Effect of varying hypoxia reoxygenation times on autophagy of cardiomyocytes.

PURPOSE: To investigate the impact of different hypoxia reoxygenation (HR) times on autophagy of rat cardiomyocytes (H9C2). METHODS: Rat cardiomyocytes were randomly divided into normal control group (group A), hypoxia group (group B), 2 h HR group (group C), 12 h HR group (group D), and 24 h HR group (group E). LC3 II/LC3 I was determined via western blotting, and cell viabilities of cardiomyocytes were measured using methyl thiazolyl tetrazolium (MTT) assay. RESULTS: Cell viabilities in HR model groups were significantly lower than those of group A (P<0.05). LC3 II/LC3 I levels in groups B to D were significantly higher than those of group A (P<0.05), and group D showed the highest LC3 II/LC3 I levels. Cell viabilities in groups B to D were significantly lower than those of group A (P<0.05), with group D showing the lowest cell viabilities (P<0.05). CONCLUSIONS: Hypoxia can induce autophagy in rat cardiomyocytes, which can be further activated by reoxygenation; most notable after 12 h. Hypoxia-induced cell injury can be aggravated by reoxygenation. The lowest cell viability was observed at 12 h after reoxygenation; however, cell viability can be recovered after 24 h.

Effect of varying hypoxia reoxygenation times on autophagy of cardiomyocytes

Abstract Purpose: To investigate the impact of different hypoxia reoxygenation (HR) times on autophagy of rat cardiomyocytes (H9C2). Methods: Rat cardiomyocytes were randomly divided into normal control group (group A), hypoxia group (group B), 2 h HR group (group C), 12 h HR group (group D), and 24 h HR group (group E). LC3 II/LC3 I was determined via western blotting, and cell viabilities of cardiomyocytes were measured using methyl thiazolyl tetrazolium (MTT) assay. Results: Cell viabilities in HR model groups were significantly lower than those of group A (P<0.05). LC3 II/LC3 I levels in groups B to D were significantly higher than those of group A (P<0.05), and group D showed the highest LC3 II/LC3 I levels. Cell viabilities in groups B to D were significantly lower than those of group A (P<0.05), with group D showing the lowest cell viabilities (P<0.05). Conclusions: Hypoxia can induce autophagy in rat cardiomyocytes, which can be further activated by reoxygenation; most notable after 12 h. Hypoxia-induced cell injury can be aggravated by reoxygenation. The lowest cell viability was observed at 12 h after reoxygenation; however, cell viability can be recovered after 24 h.

Cardiac shockwave therapy improves myocardial function in patients with refractory coronary artery disease by promoting VEGF and IL-8 secretion to mediate the proliferation of endothelial progenitor cells.

Cardiac shockwave therapy (CSWT) is a potential and effective remedy to promote revascularization in the ischemic myocardium of patients with refractory coronary heart disease (CHD). The technique is both safe and non-invasive; however, the underlying molecular mechanism remains unclear. The aim of this study was to evaluate the efficacy of CSWT in treating CHD patients and investigate a potential mechanism. A total of 26 patients with CHD were enrolled in the study, and CSWT was performed over a 3-month period. The efficacy of CSWT was assessed using several clinical parameters. Peripheral blood (PB) was collected prior to and following treatment. The number of circulating endothelial progenitor cells (EPCs) in the PB was counted using a flow cytometer, and the levels of vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), stromal cell-derived factor 1 and matrix metalloproteinase 9 in the PB were analyzed. Mononuclear cells were isolated from the PB and cultured in vitro. The EPCs and EPC-colony forming units (EPC-CFUs) in the PB mononuclear cell culture were counted using an inverted phase contrast microscope. Following CSWT, the tested clinical parameters were significantly improved. The levels of circulating EPCs, VEGF and IL-8 in the PB were significantly increased, as were the EPCs and EPC-CFUs from the PB mononuclear cell culture. We suggest that EPC proliferation, mediated by VEGF and IL-8 secretion, may be among the potential mechanisms associated with CSWT.

[A comparison of magnetic resonance spectroscopy and diffusion weighted imaging for diagnosing prostate cancer].

OBJECTIVE: To compare the clinical values of magnetic resonance spectroscopy (MRS) and diffusion weighted imaging (DWI) in diagnosing prostate cancer. METHODS: A 1. 5T MR scanner was used in this study. We measured 274 regions of interest (ROI) in the images produced by MRS and DWI from 53 patients. The biopsy confirmed 150 ROI as cancers and 124 ROI as non-cancers. The results of MRS and DWI were compared using receiver operating characteristic (ROC) curves. RESULTS: Significant differences (P<0. 05) between malignant and benign tumors were found in signal intensity (b= 0,100,800 s/mm, in DWI), ADC value(in DWI), Cit content integral, Cho content integral and (Cho+Cr)/Cit ratio (in MRS). The ROC curves showed that ADC value, signal intensity (b=800 s/mm2) and the ratio of (Cho+Cr)/Cit performed better in distinguishing prostate cancers from benign tumors. The optimal operating point (OOP) of ADC value was determined as 1. 027 x 10(-3) mm2/s, with 0. 887 specificity, 0. 953 sensitivity, 0. 84 Youden index, and the area under curve (AUC) of 0. 966. The OOP of signal intensity (b=800 s/mm2) was determined as 47. 1, with 0. 806 specificity, 0. 72 sensitivity, 0. 53 Youden index, and the AUC of 0.782; The OOP of (Cho+Cr)/Cit ratio was determined as 0.78, with 0. 806 specificity, 0. 793 sensitivity, 0. 60 Youden index, and the AUC of 0. 844. CONCLUSION: DWI is a better method than MRS in differentiating prostate cancers from benign tumors.

