MELD-XI score predict no-reflow phenomenon and short-term mortality in patient with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

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 < 0.001). Multivariate Cox regression analysis also revealed that the MELD-XI score is an independent prognostic factor for 30-day all-cause mortality (hazard ratio: 1.155, 95% CI: 1.077-1.239, P < 0.001). Moreover, according to the ROC curves, the cutoff value of the MELD-XI score to predict NRP was 9.47 (area under ROC curve: 0.739, P < 0.001). The Kaplan-Meier curves for 30-day all-cause mortality revealed lower survival rate in the group with a MELD-XI score of > 9.78 (P < 0.001). 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.

Low Serum Calcitonin Gene-Related Peptide Level is Associated with Severity of Coronary Stenosis.

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.

Over-expansion of second-generation drug-eluting stents, risk of restenosis, and relation to major adverse cardiac events.

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.

Periprocedural myocardial infarction is associated with increased mortality in patients with coronary artery bifurcation lesions after implantation of a drug-eluting stent.

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 99 th 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 < 0.05). A 10-fold increase in TNI levels resulted in similar PMI rate (5.2%) and mortality risk (adjusted HR 2.7, 95% CI 3.0-5.2) as a fivefold increase in CKMB levels. CONCLUSIONS: PMI, as defined by CKMB elevations following coronary bifurcation lesion stenting, was associated with increased one-year mortality. Additionally, to attain an equal frequency of PMI, the elevation in TNI levels needed to be twice as high as the elevation in CKMB levels.

Upregulation of TRPC1/6 may be involved in arterial remodeling in rat.

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.

Telmisartan reduces atrial arrhythmia susceptibility through the regulation of RAS-ERK and PI3K-Akt-eNOS pathways in spontaneously hypertensive rats.

Telmisartan is an angiotensin II receptor blocker that displays unique PPAR-γ modulating activity. PPAR-γ agonists have been shown to decrease susceptibility to atrial fibrillation through their antioxidant and antiapoptotic effects. The aim of this study was to determine whether telmisartan would have a greater effect on susceptibility to atrial arrhythmia in a hypertensive rat model than valsartan, which is a traditional angiotensin II receptor blocker. In this study, spontaneously hypertensive rats were treated with 10 mg·(kg body mass)(-1)·d(-1) telmisartan (TEL group), 10 mg·(kg body mass)(-1)·d(-1) valsartan (VAL group), or vehicle (saline; SHR group) for 4 weeks. Age-matched Wistar-Kyoto rats (WKY) were used as normotensive controls. After 4 weeks of treatment, we performed echocardiographic assessment, electrophysiological analysis, histological evaluation, and Western blot analysis. Telmisartan decreased systolic blood pressure to a similar extent as valsartan. Relative to the WKY controls, atrial arrhythmia susceptibility was significantly increased in the SHR group, and was significantly decreased by both telmisartan and valsartan, albeit to a greater extent with telmisartan. Arrhythmogenic atrial remodeling, including enlargement of the left atrium, myocyte hypertrophy, interstitial fibrosis, and myocyte apoptosis, was observed in the SHR group, and was accompanied by activated RAS-ERK signaling and suppressed PI3K-Akt-eNOS signaling. The results suggest that telmisartan reduced susceptibility to atrial arrhythmia to a greater extent than valsartan, ameliorated atrial remodeling, and reversed imbalances in the RAS-ERK and PI3K-Akt-eNOS pathways.

Comparison of effectiveness and cost between perventricular device occlusion and minimally invasive surgical repair for perimembranous ventricular septal defect.

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 < 0.001), where most of the cost was attributed to the occluder in the amount of Yuan 19,500. Compared with perventricular device closure, minimally invasive surgical repair can provide comparable efficacy and complication rates, without the potential for developing atrioventricular block at long-term follow-up. In addition, it is 30.5% cheaper than hybrid procedure. In the low-income countries where health-care resources are limited the medical resources must be judiciously allocated to the treatment that allows for effective treatment of the largest number of patients.

Transfemoral Device Occlusion and Minimally Invasive Surgical Repair for Doubly Committed Subarterial Ventricular Septal Defects.

Transfemoral device occlusion and minimally invasive surgical repair are performed for doubly committed subarterial ventricular septal defect (dcVSD) to reduce the invasiveness of the conventional surgical repair through a median sternotomy. However, few studies have compared them in terms of effectiveness and cost. Inpatients with isolated dcVSD who had undergone transfemoral device occlusion or minimally invasive surgical repair from January 2011 to June 2014 were reviewed for a comparative investigation between the two procedures. Procedure success was achieved in 36 transfemoral (75 %) and in 36 surgical (100 %) procedures (p = 0.001). Transfemoral patients were older, with a VSD size similar to that of surgical patients (14.5 ± 11.7 vs 4.4 ± 2.9 years, p < 0.001; 4.5 ± 1.5 vs 4.4 ± 1.3 mm, p = 0.577, respectively). No significant difference was observed in complication rates between the two treatment groups (p = 1). No large residual shunt was observed. Small residual shunt was noted in two transfemoral patients and four surgical patients (p = 0.674). All these small residual shunts closed spontaneously during follow-up. The surgical repair costs 26 % less than the device occlusion (Yuan 22063.2 ± 343.9 vs Yuan 29970.1 ± 1335.2, p < 0.001), where most of the cost was attributed to the occluder in the amount of Yuan 19,500. Compared with device occlusion, minimally invasive surgical repair can provide superior efficacy and comparable complication rates. In addition, it is 26 % cheaper than device occlusion. In low-income countries where healthcare resources are limited, medical resources must be judiciously allocated to the treatment that allows for effective treatment of the largest number of patients.

