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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, p22) was 0.772 [95% confidence interval (CI): 0.673-0.870, p22 [odds ratio (OR) =5.819, 95% CI: 2.240-15.116; p64) (OR=4.943, 95% CI: 2.020-12.095; p

Objective In a substudy of a randomized controlled trial, we investigated the effects of the valsartan/amlodipine single-pill combination and nifedipine gastrointestinal therapeutic system (GITS) monotherapy on brachial pulse pressure (bPP) and radial augmentation index (rAI) in patients with previously uncontrolled hypertension. Methods We performed measurements of clinic blood pressure (BP) and pulse rate and rAI (n = 63) and ambulatory BP monitoring (n = 42) at baseline and 12-week of follow-up. Analysis of covariance was performed to calculate the least square mean change from baseline and between-group differences [95% confidence interval (CI)]. Correlation analysis was performed to study the interrelationship between the changes in bPP and rAI and in pulse rate. Results After 12-week treatment, clinic and ambulatory SBP/DBP and pulse rate were not differently changed between the valsartan/amlodipine (n = 29) and nifedipine GITS groups (n = 34, P ≥ 0.06) except daytime SBP (P = 0.01). The reductions in 24-h and daytime ambulatory bPP were significantly greater in the former than the latter group (P ≤ 0.04). rAI increased slightly by 3.5% (P = 0.20) and 5.2% (P = 0.06) in the valsartan/amlodipine and nifedipine groups, respectively, with a between-group difference of -1.7% (95% CI -9.6 to 6.1%, P = 0.66). In the two groups combined, the changes in clinic and ambulatory bPP were not or weakly associated with that in clinic or ambulatory pulse rate (r = -0.14 to 0.36, P = 0.02-0.95), while the changes in rAI were more strongly or significantly associated with that in clinic or ambulatory pulse rate (r = -0.39 to -0.23, P = 0.02-0.16). Conclusions Antihypertensive drug-induced changes in rAI but not bPP were dependent on pulse rate.

Background: Cutaneous squamous cell carcinoma (cSCC) is a malignant proliferation of cutaneous epithelium. Ferroptosis is a new type of cell death involved in cancer progression. M2 macrophage derived exosomes promote cancer proliferation and progression. We intended to investigate the role of M2 macrophages derived exosomes on ferroptosis in cSCC and explore the underlying mechanism. Methods: cSCC samples and adjacent normal tissues were obtained from cSCC patients. Exosomes were isolated from M2 macrophages differentiated from human mononuclear macrophage (THP-1) cells by flow cytometry. Cell viability, iron level, Malondialdehyde (MDA), Lipid ROS, mitochondrial superoxide, mitochondrial membrane potential (MMP) were detected for the validation of ferroptosis. RNAs and proteins were measured using RT-qPCR and western blot. Binding relationships between miR-451a and circ_TNFRSF21 or SLC7A11 were revealed by dual luciferase assay.Results: M2 macrophages were increased in cSCC tissues. M2 macrophages inhibited erastin-induced ferroptosis, which was reversed by exosome inhibitor GW4869. SLC7A11 was up-regulated in cSCC tissues. Erastin treatment reduced cell viability, increased the level of iron and Fe2+, upregulated MDA, lipid-ROS, mitochondrial superoxide, and declined MMP, which were reversed by M2 exosomes. Interestingly, circ_TNFRSF21 knockdown antagonized these effects of M2 exosomes. Circ_TNFRSF21 targeted miR-451a to regulate SLC7A11. Erastin-induced ferroptosis was promoted by miR-451a mimics, which was reversed after SLC7A11 overexpression. M2 exosomes inhibited erastin-induced ferroptosis in cSCC cells, which was antagonized by SLC7A11 downregulation or miR-451a upregulation. Conclusion: M2 macrophage exosomes inhibited ferroptosis in cSCC through circ_TNFRSF21/miR-451a/SLC7A11 axis. It is contributed to cSCC progression and may providing a novel target for therapy.

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.

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 P P 9.78 (P Conclusion The MELD-XI score can be used to predict NRP and the 30-day prognosis in patients with STEMI who are candidates for primary PCI. It could be adopted as an inexpensive and a readily available tool for risk stratification.

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.

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.

Objectives The present study aimed to investigate the association between periprocedural myocardial infarction (PMI), defined by creatine kinase (CK)-MB or troponin I (TNI) level elevations >5 times the 99th percentile of the upper reference limit (URL) within 48 hr after implantation of a drug-eluting stent (DES), and one-year mortality in patients with coronary bifurcation. Background PMI is reported to be associated with increased one-year mortality after DES implantation. However, the prevalence and association of PMI with mortality after stenting bifurcation lesions remains unclear. Methods We prospectively followed 1,971 patients with true coronary bifurcations who underwent DES implantation as part of the multicenter DEFINITION study. These patients were grouped into categories based on PMI outcome: Non-PMI, CKMB-PMI, TNI-PMI, and CKMB/TNI-PMI. The primary endpoint was the rate of all-cause mortality at one year. Results PMI occurred in 11.4% of patients by CKMB criteria and 41.3% of patients by TNI criteria. At one-year follow-up, the mortality rate was 2.3% in the entire patient population. However, mortality was significantly higher in the CKMB-PMI (6.4%) and CKMB/TNI-PMI (6.1%) groups compared to the Non-PMI (1.7%) and TNI-PMI (2.1%) groups (all P

