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Abstract In recent years, the role of circular RNA in cancer cells has been studied broadly; however, the functional significance of circular RNA in the regulation of the tumor microenvironment (TME) is not fully understood. In this study, we aimed to reveal the role of circ_TNFRSF21 in M2 macrophage‐induced cutaneous squamous cell carcinoma (cSCC) angiogenesis. Quantitative polymerase chain reaction and Western blotting were performed to determine the levels of the indicated genes. Direct binding between circ_TNFRSF21 and miR‐3619‐5p, miR‐3619‐5p, and ROCK2 was verified by dual‐luciferase activity. The migration and invasion of human umbilical vein endothelial cells were evaluated by wound healing and transwell assays. Tube formation was performed to detect in vitro angiogenesis. Circ_TNFRSF21 and ROCK2 were upregulated in cSCC tissue, while miR‐3619‐5p was downregulated. Circ_TNFRSF21 negatively regulated the expression of miR‐3619‐5p, while miR‐3619‐5p negatively regulated the expression of ROCK2. miR‐3619‐5p suppressed tube formation by inhibiting ROCK signaling. M2 macrophages facilitated tube formation via the circ_TNFRSF21/miR‐3619‐5p/ROCK2 axis. Our present study revealed that circ_TNFRSF21 was elevated in M2 macrophages and mediated M2 macrophage‐induced tube formation in vitro.

Abstract Introduction No-reflow phenomenon (NRP) is one of the complications that mostly occur during percutaneous coronary intervention (PCI). In this study, we comprehensively examined the relationship between the model for end-stage liver disease-XI (MELD-XI) score and NRP. Moreover, we discussed whether the MELD-XI score could be considered as an accurate risk assessment score of patients with ST-segment elevation myocardial infarction (STEMI) who are candidates for PCI. Methods This retrospective study involved 693 patients with acute STEMI and who underwent an emergency PCI. They were divided into a normal reflow group or a no-reflow group on the basis of the flow rate of post-interventional thrombolysis in myocardial infarction. Univariate, multivariate logistic regression, and Cox regression analyses were performed to identify the independent predictors of NRP in both groups. Receiver operator characteristic (ROC) curves and Kaplan–Meier curves were plotted to estimate the predictive values of the MELD-XI score. Results MELD-XI score was found to be an independent indicator of NRP (odds ratio: 1.247, 95% CI: 1.144–1.360, P 9.78 (P

Abstract Challenges remain for clinicians over balancing the efficacy of active antithrombotic therapy and simultaneous bleeding reduction in patients. The clinical data of 347 patients with acute coronary syndrome (ACS) undergoing percutaneous coronary intervention (PCI) were retrospectively analyzed. On the basis of the given tirofiban, the patients were assigned into three different dose groups: high dose group (group H), medium dose group (group M), and low dose group (group L). The tirofiban efficacy was evaluated in terms of major adverse cardiovascular event (MACE) parameters and lab endpoints, including platelet count and function. The tirofiban safety was assessed by the occurrence of bleeding events. The patients were followed up for 1 month after the PCI. No significant difference in MACE events was evident among these groups (p > 0.05). Groups H and M reported an obvious reduction in platelet count (p

BACKGROUND: Intermediate coronary lesions (ICLs) are highly prevalent but ported mixed prognosis. Radial strain has been associated with plaque vulnerability, yet its role in predicting lesion progression is largely unknown. The purpose of this study was to determine the predictive value of angiography-derived radial wall strain (RWS) for progression of untreated non-culprit ICLs. METHODS: Post-hoc analysis was conducted in a study cohort including 603 consecutive patients with 808 ICLs identified at index procedure with angiographic follow-up of up to two years. RWS analysis was performed on selected angiographic frames with minimal foreshortening and vessel overlap. Lesion progression was defined as = 20% increase in percent diameter stenosis. RESULTS: Lesion progression occurred in 49 ICLs (6.1%) with a median follow-up period of 16.8 months. Maximal RWS (RWSmax), frequently located at the proximal and throat plaque regions, distinguished progressive ICLs from silent ones. The largest area under the curve value of 0.75 (95% CI: 0.67-0.82, P < 0.001) was reached at the optimal RWSmax cutoff value of > 12.6%. According to this threshold, 178 ICLs were classified as having a high strain pattern. Exposure to a high strain amplitude with RWSmax > 12.6% was independently associated with an increased risk of lesion progression (adjusted HR = 6.82, 95% CI: 3.67 -12.66, P < 0.001). CONCLUSIONS: Assessment of RWS from coronary angiography is feasible and provides independent prognostic value in patients with untreated ICLs. [ABSTRACT FROM AUTHOR]

