Development and Validation of a Random Forest Risk Prediction Pneumothorax Model in Percutaneous Transthoracic Needle Biopsy.

BACKGROUND Computed tomography (CT)-guided percutaneous transthoracic needle biopsy (PTNB) is an effective means for diagnosing various thoracic diseases. Pneumothorax is the most common complication, and when it becomes life-threatening, urgent medical intervention is required. The purpose of this study was to develop and validate a model that can be used to predict postoperative pneumothorax following CT-guided PTNB. MATERIAL AND METHODS We enrolled 245 patients who completed CT-guided PTNB to develop the model. A random forest (RF) model was built using 15 risk factors (15-RFs). The 7 most critical risk factors (7-RFs) were extracted by feature selection and used to build a new model. The independent external validation data contained 97 patients. Logistic regression (LR), support vector machine (SVM), and decision tree (DT) models were also developed using both 15-RFs and 7-RFs, and their performance was compared with the RF models. RESULTS The length of the aerated lung traversed was identified as the most important risk factor for developing pneumothorax, followed by angle of pleural puncture, lesion depth, lesion size, age, procedure time, and sex. The RF model demonstrated better performance in the development and validation datasets when compared with the LR, SVM, and DT based on 15-RFs and 7-RFs. According to DeLong's test for difference in ROC curves, the RF models based on the 15-RFs and 7-RFs achieved similar classification performance (P>0.05). CONCLUSIONS This study demonstrated the feasibility of using the 7-RFs RF model for predicting postoperative pneumothorax before patients undergo CT-guided PTNB.

Schizandrin B attenuates hypoxia/reoxygenation injury in H9c2 cells by activating the AMPK/Nrf2 signaling pathway.

Schizandrin B exhibits prominent antioxidant and anti-inflammatory effects, and plays an important role in ameliorating myocardial ischemia/reperfusion injury. However, the underlying protective mechanisms remain to be elucidated. The aim of the present study was to explore the cardioprotective effects of schizandrin B against hypoxia/reoxygenation (H/R)-induced H9c2 cell injury, focusing on the role of the adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this process. The results showed that schizandrin B attenuated the H/R-induced decrease in cell viability and the increase in lactate dehydrogenase release, as well as the apoptosis rate in H9c2 cells. Schizandrin B also mitigated H/R-induced oxidative stress, as illustrated by the decrease in intracellular reactive oxygen species generation, malondialdehyde content and NADPH oxidase 2 expression, and the increase in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities. In addition, schizandrin B reversed the H/R-induced upregulation of pro-inflammatory cytokines [interleukin (IL)-1ß (IL-1ß) tumor necrosis factor-α, IL-6 and IL-8] and the downregulation of anti-inflammatory cytokines (transforming growth factor-ß and IL-10) in the culture supernatant. Notably, schizandrin B increased the expression of Nrf2, NAD(P)H: Quinone oxidoreductase (NQO-1) and heme oxygenase-1 (HO-1) in H/R-treated H9c2 cells, activating the Nrf2 signaling pathway. The cardioprotection of schizandrin B against H/R injury was inhibited by Nrf2 knockdown induced byNrf-2-specific small interfering RNA (siRNA; si-Nrf2) transfection. Furthermore, schizandrin B enhanced phosphorylated (p)-AMPK expression, while AMPK knockdown induced by AMPK-specific siRNA(si-AMPK) transfection remarkably eliminated schizandrin B-induced cardioprotection and reduced Nrf2 expression in H/R-treated H9c2 cells. Taken together, these results suggested that schizandrin B exerts cardioprotection on H/R injury in H9c2 cells due to its antioxidant and anti-inflammatory activities via activation of the AMPK/Nrf2 pathway.

Pitavastatin Combined with Ezetimibe Treatment was an Effective Approach to Non-IRA Lesion of ST-segment Elevation Myocardial Infarction Patients with Primary Percutaneous Coronary Intervention.