Objectives The present study established criteria to differentiate simple from complex bifurcation lesions and compared 1-year outcomes stratified by lesion complexity after provisional stenting (PS) and 2-stent techniques using drug-eluting stents. Background Currently, no criterion can distinguish between simple and complex coronary bifurcation lesions. Comparisons of PS and 2-stent strategies stratified by lesion complexity have also not been reported previously. Methods Criteria of bifurcation complexity in 1,500 patients were externally tested in another 3,660 true bifurcation lesions after placement of drug-eluting stents. The primary endpoint was the occurrence of a major adverse cardiac event (MACE) at 12 months. The secondary endpoint was the rate of stent thrombosis (ST). Results Complex (n = 1,108) bifurcation lesions were associated with a higher 1-year rate of MACE (16.8%) compared with simple (n = 2,552) bifurcation lesions (8.9%) (p Conclusions Complex bifurcation lesions had higher rates of 1-year MACE and ST. The 2-stent and PS techniques were overall equivalent in 1-year MACE. However, 2-stent techniques for complex lesions elicited a lower rate of cardiac death and in-hospital MACE but higher rates of in-hospital ST and revascularization at 1 year for simple lesions.

Spontaneously hypertensive rats (SHR) was used to study left ventricular hypertrophy (LVH) and its dynamic change after the interventions with Telmisartan and Amlodipine. The results showed that the expression of TRPC1, CaN and NFATC3 increased gradually with the pathogenesis and progression of LVH. Telmisartan reduced blood pressure and LVH, and down-regulated the expression of TRPC1, CaN and NFATC3 in left ventricle of SHR. Amlodipine reduced the blood pressure in SHR but had no impact on the hypertrophy and expression of above factors. Our data suggest that the pathogenesis and progression of LVH in SHR are related to upregulation of TRPC1, CaN and NFATC3 signaling pathway.

The microstructural evolution of Al–Zn–Mg–Zr alloy with trace amount of Sc during homogenization treatment was studied by means of metallographic analysis, scanning electron microscopy (SEM), energy dispersive X-ray (EDX) and differential scanning calorimetry (DSC). The results show that serious dendritic segregation exists in studied alloy ingot. There are many eutectic phases with low melting-point at grain boundary and the distribution of main elements along interdendritic region varies periodically. Elements Zn, Mg and Cu distribute unevenly from grain boundary to the inside of alloy. With increasing the homogenization temperature or prolonging the holding time, the residual phases are dissolved into matrix α(Al) gradually during homogenization treatment, all elements become more homogenized. The overburnt temperature of studied alloy is 476.7 °C. When homogenization temperature increases to 480 °C, some spherical phases and redissolved triangular constituents at grain boundaries can be easily observed. Combined with microstructural evolution and differential scanning calorimeter, the optimum homogenization parameter is at 470 °C for 24 h.

Al-5.8Mg-0.4Mn-0.25Sc-0.1Zr (mass fraction, %) alloys were prepared by water chilling copper mould ingot metallurgy processing which was protected by active flux. The recrystallization temperature and nucleation mechanism of the alloy were studied by means of hardness tests, observations of optical microscopy and transmission electron microscopy. The results show that the anti-crystallization ability can be significantly improved by adding minor Sc and Zr into Al-Mg-Mn alloy. This can be proved by a much higher recrystalliztion temperature (450 °C) than Al-Mg-Mn alloy without Sc and Zr (150 °C). The main reason of the great increase of recrystallization temperature can be attributed to the strong pinning effect of highly disperseded Al3(Sc,Zr) particles on dislocations and sub-grain boundaries. The recrystallizing process reveals itself the nucleation mechanism of the alloy involving not only the sub-grain coalescence but also the sub-grain growth.

Percutaneous coronary intervention (PCI) in coronary bifurcation lesions is relatively common in daily practice which accounts for approximately 1/5 of all the PCI procedures. Transradial PCI of left main or non–left main bifurcation lesions can be successfully accomplished in most cases, but this practice is still restricted in many centers worldwide due to the perceived technical challenges of guiding catheter support, limitations of catheter sizes, need for the simultaneous use of stents and balloons, and consequences of procedural failure. In the past few years, Chinese interventionists have developed a few techniques, such as double kissing crushing technique, double kissing mini culotte stenting technique to increase the procedural success rate and improve the long-term prognosis of complex bifurcation intervention. In this chapter, we will give a detailed description of those bifurcation intervention techniques via transradial approach.