The relationship between stent expansion conditions and clinical outcomes is not completely understood. This prospective cohort study included patients who were successfully implanted with second-generation drug-eluting stent in 2012 and received follow-up angiography in 9-12 months. Stent over-expansion was defined as ≥ 1.05 of the stented segment over the reference artery diameter. Imaging parameters were measured, and the follow-up period was 7 years. A total of 123 patients with 161 lesions were enrolled, and 75 (46.58%) stents were found to be over-expanded. The baseline clinical and procedural data were comparable. Stent over-expansion showed a markedly increased diameter stenosis percentage (DSP) at 1-year follow-up (24.12 ± 21.10% vs. 14.65 ± 16.75%, P = 0.002) and high late lumen loss (LLL) in-segment (0.54 ± 0.62 mm vs. 0.31 ± 0.55 mm, P = 0.014). Furthermore, 63 patients with ≥ 1 over-expanded stented lesions were classified into the over-expansion group. Cumulative major cardiac adverse event (MACE) was higher in the over-expansion group than the norm-expansion group (17.5% vs. 8.3%, P = 0.133). Target lesion revascularization/target vessel revascularization increased during the 7-year follow-up period in the over-expansion group compared with the norm-expansion group (11.1% vs. 3.3%, P = 0.098). The Kaplan-Meier cumulative MACE-free survival showed a better tendency for statistical differences in the norm-expansion group than in the over-expansion group (log-rank test; P = 0.083). Conclusion: Stent over-expansion is associated with a significant increase in LLL and DSP at 1-year angiographic follow-up and with the increasing trend of cumulative MACE during 7-year clinical follow-up period compared with stent norm-expansion. Stent over-expansion needs to be avoided. [ABSTRACT FROM AUTHOR]

Background. Percutaneous device occlusion and minimally invasive surgical repair for perimembranous ventricular septal defect (pmVSD) are two typical methods to reduce the invasiveness of the conventional operation through a median sternotomy. However, few studies have compared them in terms of effectiveness and cost. Methods. Inpatients with isolated pmVSD who had undergone percutaneous device occlusion or minimally invasive surgical repair from June 2009 to June 2012 were reviewed for a comparative investigation between the two procedures. Results. Procedure success was achieved in 80 percutaneous (93.0%) and in 113 surgical (98.3%) procedures (p = 0.076). Percutaneous patients were older, with a smaller VSD size than surgical patients (16 ± 11.7 vs 3.8 ± 2.4 mm, p<0.001; 4.0 ± 1.2 vs 4.3 ± 1.3 mm, p = 0.034, respectively). Major complications occurred in 1 percutaneous (1.2%) and in 4 surgical (3.5%) procedures (p = 0.602), and minor complications occurred in 27 percutaneous (33.3%) and in 37 surgical (32.2%) procedures (p = 0.991). The surgical repair cost 31% less than the device occlusion (¥20,565 ± ¥3,497 vs ¥29,795 ± ¥2,643, p < 0.001), where most of the cost was attributed to the occluder in the amount of ¥19,500. Conclusions. Compared with device occlusion, minimally invasive surgical repair can provide comparable efficacy and complication rates. In addition, it is 31% cheaper than device occlusion. In low-income countries where health care resources are limited, medical resources must be judiciously allocated to the treatment that allows for effective treatment of the largest number of patients. [ABSTRACT FROM AUTHOR]

