[Show abstract][Hide abstract] ABSTRACT: Cardiac troponin-I (cTnI) and -T (cTnT) are sensitive and specific markers of myocardial injury. However, the role of increased cTnI and cTnT in percutaneous coronary intervention (PCI)-related myocardial injury remains controversial. In this prospective, single-center and double-blind study, we aimed to determine the diagnostic and prognostic value of cTnI as well as cTnT (cTns) in PCI-related myocardial injury in a Chinese population. A total of 1,008 patients with stable angina pectoris and non-ST-segment elevation acute coronary syndrome were recruited. The levels of cTnI and cTnT were examined before and after PCI. All patients were followed up for 26±9 months to observe the incidence of major adverse cardiac events (MACEs). Our results showed that post-PCI cTnI and/or cTnT levels were increased to more than the 99(th) percentile upper reference limit (URL) in 133 (13.2%) patients, among which 22 (2.2%) were more than 5 × 99(th) percentile URL. By univariate analysis, an elevation in cTns after PCI was not an independent predictor of increased MACEs, HR 1.35 (P = 0.33, 95%CI: 0.74-2.46). In conclusion, our data demonstrate that the incidence of PCI-related myocardial injury is not common in a Chinese population and minor elevated cTns levels may not be a sensitive prognostic marker for MACEs.
Journal of biomedical research. 03/2014; 28(2):98-107.
[Show abstract][Hide abstract] ABSTRACT: gender - Male, age - 63 year-old.
Acute myocardial infarction.
Aspirin • beta-blocker • captopril.
CABG • autologous skeletal myoblast transplantation • PCI.
Unusual or unexpected effect of treatment.
Cell transplantation has been viewed as a promising strategy for end-stage heart failure, but long-term follow-up results are lacking.
In December 2002 we began transplanting autologous skeletal myoblasts in one patient because of serious coronary heart disease. Here, we present the 9-year follow-up results of this patient. No ventricular tachyarrhythmias were detected after treatment. The patient had another myocardial infarction in April 2012 and was treated successful with PCI.
Autologous skeletal myoblast transplantation with bypass surgery is associated with improvement in cardiac function and lack of adverse effects in long-term follow-up, making it a promising therapy for patients with heart failure.
The American journal of case reports. 01/2013; 14:139-42.
[Show abstract][Hide abstract] ABSTRACT: VEGF and angiopoietin-1 (Ang1) are two major angiogenic factors being investigated for the treatment of myocardial infarction (MI). Targeting VEGF and Ang1 expression in the ischemic myocardium can increase their local therapeutic effects and reduce possible adverse effects. Adeno-associated viral vectors (AAVs) expressing cardiac-specific and hypoxia-inducible VEGF [AAV-myosin light chain-2v (MLC)VEGF] and Ang1 (AAV-MLCAng1) were coinjected (VEGF/Ang1 group) into six different sites of the porcine myocardium at the peri-infarct zone immediately after ligating the left descending coronary artery. An identical dose of AAV-Cytomegalovirus (CMV)LacZ or saline was injected into control animals. AAV genomes were detected in the liver in addition to the heart. RT-PCR, Western blotting, and ELISA analyses showed that VEGF and Ang1 were predominantly expressed in the myocardium in the infarct core and border of the infarct heart. Gated single-photon emission computed tomography analyses showed that the VEGF/Ang1 group had better cardiac function and myocardial perfusion at 8 wk than at 2 wk after vector injection. Compared with the saline and LacZ controls, the VEGF/Ang1 group expressed higher phosphorylated Akt and Bcl-xL, less Caspase-3 and Bad, and had higher vascular density, more proliferating cardiomyocytes, and less apoptotic cells in the infarct and peri-infarct zones. Thus, cardiac-specific and hypoxia-induced coexpression of VEGF and Ang1 improves the perfusion and function of porcine MI heart through the induction of angiogenesis and cardiomyocyte proliferation, activation of prosurvival pathways, and reduction of cell apoptosis.
Proceedings of the National Academy of Sciences 02/2011; 108(5):2064-9. · 9.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: We wanted to determine whether zinc supplementation can inhibit bone marrow-derived mesenchymal stromal cell (MSC) apoptosis and enhance their tissue regenerative potential a in mouse ischemic hindlimb model.
Rat bone marrow cells were cultured and the resulting MSC were passaged for 3-7 generations. The proliferation and apoptosis of MSC was examined by 3-[4,5-dimethyl-2-thiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis. The activation of protein kinases B (Akt) was determined by Western blots. Vascular endothelial growth factor (VEGF) levels were examined by enzyme-linked immunosorbent assay. The mouse hindlimb ischemic model was established by ligating the right femoral artery. Mice received MSC, zinc-treated MSC or vehicle. The blood flow was assessed by laser Doppler imaging. The survival rate of donor cells was quantified by real-time polymerase chain reaction for the sex-determining region of the Y-chromosome (Sry). Angiogenesis was assessed by histochemical staining and immunofluoresence staining.