The present study was designed to examine whether astaxanthin (ASX, 3,3-dihydroxybeta, beta-carotene-4,4-dione, CAS 472-61-7), a dietary antioxidant carotenoid that is naturally present in algae, crustaceans, and fish, has a protective effect on endothelial dysfunction of aortas in diabetic rats and the possible molecular mechanism involved. Male Wistar rats were randomly divided into four groups: control rats, diabetic rats, diabetic rats treated with ASX (10 mg/kg/d), and control rats treated with ASX. Type 1 diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 60 mg/ kg). STZ-induced diabetes in rats was complicated with excessive oxidative stress and endothelial dysfunction, increased serum oxidized low-density lipoprotein (ox-LDL) and aortic malondialdehyde (MDA) levels, inhibited endothelium-dependent vasorelaxation to acetylcholine (ACh) and unaffected endothelium-dependent vasorelaxation to sodium nitroprusside (SNP). Simultaneously, lectin-like oxLDL receptor-i (LOX-1) expression was enhanced and endothelial nitric oxide (NO) synthase (eNOS) expression was reduced in the aortas of diabetic rats. ASX treatment could significantly decrease serum oxLDL and aortic MDA levels, attenuate blunted endothelium-dependent vasodilator responses to ACh, upregulate eNOS expression, and decrease LOX-1 expression. These results indicated that ASX could ameliorate diabetic endothelial dysfunction by inhibiting the ox-LDLLOX-1-eNOS pathway. Treatment with ASX might be clinically useful for diabetic complications associated with endothelial dysfunction.

IntroductionProvisional stenting (PS) for simple coronary bifurcation lesions is the mainstay of treatment. A systematic two-stent approach is widely used for complex bifurcation lesions (CBLs). However, a randomised comparison of PS and two-stent techniques for CBLs has never been studied. Accordingly, the present study is designed to elucidate the benefits of two-stent treatment over PS in patients with CBLs.Methods and analysisThis DEFINITION II study is a prospective, multinational, randomised, endpoint-driven trial to compare the benefits of the two-stent technique with PS for CBLs. A total of 660 patients with CBLs will be randomised in a 1:1 fashion to receive either PS or the two-stent technique. The primary endpoint is the rate of 12-month target lesion failure defined as the composite of cardiac death, target vessel myocardial infarction (MI) and clinically driven target lesion revascularisation. The major secondary endpoints include all causes of death, MI, target vessel revascularisation, in-stent restenosis, stroke and each individual component of the primary endpoints. The safety endpoint is the occurrence of definite or probable stent thrombosis.Ethics and disseminationThe study protocol and informed consent have been approved by the Institutional Review Board of Nanjing First Hospital, and accepted by each participating centre. Written informed consent was obtained from all enrolled patients. Findings of the study will be published in a peer-reviewed journal and disseminated at conferences.Trial registration numberNCT02284750; Pre-results.

Biodegradable and biocompatible materials are the basis for medical application. As an initial step for developing bone internal fixation materials, the biological evaluation of poly-l-lactic acid/bioactive glass (PLLA/BG) composite in vitro and in vivo, including the hemolysis test, pyrogen test, acute systemic toxicity test, genetic toxicity test, anaphylaxis test, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test, direct cell culture and in vivo implant experiment, was performed. The results indicated that PLLA/BG composite showed no acute systemic toxicity, genetic toxicity, anaphylaxis reaction, and pyrogen reaction, and the hemolysis ratio was 0.39%. MTT assay indicated that no cytotoxic effect was observed for the PLLA/BG composite, and in addition, a significant increase in cellular activity compared to the negative control group was found. Excellent adhesion between fibroblast and PLLA/BG material was observed, the fibroblasts cultured on the PLLA/BG composite substrates revealed a higher proliferation and differentiation rate than those on the pure PLLA substrates. In vivo implant experiment showed that the PLLA/BG composite could maintain the mechanical properties during the course of fracture therapy, and the malleolar fracture of rabbits was healed in 8 weeks on the whole. Therefore, PLLA/BG composites have a promising biological response as a potential implant material.

Bioactive and bioresorbable composite materials were fabricated from poly-L-lactide and bioactive glass (average particle size 6.8 μm) by a solvent evaporation technique. Cellular cultivation in vitro and MTT assay were conducted for evaluating the influence on morphology, growth and proliferation of cultured fibroblasts. The results of cytotoxicity testing show that cells cultured in extracts of PLLA/BG and on the surface of composites demonstrate normal growth and proliferation. The bioactive glass in PLLA composite facilitates both adhesion and proliferation of rat fibroblasts on PLLA/bioactive glass composite film.

Perventricular 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 median sternotomy. However, few comparative studies have been made between them in terms of effectiveness and cost. A review was made of the inpatients with isolated pmVSD, who had undergone perventricular device occlusion or minimally invasive surgical repair from June 2011 and January 2013 for a comparative investigation between the two procedures. The two treatment groups had similar baseline characteristics. Procedural success was achieved in 163 (94.8 %) of the perventricular and 137 (98.6 %) of the surgical (P = 0.136). Major complications occurred in 2 (1.2 %) of the perventricular and 4 (2.9 %) of the surgical (P = 0.497), and minor complications, in 57 (33 %) of the percutaneous and 49 (35.2 %) of the surgical (P = 0.696). In cost, the surgical repair was 30.5 % cheaper than the device occlusion (Yuan 20139 ± 3760 vs. 28970 ± 3343, P

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.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.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, p0.001; 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, p0.001), where most of the cost was attributed to the occluder in the amount of ¥19,500.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.

