.8% (P=0.11) and 6.21% with 95%CI -10.07% to -2.36% (P<0.01) respectively at 6 months postoperatively compared with preoperative value. ConclusionLeft ventricular morphology and contractile function of patients with mitral stenosis and small left ventricle recovers well after mitral valve replacement.