Supplementation with physiologic amounts of zinc caused a marked attenuation of cell apoptosis, enhanced cell viabilities, increased VEGF release and up-regulated Akt activation. Zinc-treated MSC delivered into ischemic hindlimbs resulted in significant improvements in limb blood perfusion by increased implanted MSC survival and stimulated angiogenesis.
This study demonstrates the potential of zinc supplement to enhance survival of engrafted MSC and ameliorate their tissue regenerative potential in a mouse ischemic hindlimb model.
[Show abstract][Hide abstract] ABSTRACT: Iodinated contrast media (CM) can induce apoptosis and necrosis of renal tubular cells. The injuries of endothelial cells induced by CM on the systemic condition have not been fully understood. To assess the toxic effects of non-ionic CM on the glomerular and aortic endothelial cells, iopromide and iodixanol, two kinds of representative non-ionic CM, were used for the in vivo study. Sixty aged rats were respectively received the agents or normal sodium intravascularly. No obvious apoptosis and morphological change was detected in the glomerular and aortic endothelial cells apart from renal tubules after CM administration. However, expressions of the nitric oxide synthase (eNOS) in glomerular endothelium were decreased at 12h after CM injection. Furthermore, plasma creatinine and endothelin-1 were increased and plasma nitric oxide (NO) was decreased significantly after CM administration. However, we failed to observe the significant increase of plasma von Willebrand Factor. These results suggest that non-ionic iodinated CM do not induce apoptosis and necrosis of glomerular and aortic endothelial cells in vivo. Decreased eNOS expression and increased plasma endothelin-1 may be involved in non-ionic iodinated CM-induced endothelial dysfunction and kidney injury.
[Show abstract][Hide abstract] ABSTRACT: Calcium-sensing receptors (CaSRs) are G-protein coupled receptors which maintain systemic calcium homeostasis and participate in hormone secretion, activation of ion channels, cell apoptosis, proliferation, and differentiation. Previous studies have shown that CaSRs induce apoptosis in isolated adult rat heart and in normal neonatal rat cardiomyocytes by G-protein-PLC-IP3 signaling transduction. However, little knowledge is presently available concerning the role of CaSRs in the apoptosis induced by ischemia and reperfusion in neonatal cardiomyocytes.
Primary neonatal rat ventricular cardiomyocytes were incubated in ischemiamimetic solution for 2 h, and then re-incubated in normal culture medium for 24 h to establish a model of simulated ischemia/reperfusion (I/R). Cardiomyocyte apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The expression of CaSRs mRNA was detected by real-time reverse transcription polymerase chain reaction (RT-PCR). In addition, the expressions of caspase-3 and Bcl-2 were analyzed by western blot.
The simulated I/R enhanced the expression of CaSRs and cardiomyocyte apoptosis. GdCl3, a specific activator of CaSRs, further increased the expression of CaSRs and cardiomyocyte apoptosis, along with up-regulation of caspase-3 and down-regulation of Bcl-2.
CaSRs are associated with I/R injury and apoptosis in neonatal rat ventricular cardiomyocytes via suppressing Bcl-2 and promoting caspase-3 expression.
Journal of biomedical research. 07/2010; 24(4):301-7.
[Show abstract][Hide abstract] ABSTRACT: Bone marrow stem cells are able to repair infarcted human myocardium following intracoronary transplantation via the infarct-relative artery. However, traditional reperfusion strategies fail to open the artery in some patients, making effective delivery impossible. Our previous study demonstrated a safe and efficient approach to delivering bone marrow stem cells via a noninfarcted artery in an animal myocardial infarction model. The objective of the present study was to evaluate the safety and feasibility of autologous bone marrow mesenchymal stem cell transplantation via such an approach in patients with acute myocardial infarction (AMI). Sixteen patients with anterior AMI who had successfully undergone percutaneous coronary intervention (PCI) were enrolled in this pilot, randomized study. Three weeks after PCI, cultured bone marrow mesenchymal stem cells were injected into the myocardium via either the infarct-relative artery (left anterior descending branch artery, LAD) or a noninfarct-relative artery (right coronary artery, RCA). The safety and feasibility of the cell infusion were evaluated during the procedure and during 6 months of follow-up. In addition, 2D echocardiography, technetium-99m methoxyisobutylisonitrile (99mTc-MIBI) and 18F-deoxyglucose single photon emission computed tomography were employed to examine cardiac function, myocardial perfusion, and viable cardiomyocytes, respectively, at day 4 after PCI and 6 months after the cell infusion. There were no arrhythmia and any other side-effects, including infections, allergic reactions or adverse clinical events, during, immediately after, or 6 months after cell transplantation. Cardiac function and myocardial perfusion had improved 6 months after PCI/bone marrow stem cells transplantation. Viable cardiomyocytes metabolism was detected in the infarcted areas in both groups after the cell infusion, as demonstrated by 18F-deoxyglucose. Intracoronary infusion of autologous bone marrow mesenchymal stem cells via a noninfarct-relative artery appears safe and feasible in the treatment of patients with AMI.