Current hypertension guidelines recommend single-pill combinations because they not only improve convenience and compliance to therapy and thus blood pressure (BP) control, but also reduce health-care costs. This study compared the efficacy and safety of valsartan/amlodipine single-pill combination with nifedipine gastrointestinal therapeutic system (GITS) in Chinese patients with hypertension who were inadequately controlled with monotherapy.In this multicenter, open-label, active-controlled, parallel-group study, 564 patients with hypertension not adequately controlled by prior monotherapy were randomized to receive valsartan/amlodipine 80/5 mg or nifedipine GITS 30 mg once daily for 12 weeks.In the intention-to-treat analysis (n = 540), valsartan/amlodipine (n = 272) showed a least-square mean reduction of -16.6 versus -10.8 mmHg by nifedipine GITS (n = 268; mean between-treatment difference: -5.8 mmHg; P 0.0001) from baseline to week 12. The corresponding results for mean sitting diastolic BP were -8.6 and -4.6 mmHg, respectively (difference: -4.0 mmHg; P 0.0001). The percentage of patients achieving the BP target (140/90 or130/80 mmHg in the absence or presence of diabetes mellitus, respectively) was significantly higher with valsartan/amlodipine (79.0%) versus nifedipine GITS (57.4%; P 0.0001). The overall incidence rate of adverse events was lower with valsartan/amlodipine (19.2%) than with nifedipine GITS (29.4%; P = 0.004).The valsartan/amlodipine 80/5 mg single-pill combination is well tolerated and more effective than nifedipine GITS 30 mg for BP control in Chinese patients with hypertension.

The optimal stenting strategy for the treatment of coronary bifurcation lesions (CBLs) remains uncertain. The present study observed technical feasibility and reliability, 9-month clinical and angiographic outcomes of the modified culotte stenting (MCS) in the treatment of CBLs with drug-eluting stents.A total of 34 consecutive patients with CBLs that required stenting the parent vessel (PV), the main branch (MB) and the side branch (SB) were included. All patients were first assigned to receive MCS for CBL interventions (per MCS), and might be switched to receive the double-kissing-crush stenting (DKS) in case of temporally acute branch occlusion (per protocol).The immediate angiographic or procedural success was achieved in 33/34 (97%) lesions (patients) per MCS, 34/34 (100%) lesions (patients) per protocol with 100% successful final balloon kissing. The long-term clinical success at 9 months was 94% per MCS and 94% per protocol, only 2 patients had reoccurrence of angina but none of them needed target lesion revascularization. There were no procedure-related biomarker elevation, no in-stent thrombosis peri-procedurally and at 9-month follow-up. Quantitative coronary angiography data at 9 months showed that in-stent (6%) or in-segment (6%) binary stenosis was infrequent, and minimal lumen diameter was significantly reduced but late lumen loss was acceptable with only (0.10 ± 0.14) mm for PV, (0.21 ± 0.23) mm for MB and (0.27 ± 0.32) mm for SB.MCS for treatment of CBLs that required dual-stent implantation was technically easier and safer, readily to complete final balloon kissing, and was associated with high immediate success and optimal 9-month outcomes.

Background Lifestyle interventions, including physical exercise, are feasible options for the prevention and treatment of cardiovascular diseases. In this study, the effects of exercise of different intensities on the infarct region, function, and angiogenesis of the left ventricle (LV) in postmyocardial infarction (MI) rats were investigated and the levels of vascular endothelial growth factor (VEGF) proteins in the LV and plasma were examined. Materials and methods Male Sprague-Dawley rats were randomly assigned to six groups. The exercise-trained rats observed a daily 60-min treadmill routine 5 days/weeks for 6 weeks. Different treadmill speeds were used in the high-intensity exercise (HIE), moderate-intensity exercise (MIE), and low-intensity exercise (LIE) groups, whereas the untrained rats remained sedentary (Sed). At 6 weeks, all rats underwent either an acute MI operation or a sham (Sh) MI operation 24 h after their last treadmill exercise or the corresponding Sed protocol. They were then killed 7 days after recovery. Echocardiographic and hemodynamic measurements were taken at the end of the experimental protocol. The infarct regions were analyzed using Masson's trichrome staining, whereas intramyocardial microvessels were detected using Factor VIII-related antigen staining. The cardiac VEGF protein levels were determined by western blotting analysis, and plasma VEGF concentrations were examined by enzyme-linked immunosorbent assay. Results Compared with the corresponding parameters in the Sed-Sh group, LV function did not significantly ameliorate and microvessel density did not increase in the MIE-Sh group. Compared with the Sed-MI group, the MIE-MI and HIE-MI groups had significantly reduced LV infarct size, improved hemodynamic parameters, and increased fractional shortening, scar thickness, and microvessel density, these parameters did not significantly change in the LIE-MI group. In addition, the MIE-MI and HIE-MI rats had significant differences in hemodynamic parameters and microvessel density. Compared with those of the Sed-MI group, the heart and plasma of the exercise-trained rats in the MIE-MI and HIE-MI groups displayed higher levels of VEGF protein, but the difference between the MIE-MI and HIE-MI groups was not significant. Conclusions Moderate-intensity running before acute MI improved LV function, reduced scar size, and increased scar thickness and microvessel density in post-MI rats. Exercise at a higher intensity could have further small effects. LIE may be beneficial, but it would not be sufficient to improve MI. Moderate-intensity and high-intensity running upregulated the expression of VEGF protein and increased microvessels, which may have partly improved cardiac function after MI in this study.