[Extracorporeal cardiac shock wave therapy for treatment of coronary artery disease].

OBJECTIVE: To evaluate the feasibility and efficiency of extracorporeal cardiac shock wave therapy (CSWT) for treatment of coronary artery disease. METHODS: Twenty-five patients with 1 - 16 years history of chronic angina pectoris underwent the CSWT. Before and after the treatment, low-dose Dobutamine stress echocardiography and (99)Tc(m)-MIBI myocardial perfusion SPECT were applied to locate the ischemic segments, detect the viable myocardium and evaluate the effect of CSWT. Under the guidance of echocardiography, CSWT was applied in R-wave-triggered manner with low energy (0.09 mJ/mm(2)) at 200 shoots/spot for 9 spots (-1-0-+1 combination). Patients were divided group A and group B. Sixteen patients in group A were applied 9 sessions on 29 segments within 3 month and nine patients in group B were applied 9 sessions on 13 segments within 1 month. Ten chronic angina pectoris patients receiving standard medication served as controls. RESULTS: All patients completed the 9 sessions without procedural complications or adverse effects. CSWT significantly improved symptoms as evaluated by NYHA, Canadian Cardiovascular Society (CCS) class sores, Seattle angina questionnaire (SAQ), 6-min walk and the use of nitroglycerin (P < 0.05). CSWT also improved myocardial perfusion and regional myocardium function as evaluated by rest SPECT and stress peak systolic strain rate (PSSR) (P < 0.01). Myocardial perfusion improvement was more significant in group A compared with group B (1.21 ± 0.86 vs. 0.83 ± 0.80, P < 0.01). All parameters remained unchanged in control group during follow up. CONCLUSION: These preliminary results indicate that CSWT is safe and effective on ameliorating anginal symptoms for chronic angina pectoris patients.

Cardiac shock wave therapy reduces angina and improves myocardial function in patients with refractory coronary artery disease.

BACKGROUND: Safe and effective therapeutic management of refractory coronary artery disease (CAD) in heart patients is critical to enhance cardiovascular function and improve quality of life. Current therapies for refractory CAD are inadequate in ameliorating angina and promoting revascularization of ischemic myocardium. HYPOTHESIS: Cardiac shock wave therapy (CSWT) is a safe and effective noninvasive intervention in the management of patients with refractory CAD. METHODS: The study enrolled 9 male patients age 50 to 70 years (5.11 ± 5.46 years) with a diagnosis of CAD and stent implantation (3.00 ± 2.24 stents). CSWT was carried out for 3 months at 3 intervals during the first week of each month (first, third, and fifth day), for a total of 9 therapies per patient. Dobutamine stress echocardiography and radionuclide angiography identified the myocardial ischemic segments. The effects of CSWT on myocardial perfusion and systolic function were examined. Other outcome measures included myocardial injury enzyme markers, angina scale, nitroglycerin dosage, and cardiopulmonary fitness assessments. RESULTS: Improved myocardial blood flow and regional systolic function (stress peak systolic strain rate - 1.10 to - 1.60 s(-1), P = 0.002) were detected in patients following CSWT. Reductions in creatine kinase (87.89 ± 36.69 to 86.22 ± 35.96 IU/L, P = 0.046), creatine kinase MB (10.89 ± 5.73 to 10.11 ± 5.93 IU/L, P = 0.008), aspartate transaminase (interquartile range [IQR], 28.00 to 27.00 IU/L, P = 0.034) were also found. Angina (Canadian Cardiovascular Society scale IQR 3.0 to 2.0, P = 0.035) and nitroglycerin dose reduction (IQR 3.0 to 1.0 times/wk, P = 0.038) were reported. CONCLUSIONS: This study is a preliminary assessment of CSWT in patients with refractory CAD. We report that CSWT is a noninvasive, effective, and safe intervention in the treatment of refractory CAD.

A risk-predictive score for cardiogenic shock after acute myocardial infarction in Chinese patients.

BACKGROUND: Cardiogenic shock after acute myocardial infarction (AMI) remains a poor prognosis. Although numerous studies discussed the predictors of cardiogenic shock complicating AMI, the data in Chinese patients is still absent. The goal of this study is to develop a risk-predictive score for cardiogenic shock after AMI, among Chinese patients, so as to guide clinicians to prevent cardiogenic shock. METHODS: Patients with ST-segment elevated AMI were provided by two Chinese hospitals from 1994 to 2004. Baseline characteristics of each case were documented. Multivariable logistic regression modeling techniques were used to develop a model to predict the occurrence of cardiogenic shock within 72 h after admission. On the basis of the coefficients in the model, a risk score was developed for the probability of cardiogenic shock. To test its viability, another population, which was consistent with the original population, confirmed the scoring. RESULTS: Among 2,077 patients, 184 cases developed cardiogenic shock within 72 h. Age, gender, BMI, killip class, MI location, multivessel disease, previous MI, family history of CAD, and thrombolytic therapy were strong predictors for shock after AMI. A risk-predictive score for shock was developed. It predicted cardiogenic shock accurately in another Chinese population. CONCLUSIONS: A predictive model is developed in Chinese patients with AMI for the first time. It is based on some simple parameters, which can be easily obtained by clinicians. The risk score derived from the model can predict cardiogenic shock accurately.