OBJECTIVE: ST-Segment Elevation Myocardial Infarction (STEMI) patients with the multivessel disease have distinctive plaque characteristics in non-IRA lesions. Intensive statin therapy was a potential approach to treat STEMI patients with the non-IRA disease. However, there is still poor evidence about the therapeutic effect. In this study, we have evaluated the detailed therapeutic effect of statin plus ezetimibe intensive therapy. METHODS: For STEMI patients with non-IRA disease undergoing primary Percutaneous Coronary Intervention (PCI), 183 control STEMI patients without non-IRA disease undergoing primary PCI, and 200 STEMI patients with non-IRA disease undergoing primary PCI were introduced into this study. 200 STEMI patients with non-IRA disease undergoing primary PCI were divided into Normal group, Intensive group, Normal & Combined group, and Intensive & Combined group. The baseline information for each participant was recorded. Meanwhile, the physiological and biochemical indicators of each member with different treatments were collected after one-year follow-up. RESULTS: For STEMI patients with non-IRA disease undergoing primary PCI, no differences could be detected in multiple indexes such as OCT examination results, age, stroke, etc. However, diabetes mellitus, smoking, and coronary Gensini score were different between different groups (P<0.05). After one year follow-up, cholesterol, low-density lipoprotein, coronary Gensini score, thin-cap fibroatheroma, length of non-infarcted arterial lesions, non-infarct artery lesion range, myocardial infarction again, and revascularization again were significantly different between different groups (P<0.05). CONCLUSION: The results mentioned above suggested that pitavastatin combined with ezetimibe was an effective approach for STEMI patients with non-IRA disease undergoing primary PCI. The results obtained in this study have provided a novel method for the treatment of STEMI patients with non-IRA disease undergoing primary PCI.

[Prognostic significance of admission N-terminal pro-brain natriuretic peptide in predicting angiographic no-reflow phenomenon during percutaneous coronary intervention in patients with acute myocardial infarction].

OBJECTIVE: To determine the relationship between N-terminal pro-brain-type natriuretic peptide (NT-proBNP) and angiographic no-reflow phenomenon in patients with acute myocardial infarction (AMI) after primary percutaneous coronary intervention (PCI). METHODS: The data of 106 consecutive AMI patients undergoing primary PCl were collected and analyzed retrospectively. NT-proBNP was obtained pre-PCI at admission. According to the NT-proBNP level, they were divided into normal and elevated NT-proBNP groups. The no-reflow phenomenon was defined as an angiographic outcome of Thrombolysis In Myocardial Infarction (TIMI) grade < 3 without accompanying mechanical factors. RESULTS: The patients with elevated NT-proBNP on admission had a higher incidence of no-reflow phenomenon than those with NT-proBNP level. Compared to normal reflow counterparts, no-reflow patients had a higher NT-proBNP level [1883 ng/L (484 ∼ 5500 ng/L) vs 220 ng/L (87 ∼ 926 ng/L) P = 0.046]. Multivariate analysis showed that a high NT-proBNP level (NT-proBNP > 1765 ng/L) on admission was an independent predictor of no-reflow. This cut-off value yielded a sensitivity of 60.0% and a specificity of 87.5% respectively. CONCLUSION: The NT-proBNP level on admission may be a prognostic biomarker in the prediction of the development of angiographic "no-reflow" phenomenon after primary PCI for AMI patients.

[Effect of tirofiban in acute anterior myocardial infarction patients without ST segment resolution after primary percutaneous coronary intervention].

OBJECTIVE: To observe the effect of glycoprotein receptor blockade tirofiban in acute anterior myocardial infarction patients without ST segment resolution after primary percutaneous coronary intervention (PCI). METHODS: From April 2006 to April 2008, 157 acute anterior myocardial infarction patients without ST segment resolution after PCI were randomly allocated to tirofiban (intravenous bolus 10 microg/kg followed by intravenous infusion of 0.15 microgxkg(-1)xmin(-1) for 48 h, n = 80) or equal volume saline (control group, n = 77). Baseline characteristics, PCI features and clinical outcomes during hospitalization, left ventricular ejection fractions (LVEF) and major adverse cardiac events (MACE, including death, re-infarction and target vessel revascularization) at 30 and 180 days after discharge were compared between the two groups. RESULTS: The baseline clinical characteristics were comparable between the two groups. Compared to control group, the MACE rates and re-infarction rates at 30 days (6.3% vs.18.2%, P < 0.05; 1.3% vs.9.1%, P < 0.05, respectively) and 180 days (10.0% vs.23.4%, P < 0.05; 2.5% vs.10.4%, P < 0.05, respectively) were significantly reduced in tirofiban group. LVEF value was significantly higher in tirofiban group at 30 days and 180 days compared with those in control group [(51 +/- 6)% vs. (46 +/- 8)%, P < 0.05; (57 +/- 7)% vs. (50 +/- 9)%, P < 0.05]. Hemorrhagic complications were similar between the two groups. CONCLUSION: Use of tirofiban for acute anterior myocardial infarction patients without ST segment resolution after PCI is safe and can significantly improve 30 and 180 days clinical outcomes after discharge.