to investigate the combined effect of rosuvastatin (RSV) and ischemic postconditioning (PC) on myocardial ischemia-reperfusion (I/R) injury in a type 2 diabetic rat model.type 2 diabetic (induced by streptozotocin plus nicotinamide) rats, undergoing 30 min ischemia and 120 min reperfusion, were divided into six groups (n = 10 each): Sham, I/R without other interventions, RSV before reperfusion, PC with 3 cycles of 10 s reperfusion and 10 s ischemia, RSV + PC and RSV + PC + PI3-K inhibitor LY294002. Myocardial infarct size (IS), ultrastructural change and myocardial expression of phosphorylated eNOS/total eNOS were determined.IS and ultrastructural damages were all significantly reduced and myocardial eNOS phosphorylation was significantly increased in RSV and PC groups compared with the I/R group (all P0.05) these beneficial effects were further enhanced by RSV + PC (all P0.05 vs. RSV and PC, respectively). The beneficial effects were significantly attenuated by PI3K inhibitor LY294002.the results indicate that RSV + PC could alleviate myocardial ischemia-reperfusion injury in this type 2 diabetic model by activating PI3K/AKT/eNOS signaling pathway.

The optimal stenting strategy in true coronary artery bifurcation lesions has not been determined. In this study, a strategy of always stenting both the main vessel and the side branch (MV plus SB) was compared with a strategy of stenting the MV only with optional stenting of the SB. Stents used were sirolimus-eluting stents and paclitaxel-eluting stents.A total of 108 patients with true coronary bifurcation lesions were randomly assigned to either routine stenting with drug-eluting stents (DES) in both the branches (group MV plus SB) or provisional stenting with DES placement in the main branch and DES placement in the SB only if MV stenting alone provided inadequate results (group MV). The primary end points were major adverse cardiac events (MACE) at 8 months, including myocardial infarction, cardiac death, and stent thrombosis or target vessel revascularization by either percutaneous coronary intervention or coronary artery bypass grafting.Angiographic follow-up revealed 28.91+/-20.43% stenosis of the SB after provisional stenting and 18.93+/-15.34% (P0.01) after routine stenting. The corresponding binary restenosis rates were 35.2 and 14.8% (P=0.015). SB stents were implanted in 16.7% of patients in the provisional stenting group and 94.4% of patients in the routine stenting group. In the main branch, binary restenosis rates prebifurcation were 11.1% after provisional and 7.4% after routine stenting (P=0.51), whereas binary restenosis rates postbifurcation were 14.8 and 9.3% (P=0.38), respectively. The overall 8-month incidence of target lesion reintervention was 31.5% after provisional and 7.4% after routine stenting (P0.01), and cumulative MACE were 38.9 and 11.1% (P0.01), respectively.Routine stenting significantly improved the MACE outcome of percutaneous coronary intervention in true coronary bifurcation and bifurcation angle of 60 or less lesions as compared with provisional stenting.

The objective of this study was to evaluate the effects of specific NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) on inflammatory response and cardiac function in a rat model of coronary microembolization (CME). CME was developed by injecting a suspension of microthrombotic particles (MTPs) into the left ventricle when obstructing the ascending aorta. MTPs were generated from the rat clots sized by filtration through 38 microm screen. Thirty-two Sprague-Dawley rats served as sham group, 128 CME rats were randomized to untreated (CMEU) and PDTC-treated (CMEp) group. Rats in CMEp were administered intraperitoneally with 50, 100, 200 mg kg-1 day-1 PDTC, respectively, from 1 h before to 7 days after operation. The rats were sacrificed on day 1, 3, 7, 14 post-operationally and each subgroup consisted of eight rats. The general morphological characteristics were observed in sections with HE staining, and the severity of myocardial loss (SML) was determined by percent micro-necrotic area in sections with hematoxylin basic fuchsin picric (HBFP) staining 1 day or by percent micro-fibrotic area in sections with Masson's trichrome staining 14 days post-operationally. Left ventricular (LV) function was evaluated echocardiographically and hemodynamically. Activity of NF-kappaB/DNA-binding was analyzed by electrophoresis mobility shift assays (EMSA), and expressions of TNF-alpha, IL-6, and ICAM-1 genes and proteins were detected by Real-time PCR and western blots, respectively. CME rats exhibited pathological changes evidenced by multi-focal myocardial necrosis, inflammatory cell infiltration with remarkably increased SML and persistent reduction of LV function. Activity of NF-kappaB/DNA-binding was markedly increased, also TNF-alpha, IL-6 and ICAM-1 transcripts and their protein expressions were upregulated strongly in the myocardium following CME. PDTC in a dose-dependency significantly suppressed the myocardial inflammatory cytokine transcriptions, decreased SML and improved LV function. Thus, NF-kappaB is markedly activated in CME hearts, and inhibition of NF-kappaB by PDTC prevents the subsequent inflammatory activation and improves cardiac function. Patients with or at risk of CME may benefit from acute anti-inflammatory treatment with PDTC.