[Show abstract][Hide abstract] ABSTRACT: Objectives. To observe the short- and long-term outcomes after percutaneous coronary intervention (PCI) in octogenarians (>80 y.o.) at our institution. Method. All octogenarians who underwent PCI during the study period were retrospectively retrieved from our database and clinically followed. Major adverse cardiac (and cerebral) events (MAC(C)E) was considered as primary outcome. Results. From January 2003 to December 2007, 140 octogenarians (mean age: 85+/-3 y.o., 79% of male) underwent PCI and were clinically followed 14+/-11 months. Procedural success was obtained in 100 percent of patients with single vessel disease, in 96 percent of patients with double vessel disease, and in 75 percent of patients with triple vessel disease. In-hospital, 30 days, and one year MACE rates were 5%, 5%, and 10.7%, respectively. Impaired left ventricular (LV) ejection fraction (hazard ratio (HR) = 0.909, 95% confidence interval (CI) = 0.856 to 0.964, P = .002), diabetes mellitus (HR = 5.792, 95% CI = 1.785 to 18.796, P = .003), and low GFR (HR = 2.943, 95% CI = 1.161, to 7.464, P = .023) were independently associated with an increase risk of MACE at long-term followup. Conclusion. Coronary angiography can be successfully performed in elderly patients with single and double vessel disease. The results in triple vessel disease are encouraging. Low LV function, diabetes, and impaired renal function increase the risk of long-term major adverse cardiac events.
Cardiology research and practice. 01/2010; 2010:263685.
[Show abstract][Hide abstract] ABSTRACT: The pathogenesis of intestinal carcinoma is characterized as progressing through multiple steps, which begin with atrophic gastritis followed by intestinal metaplasia, dysplasia and carcinoma. However, the clonal status of gastric precancerous lesions and its association with proliferative kinetics have not been fully understood. In this study, gastric lesions and normal epithelial cells were isolated from formalin-fixed paraffin embedded tissues using a laser capture microdissection (LCM) system, the clonality was analyzed with human androgen receptor gene (HUMARA) polymerase chain reaction (PCR), and the PCR products were examined using Applied Biosystems 3730 DNA Analyzer. The relationship between the clonal status and Ki-67 protein expression was also investigated. Ki-67 was detected by two-step immunohistochemical staining. 5/32 intestinal metaplasia lesions, 10/45 low grade intraepithelial neoplasia, 25/36 high grade intraepithelial neoplasia and 20/20 intestinal gastric carcinoma were of monoclonal origin. Similar to monoclonal inactivation, the expression rate of Ki-67 also increased along the multi-step gastric carcinogenesis. Clonal status was associated with the expression rate of Ki-67 to a certain extent, which may be useful in assessing susceptibility to gastric carcinoma. Key words: gastric carcinoma; precancerous lesion; clonal analysis; Ki-67.
[Show abstract][Hide abstract] ABSTRACT: ObjectiveTo investigate the relationship of Matrix metalloproteinase-9 polymorphism to acute coronary syndrome and its affect on the severity of coronary artery disease.MethodsBy means of polymerase chain reaction (PCR) and restriction fragment length polymorphism, Genotypes of 245 patients with acute coronary syndrome (ACS) and 205 healthy subjects were tested. Genotypes displaying C-1562T functional promoter polymorphism (of the MMP-9 gene) were determined. The relationship between the polymorphism of the MMP-9 gene and ACS and the severity of coronary vessels diseased was analyzed.ResultsThe frequency of C/ T plus T/ T genotypes and T allele in patients with ACS was significantly higher than that in healthy subjects (22.1%vs12.7 % and 11.4 %vs6.6% respectively). But they were not associated with the number of coronary arteries diseased.ConclusionThe MMP-9 polymorphism may be susceptible to ACS. But there was not significant difference between the AMI and UAP subgroups
[Show abstract][Hide abstract] ABSTRACT: Objective
To assess the acute and mid-term results of cardiac function improvements and left ventricular outflow tract gradient (LVOTG) changes in 30 patients displaying hypertrophic obstructive cardiomyopathy (HOCM) treated with percutaneous transluminal septal myocardial ablation (PTSMA)
Journal of Nanjing Medical University 04/2007; 21(3):143-146.
[Show abstract][Hide abstract] ABSTRACT: Three patients, all with a history of coronary heart disease, underwent coronary artery bypass grafting and implantation of autologous satellite cells. Satellite cells were isolated from muscle biopsies of the right vastus lateralis muscle after enzymatic treatment. While the heart was still under hypothermic cardioplegia, 4 mL of cell suspension divided into approximately 40 doses was injected into the ventricular wall of the ischemic area. Less than 5 minutes were required to complete the cell implantation. All patients survived the procedure, without obvious arrhythmia, had an uneventful recovery, and were discharged from the hospital. At 3 to 4 months follow-up examination, increased left ventricular ejection fraction, decreased left ventricular diastolic diameter, as well as improved ventricular wall thickness and perfusion at the satellite cell implantation sites were observed. Our experience indicated the safety and early benefit of cellular cardiomyoplasty using autologous satellite cells.
Journal of Cardiac Surgery 01/2003; 18(3):268-73. · 1.35 Impact Factor