[Clinical outcomes of trimetazidine in patients with acute ST segment elevation myocardial infarction without ST segment resolution after primary percutaneous coronary intervention].

OBJECTIVE: To evaluate prospectively the clinical outcomes of trimetazidine (TMZ) in patients with acute ST segment elevation myocardial infarction (STEMI) without ST segment resolution (STR) after primary percutaneous coronary intervention (PPCI). METHODS: From August 2005 to October 2007, 138 acute STEMI patients without STR after PPCI were randomly assigned to either with TMZ therapy (TMZ group, n = 70) or without TMZ (control group, n = 68). Baseline characteristics, PCI features and clinical outcomes during hospitalization were compared between the two groups. Left ventricular ejection fraction (LVEF) and major adverse cardiac events (MACE, including death, re-infarction and target vessel revascularization) at Days 30 and 180 after discharge were also compared. RESULTS: The baseline clinical characteristics were comparable between the two groups. There was no significant difference in MACE rates at Days 30 and 180 between the two groups (10/70 vs 11/68, P > 0.05; 15/70 vs 13/68, P > 0.05, respectively). The LVEFs of TMZ group at Days 30 and 180 were significantly superior to the control group (51 +/- 8)% vs (45 +/- 7)%, P < 0.05; (56 +/- 7)% vs (49 +/- 8)%, P < 0.05, respectively). CONCLUSION: Use of TMZ for patients with acute STEMI without STR after primary PCI can improve the left ventricular function at Days 30 and 180.

[Activities of circulating endothelial progenitor cells in patients with in-stent restenosis].

OBJECTIVE: To observe the number and activities of circulating endothelial progenitor cells (EPCs) in patients with in-stent restenosis. METHODS: Peripheral blood samples were collected from 15 patients with angiographically restenosis, and 17 baseline characteristics-matched patients without angiographically restenosis (control group). Mononuclear cells were isolated by Ficoll density-gradient centrifugation and plated on dishes coated with human fibronectin. After 7 days in culture, the nature of EPCs was characterized with anti-CD34 and anti-KDR, specific surface antibodies of EPC, and confirmed further with the use of fluorescein isothiocyanate-labeled ulex europaeus agglutinin-I (FITC-UEA-I) and DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine percolate)-labeled acetylated low-density lipoprotein (DiI-acLDL) by laser scanning confocal microscopy. The number of EPCs was counted in a blinded manner. EPCs were inoculated onto the culture plate and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-2H-tetrazolium bromide assay was used to measure the A value by enzyme labeling instrument to evaluate the proliferation. The migration of EPCs was assayed by scratch assay. EPC adhesion was performed by replating cells on fibronectin-coated dishes and then counting the adherent cells. Results The number of EPCs of the patients with in-stent restenosis was 4.97 +/- 1.42/well, significantly lower than that of the control group (17.2 +/- 3.90/well, P = 0.001). MTT assay showed that the proliferative activities of the in-stent restenosis group was 1.37 +/- 0.32 times the baseline value, significantly lower than that of the control group (2.01 +/- 0.62, P < 0.05). The number of migrating EPCs of the in-stent restenosis group was remarkably lower than that of the control group. There was no significant difference in the adherent activity between the two groups. Conclusion The number, proliferation activity, and migration activity of the EPCs patients with in-stent restenosis are all significantly lower, which may contribute to the mechanism of in-stent restenosis.