Transcatheter Amplatzer occlusion of patent ductus artertiosus (PDA) has emerged as a minimally invasive alternative to surgical closure. The goal of this study was to compare long-term clinical outcomes between two procedures, especially on chronic residual shunt, late or very late procedure-related complications, and regression of pulmonary hypertension and left ventricular dilation.A total 255 patients having isolated PDA with a minimal diameter ofor= 4 mm treated from January 2000 to July 2003 were included in this study and have been followed up until July 2008. The patients were assigned to either the device or surgical closure group according to the patients' and/or their parents' preference. Baseline physical exams, chest roentgenography, electrocardiography, and echocardiography were performed preprocedure and at each follow-up.Seventy-two patients accepted the transcatheter procedure (Group-TC) and 183 underwent surgical operation (Group-SO) for PDA closure, both groups were similar in their demographics and preoperative clinical characteristics. There were no cardiac deaths and late complications such as infectious endocarditis and Amplatzer duct occluder (ADO) dislodge in either group. More acute procedure-related complications were recorded in Group-SO (13.7%) compared with Group-TC (1.4%) (P = 0.004). The recovery time was (8.7 +/- 2.3) days for the Group-SO and (1.3 +/- 0.5) days for the Group-TC (P0.001). The survival freedom from persistent residual shunt, defined as residual shunt that can not resolve automatically, was 91.3% for Group-SO and 98.6% for Group-TC (P = 0.037 by Log-rank test). There was no significant difference in regression of pulmonary hypertension and left ventricular dilation; neither survival freedom from pulmonary hypertension nor abnormal left ventricular end-diastolic volume index were significantly different between the surgical group and the Amplatzer group.Our study confirmed the long-term safety and efficacy of transcatheter Amplatzer occlusion. In comparison to the time-proven surgical closure, transcatheter Amplatzer occlusion was less invasive and associated with fewer complications and residual shunt, and as effective in the regression of pulmonary hypertension and left ventricular dilation.

To investigate the time course of myocardial NF-kappaB activation and association with cardiac function and other pro-inflammation cytokines following coronary microembolization (CME).CME was induced by homologous microthrombotic particle suspension injection into left ventricle with simultaneous short-term ascending aorta clamping. The CME rats were randomized to untreated group and pyrrolidine dithiocarbamate (PDTC, a specific NF-kappaB inhibitor) treated group (n = 32 respectively). The rats were sacrificed on day 1, 3, 7 and 14 post-operationally (n = 8 each). Twenty-four rats were sham-operated and served as controls. NF-kappaB DNA-binding activity was evaluated by electrophoretic mobility shift assay (EMSA), protein expressions of TNFalpha, IL-6 and ICAM-1 were analyzed by Western blotting, the dynamic alterations of TNFalpha, IL-6 and ICAM-1 mRNA were quantitatively assessed by Real-time PCR post hemodynamic measurements.NF-kappaB DNA-binding activity in CME group was significantly increased than that of sham group on day 1, peaked at day 3 and was similar as that in sham rats on day 14. The protein and mRNA expressions of TNFalpha, IL-6 and ICAM-1 were significantly increased in CME group at various time points compared those in sham rats. NF-kappaB DNA-binding activity positively correlated with mRNA expressions of TNFalpha, IL-6, ICAM-1, respectively (r = 0.72, P0.05; r = 0.94, P0.01; r = 0.62, P0.05). PDTC significantly suppressed protein and mRNA expressions of TNFalpha, IL-6 and ICAM-1 (P0.05) and improved left ventricular function.NF-kappaB activation post CME could upregulate the gene transcriptions of TNFalpha, IL-6, ICAM-1 and enhance inflammatory responses and aggravate left ventricular dysfunction.

To investigate the effects of granulocyte colony stimulating factor (G-CSF) on myocardial apoptosis following coronary microembolization (CME) and possible role of Janus kinase/singnal transducer and activator of transcription (JAK/STAT) pathway in this process.A total of 92 male Sprague Dawley rats were randomized into CME (n = 24), G-CSF (100 microg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), JAK2 inhibitor AG490 (G-CSF plus AG490, 5 mg x kg(-1) x d(-1) i.p. 2 hours post CME for 5 days, n = 24), all rats received left ventricular injection of homologous microthrombotic particle suspension post clamping the ascending aorta. Sham-operated group (n = 20) served as control. The rats were sacrificed at day 3, 7, 14 and 28 after operation. The myocardial mRNA expressions of Bcl-2, Bax, Fas, FasL and GAPDH which was used as the intercomparison, were evaluated by real time PCR. The ratio of Bcl-2/Bax was compared. The protein expression of Caspase-3, cleaved PARP, t-JAK2, p-JAK2, t-STAT3 and p-STAT3 were detected by western blot. Myocardial apoptosis were examined by TUNEL staining.Compared with Sham rats, the mRNA of Bcl-2, Bax, Fas and FasL significantly increased whereas the ratio of Bcl-2/Bax (0.28 +/- 0.04 vs. 2.98 +/- 0.49) significantly decreased and the protein expression of Caspase-3 (0.762 +/- 0.129 vs. 0.133 +/- 0.027), PARP (0.992 +/- 0.146 vs. 0.386 +/- 0.074) and the myocardial apoptosis index (17.2 +/- 1.9 vs. 1.2 +/- 0.6) significantly increased in CME hearts (all P0.05). rhG-CSF significantly attenuated CME induced changes and cotreatment with JAK2 inhibitor AG490 abolished the effects of rhG-CSF. The protein expressions of t-JAK2 and t-STAT3 among the groups were similar. P-JAK2 and p-STAT3 protein expressions were significantly increased in G-CSF group compared to other groups (P0.05).G-CSF attenuated myocardial apoptosis induced by CME via JAK2/STAT3 pathway.