AbstractAim:This study aimed to compare the efficacy and safety between standard and low-dose tirofiban in the treatment of elderly high-risk non-ST-segment elevation acute coronary syndrome (NSTE-ACS) patients who underwent percutaneous coronary intervention (PCI).Methods:Ninety-four very elderly (≥80 years) high-risk patients with NSTE-ACS were randomly assigned to the standard or the low-dose group. Upstream tirofiban was administered intravenously with a bolus dose of 0.4 μg·kg−1·min−1 over a period of 30 min after the diagnosis had been confirmed, and was followed by a 36−48 h infusion of 0.10 μg·kg−1·min−1 or 0.075 μg·kg−1·min−1. PCI was performed within 24 h of admission. Platelet aggregation inhibition and thrombolysis in myocardial infarction (TIMI) grade flow were assessed. The major adverse cardiac events (MACEs), including death, myocardial infarction, recurrent angina and urgent target-vessel revascularization (TVR), were documented at 7 d, 30 d, and 6 months, and bleeding events were recorded at 7 d.Results:Although a significantly higher inhibition of platelet aggregation was observed in the standard-dose group (P<0.05), angiographic PCI success was similar between the two groups (P>0.05). The rate of MACEs was not significantly different at 7 days (2.1% vs 4.4%, P=0.61), 30 days (6.3% vs 8.7%, P=0.71) and 6 months (14.6% vs 17.4%, P=0.71). Major bleeding events were significantly higher in the standard-dose group (10.4% vs 0.0%, P=0.03).Conclusion:In very elderly high-risk patients with NSTE-ACS undergoing PCI, low-dose tirofiban offered about the same level of protection from major ischemic events that standard doses did, with less associated bleeding.Acta Pharmacologica Sinica (2009) 30: 553–558; doi: 10.1038/aps.2009.38 [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the relationship between the serum calcitonin gene-related peptide (CGRP) level and severity of coronary stenosis.Methods: A total of 233 eligible patients who underwent coronary angiography were divided into two groups: a control and a coronary heart disease (CHD) group. The angiographic severity of coronary stenosis was evaluated by SYNTAX and Gensini scores. The incidence of major adverse cardiovascular events within two years was collected.Results: A negative correlation between serum CGRP levels and Gensini scores was observed in all patients (r=-0.352, p<0.001), the control group (r=-0.422, p<0.001) and the CHD group (r=-0.393, p<0.001). Serum CGRP levels were negatively associated with SYNTAX scores in the CHD group (r=-0.522, p<0.001). The area under the curve of CGRP for identifying high SYNTAX scores (>22) was 0.772 [95% confidence interval (CI): 0.673-0.870, p<0.001], and for identifying high Gensini scores was 0.744 (95% CI: 0.646-0.842, p<0.001). A CGRP concentration of 25.05 pg/ml was selected as the cutoff point. A low CGRP level (<25.05 pg/ml) was an independent predictor of severe coronary stenosis, a SYNTAX score >22 [odds ratio (OR) =5.819, 95% CI: 2.240-15.116; p<0.001] and a high Gensini score (>64) (OR=4.943, 95% CI: 2.020-12.095; p<0.001). The low CGRP group had a higher incidence of major adverse cardiovascular events within two years (11.1 vs. 3.1%, p=0.031).Conclusion: In coronary atherosclerosis patients without acute myocardial injury, serum CGRP levels were negatively associated with the severity of coronary stenosis. [ABSTRACT FROM AUTHOR]

Objective: The present study aims to investigate the incidence and predictors of atrial high-rate events (AHREs) in patients with permanent pacemaker implants.Methods: A total of 289 patients who were implanted with a dual-chamber pacemaker due to complete atrioventricular block or symptomatic sick sinus syndrome (SSS) and had no previous history of atrial fibrillation were included in the present study. AHREs are defined as events with an atrial frequency of ≥175 bpm and a duration of ≥5 min. The patients were divided into two groups according to whether or not AHREs were detected during the follow-up: group A (AHRE+, n = 91) and group N (AHRE–, n = 198).Results: During the 12-month follow-up period, AHREs were detected in 91 patients (31.5%). The multivariate Cox regression analysis revealed that patient age [odds ratio [OR] = 1.041; 95% confidence interval [CI], 1.018–1.064; and P < 0.001], pacemaker implantation due to symptomatic SSS (OR = 2.225; 95% CI, 1.227–4.036; and P = 0.008), and the percentage of atrial pacing after pacemaker implantation (OR = 1.010; 95% CI, 1.002–1.017; and P = 0.016) were independent AHRE predictors.Conclusion: The AHRE detection rate in patients with pacemaker implants was 31.5%. Patient age, pacemaker implantation due to symptomatic SSS, and the percentage of atrial pacing after pacemaker implantation were independent AHRE predictors.