As a kind of sirolimus-eluting stent (SES) made in China, Firebird SES is more effective than bare metal stent (BMS) and not inferior to Cypher SES for short coronary lesions in terms of reduction of restenosis and revascularization. However, Firebird SES does not show any benefits in patients with a very long coronary lesion (VLCL). The present study was undertaken to evaluate the safety and efficacy of Firebird SES for VLCL by comparison of Cypher SES and BMS.In this prospective, nonrandomized and comparative study, eligible patients with de novo coronary lesion (or = 30 mm) between January 2005 and June 2006 were allocated into Firebird SES group, Cypher SES group or BMS group. They were subjected to an angiographic follow-up of 6 months and a clinical follow-up of 12 months. The primary endpoints constitute the in-stent and in-segment restenosis rates at 6 months. The secondary endpoint was defined as a major adverse cardiovascular event (MACE) that was a 12-month combined endpoint of all-cause deaths, reinfarction or in-stent thrombosis, and target-lesion revascularization. The 12-month in-stent thrombosis was also evaluated to address the safety of Firebird SES implantation exceptionally.A total of 468 patients were assessed for eligibility. Of 113 patients who were finally included according to the prior inclusion and exclusion criteria, 39 (41 lesions) were treated with Firebird SES, 37 (39 lesions) with Cypher SES, and 37 (37 lesions) with BMS. There were no significant differences in the baseline characteristics between the three groups; but there were longer lesions, more frequent use of overlapping stent in the Firebird SES group and the Cypher SES group. Angiographic follow-up showed that the rates of binary stenosis were similar between the Firebird SES group and the Cypher SES group (in-segment: 14.6% vs 12.8%, relative risk (RR) 1.14, P = 0.81; in-stent: 9.8% vs 10.3%, RR 0.95, P = 0.94), and significantly lower than those in the BMS group (in-segment: vs. 36.1%, RR 0.41 or 0.36, P = 0.04 or 0.03, respectively; in-stent: vs 30.6%, RR 0.32 or 0.34, P = 0.03 or 0.04, respectively). The total MACE rate up to 12 months was also similar in both SES groups (7.7% vs 5.4%, P = 1.000), and significantly lower than that in the BMS group (27.0%, P = 0.034 or 0.024, respectively). The in-stent thrombosis rate in the follow-up period was 2.6% in the Firebird SES group, not higher in the Cypher SES and BMS groups (2.7% and 2.7%, respectively, P = 1.000).In the treatment of VLCL, Firebird SES would be safer and more effective than BMS. Firebird SES may be not inferior to Cypher SES in terms of restenosis and MACE.

To investigate the effects of preconditioning with doxycycline on ischemia/reperfusion (I/R) injury and expressions of matrix metalloproteinase-1 (MMP-1) and MMP-9 in myocardium in rat in vivo.Sixty-four healthy male SD rats, weighing 300-350 g, were randomly divided into three groups: sham operation group (n = 16), I/R group (n = 24), and doxycycline preconditioning group (n = 24). The heart function, plasma level of creatine kinase (CK) and lactate dehydrogenase (LDH), and the activity of myeloperoxidase (MPO) were respectively determined in rat myocardium after ischemia for 60 minutes and reperfusion for 120 minutes or with the same procedure but with precondition of Doxycycline. Also the expressions of MMP-1 and MMP-9 was determined by immunohistochemistry.In I/R group, left ventricular systolic pressure (LVSP) and the maximum and minimum first derivative of LVSP (+/-dp/dtmax) were significantly less, and left ventricular end diastolic pressure (LVEDP), CK, LDH, the activity of MPO, and the protein expressions of MMP-1 and MMP-9 were remarkably higher compared with the sham operation group (P0.05 or P0.01). Heart function was improved, CK, LDH, MPO and the expressions of MMP-1 and MMP-9 were reduced obviously by doxycycline preconditioning compared with the I/R group (P0.05 or P0.01).Precondition with doxycycline could remarkably abate I/R injury of rat myocardium in vivo and inhibit the expressions of MMP-1 and MMP-9.

To analyze the evaluation and treatment of blood loss during total hip arthroplasty (THA) and total knee arthroplasty (TKA) in the aged .We retrospectively surveyed the blood loss and the rehabilitation of 46 cases of TKA and 146 cases of THA older than 60.In the group younger than 70, the mean total blood loss of THA was 1425 mL and the hidden hemorrhage 729 mL (51%); following the TKA, the mean total loss was 1386 mL and the hidden hemorrhage was 890 mL (64%). In the group 70 and older, the mean total blood loss of THA was 1435 mL and the hidden hemorrhage was 769 mL (53%)û following the TKA, the mean total loss was 1380 mL and the hidden hemorrhage was 910 mL (65%). The difference of hidden hemorrhage between the THA and the TKA was both significant by different (p0.05). Age played an important part in the THA group (p0.05), but not in the TKA group (0.05).The aged have poor resistance to blood loss. Hidden hemorrhage in the TKA or THA perhaps is the primary part of the blood loss. Prompt treatment is helpful for the rehabilitation.

Background Dobutamine stress echocardiography has been proposed as a diagnostic tool to identify viable myocardium. How regional wall thickening responds to dobutamine in the ischemic or short-term hibernating myocardium has not been adequately defined. We hypothesized that regional wall thickening would improve initially and subsequently deteriorate with incremental doses of dobutamine in viable myocardial regions supplied by a stenotic coronary artery. This study was undertaken to determine whether this biphasic pattern of regional function characterizes the response of ischemic or hibernating myocardium to dobutamine and to explore the factors and mechanisms that determine this response. Methods and Results Twenty-six pigs in four groups were studied: a control group (n=5) to assess the response of myocardium perfused by nonstenotic coronary artery to incremental doses of dobutamine, and three experimental groups with a left anterior descending coronary artery stenosis producing acute myocardial ischemia (n=7), short-term myocardial hibernation for 90 minutes (n=7), and short-term hibernation for 24 hours (n=7) to determine the functional and metabolic response to dobutamine under these conditions. Regional coronary flow was reduced to 40% to 60% of baseline, with significant reductions of regional wall thickening as measured by two-dimensional echocardiography and sonomicrometers. An incremental dobutamine infusion from 2.5 to 25 μg · kg −1 · min −1 increased wall thickening and coronary flow without lactate production in the control group. In the other three groups, during the incremental dobutamine infusion, regional wall thickening improved initially, from 11.4±7.5% to 19.8±11.4%, P −1 · kg −1 but deteriorated subsequently to 5.0±5.8% at the maximal dose of dobutamine of 12.6±4.1 μg · min −1 · kg −1 . The initial improvement of regional wall thickening was associated with a small increase in regional coronary flow (from 0.53±0.18 to 0.68±0.25 mL · min −1 · g −1 myocardium, P P Conclusions A biphasic response of wall thickening to incremental dobutamine with initial improvement and subsequent deterioration is characteristic of ischemic or short-term hibernating myocardium. The initial low-dose dobutamine infusion improved wall thickening in the ischemic or hibernating myocardial region to a modest level. This initial modest improvement was transient and at the expense of metabolic deterioration of myocardial ischemia, so that at higher doses during prolonged dobutamine infusion, wall thickening deteriorated, lactate accumulated, and myocardial acidosis developed.

Objective Lifestyle interventions including exercise training have been shown to be a feasible option for the prevention and treatment of cardiovascular diseases. In this study, we investigated the effects of prior different intensities of exercise on infarct region and function and angiogenesis of the left ventricle (LV) in post-myocardial infarction (MI) rats, and further examined the expression of VEGF proteins in the left ventricle. Methods Male Sprague–Dawley rats were randomly assigned to six groups. The exercised rats underwent a daily 60-min treadmill exercise, 5 d/wk, for 6 wk. Different treadmill speeds were carried out in the high intensity exercise group (HIE-MI group, 30 m/min), moderate intensity exercise groups (MIE-Sh and MIE-MI groups, 21 m/min), low intensity exercise group (LIE-MI group, 12 m/min), respectively, whereas the untrained rats (Sed-Sh and Sed-MI groups) remained sedentary. At 6 wk, 24 h after the last treadmill exercise or the corresponding sedentary protocol, all rats underwent either acute MI (LIE-MI, MIE-MI, HIE-MI and Sed-MI groups) or sham MI operation (MIE-Sh and Sed-Sh groups). Then, all rats were sacrificed at 7d after recovery. Echocardiographic and haemodynamic measurements were performed at the end of the experimental protocol, and hearts were sampled for histological and molecular analysis. The infarct regions were analysed by using Masson9s trichrome staining; intramyocardial microvessels were detected by using Factor VIII-related antigen staining; and cardiac VEGF protein levels were determined by Western blotting analysis. Results Compared with Sed-Sh group, MIE-Sh group ameliorated left ventricular function and increased microvessels intensity, though the difference was not significant. Compared with Sed-MI group, MIE-MI and HIE-MI groups significantly reduced left ventricular infarct size, improved haemodynamic parameters, increased fractional shortening, scar thickness and microvessel density, but LIE-MI rats only had slight, and non-significant effect on these parameters. In addition, the differences between MIE-MI and HIE-MI rats were significant in haemodynamic parameters and microvessel density. Interestingly, compared with Sed-MI group, the exercised hearts displayed higher levels of VEGF protein in MIE-MI and HIE-MI groups. However, there was no significant difference between MIE-MI and HIE-MI groups. Conclusion Moderate intensity running exercise before acute MI improved LV function, reduced scar size, increased scar thickness and microvessel density in the post-MI rat. Additional higher intensity exercise could have little further effect. Low intensity exercise may be beneficial, but not sufficient to improve MI. Moderate and high intensity running upregulated the expression of VEGF protein, and contributed to the increased microvessels, which may partly benefit cardiac function after MI.