Introduction: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is involved in the pathophysiology of atherosclerosis and acute coronary syndromes (ACS). Circulating soluble LOX-1 (sLOX-1) has been linked to the risk of coronary artery disease (CAD). Our aim was to test if baseline serum sLOX-1 was associated with major adverse cardiovascular events (MACE) in patients with stable CAD. Materials and methods: This multicentre pilot study enrolled 833 stable CAD patients. All patients were followed for two years. Serum sLOX-1 concentrations were detected by enzyme-linked immunosorbent assay (ELISA). The association between sLOX-1 concentrations and MACE was assessed by logistic regression, Kaplan-Meier survival curves and Cox proportional hazards analyses. Logistic regression analysis was employed to assess the predictors of complex lesion. Results: Multivariate logistic regression analysis revealed that sLOX-1 concentration was an independent predictor of MACE (OR 2.07, 95%CI 1.52 - 2.82; P < 0.001). Kaplan-Meier cumulative survival curves showed that the incidence of MACE in patients with a high sLOX-1 concentration was significantly higher than in patients with an intermediate or low sLOX-1 concentration (P < 0.001). Soluble LOX-1 concentrations were independently correlated with coronary complex lesions (OR 2.32, 95%CI 1.81 - 2.97; P < 0.001). Conclusions: Baseline sLOX-1 concentrations were correlated with 2-year MACE in stable CAD patients. Furthermore, patients with high serum sLOX-1 concentrations had higher cumulative incidence of MACE compared to those with low serum sLOX-1 concentrations. [ABSTRACT FROM AUTHOR]

The article offers an interpretation of various radiography performed on a 72-year-old male patient with dextrocardia. A stenosis at ostium of the left circumflex coronary artery (LCx) and stenosis at the mid, as well as proximal stenosis of a large right coronary artery were observed from transradial coronary angiography. The prevalence of dextrocardia in the general population is assessed.

Background Hypertension and its complications are associated with arterial remodeling. Transient receptor potential cationic channels (TRPCs) are important nonselective cationic channels that regulate calcium homeostasis in mammalian cell membranes. We aimed to study the expression of various TRPC isoforms in spontaneously hypertensive rat (SHR) carotid arterial remodeling and explore the relationship between SHR carotid arterial remodeling and TRPC expression. Materials and methods Thirty male SHRs were randomly divided into three groups and sacrificed at ages 4, 8, and 18 wk, respectively, with matching control male Wistar-Kyoto rats (n = 10). Caudal artery systolic blood pressure (SBP) was measured every 2 wk. Carotid artery remodeling parameters including carotid artery wall thickness (MT), lumen diameter (LD), medial area, collagen area rate, and average nuclear area in media cells were determined after histologic staining. Real-time polymerase chain reaction and immunoblot assays were performed to assess TRPC expression. Carotid artery remodeling and TRPC expression were reevaluated after ginsenoside Rb1 treatment from eighth to eighteenth week. Results Carotid artery remodeling of SHRs was aggravated gradually with age and SBP, as well as MT, LD, MT/LD, medial area, average nuclear area in media cells, and collagen deposition, most obvious at 18 wk. Interestingly, expression of TRPC1, 3, and 6 increased with age and SBP, with TRPC1/6 showing significant differences between the Wistar-Kyoto and 18 wk groups; TRPC4/5 expression was unchanged and TRPC7 was barely detected. Importantly, after ginsenoside Rb1 treatment, TRPC1/6 expressions were significantly inhibited, SBP decreased, and the carotid artery remodeling in SHRs relieved. Conclusions Upregulation of TRPC1 and TRPC6 may be involved in carotid arterial remodeling in SHRs. [ABSTRACT FROM AUTHOR]