Stem cells with FGF4-bFGF fused gene enhances the expression of bFGF and improves myocardial repair in rats.

The aim of this study was to investigate whether the modification of bone marrow-derived mesenchymal stem cells (BMSCs) with the fused FGF4 (fibroblast growth factor 4)-bFGF (basic fibroblast growth factor) gene could improve the expression and secretion of BFGF, and increase the efficacies in repairing infarcted myocardium. We used In-Fusion technique to construct recombinant lentiviral vectors containing the individual gene of bFGF, enhanced green fluorescent protein (EGFP), or genes of FGF4-bFGF and EGFP, and then transfected these lentiviruses into rat BMSCs. We conducted an in vitro experiment to compare the secretion of bFGF in BMSCs infected by these lentiviruses and also examined their therapeutic effects in the treatment of myocardial infraction in a rodent study. Sixty rats were tested in the following five conditions: Group-SHAM received only sham operation as controls; Group-AMI received only injection of placebo PBS buffer; Group-BMSC, Group-bFGF and Group-FGF4-bFGF received implantation of BMSCs with empty lentivirus, bFGF lentivirus, and FGF4-bFGF lentivirus, respectively. Our results found out that the transplanted FGF4-bFGF BMSCs had the highest survival rate, and also the highest myocardial expression of bFGF and microvascular density as evidenced by Western blotting and immunohistochemistry, respectively. As compared to other groups, the Group-FGF4-BFGF rats had the lowest myocardial fibrotic fraction, and the highest left ventricular ejection fraction. These results suggest that the modification of BMSCs with the FGF4-bFGF fused gene can not only increase the expression of bFGF but also improve its secretion. The FGF4-bFGF BMSCs thus can enhance the survival of the transplanted cells, diminish myocardial fibrosis, promote myocardial angiogenesis, and improve cardiac functions.

Circ_TNFRSF21 promotes cSCC metastasis and M2 macrophage polarization via miR-214-3p/CHI3L1.

BACKGROUND: Cutaneous squamous cell carcinoma (cSCC) is a highly invasive disease with the potential to metastasize and cause fatality. Therefore, it is crucial to understand the mechanism behind cSCC in order to devise effective strategies to combat this disease. OBJECTIVE: We investigated the function of circ_TNFRSF21/miR-214-3p/CHI3L1 axis in cSCC. METHODS: The features of circ_TNFRSF21 was characterized using Sanger sequencing, and RNase R/actinomycin D treatment. Genes and M1/M2 markers levels were assessed by qRT-PCR and IHC. The proliferation, migration, and invasion of cells were evaluated by CCK-8, colony formation, EdU incorporation, and transwell assays. Tumor growth and metastasis in vivo were evaluated by nude mouse xenograft model. Interactions of circ_TNFRSF21/miR-214-3p and miR-214-3p/CHI3L1 were validated by RNA immunoprecipitation and dual luciferase assay. RESULTS: Circ_TNFRSF21 and CHI3L1 expression were elevated in both human cSCC tissues and cells, whereas miR-214-3p was reduced. Circ_TNFRSF21 silencing or miR-214-3p overexpression suppressed cSCC cell proliferation, migration, invasion, and M2 macrophage polarization. Circ_TNFRSF21 functioned as a sponge for miR-214-3p while miR-214-3p directly targeted CHI3L1. Knockdown of miR-214-3p reversed the effects of circ_TNFRSF21 knockdown on cSCC development, while CHI3L1 upregulation reversed the effects of miR-214-3p overexpression. Furthermore, knockdown of circ_TNFRSF21 inhibited cSCC tumor growth and metastasis in vivo. CONCLUSION: Circ_TNFRSF21 plays a significant role in cSCC progression by enhancing cell proliferation, migration, invasion, and M2 macrophage polarization through inhibiting miR-214-3p and subsequent disinhibition of CHI3L1. These findings deepen our understanding of the molecular mechanism of cSCC and propose the circ_TNFRSF21/miR-214-3p/CHI3L1 axis as promising diagnosis markers or therapeutic targets for cSCC.

M2 macrophage facilitated angiogenesis in cutaneous squamous cell carcinoma via circ_TNFRSF21/miR-3619-5p/ROCK axis.

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.

Angiography-derived radial wall strain predicts coronary lesion progression in non-culprit intermediate stenosis.

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.

Clinical efficacy and safety of tirofiban combined with conventional dual antiplatelet therapy in ACS patients undergoing PCI.

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 < 0.05 for both) and an increased platelet inhibition rate (p < 0.05 for both). Group H showed a higher rate of total bleeding events than the other groups (Group H vs. Group M: 34.4% vs. 16.5%; Group H vs. Group L: 34.4% vs. 10.3%; p < 0.05 for both). A proper administration of a low dose of tirofiban may be a superior alternative in treating ACS patients, which can produce a similar favorable clinical outcome and a decrease in bleeding complication.

Effects of the valsartan/amlodipine combination and nifedipine gastrointestinal therapeutic system monotherapy on brachial pulse pressure and radial augmentation index in hypertensive patients.

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.

Atrial High-Rate Event Incidence and Predictors in Patients With Permanent Pacemaker Implantation.

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.

[Rosuvastatin enhances the protective effects of ischemic postconditioning on myocardial ischaemia-reperfusion injury in type 2 diabetic rat].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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 P < 0.05) these beneficial effects were further enhanced by RSV + PC (all P < 0.05 vs. RSV and PC, respectively). The beneficial effects were significantly attenuated by PI3K inhibitor LY294002. CONCLUSIONS: 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 impact of echocardiographic parameter ratio of E/E' on the late recurrence paroxysmal atrial fibrillation in patients accepted radiofrequency catheter ablation: A retrospective clinical study.

This study aimed to evaluate the impact of the echocardiographic parameter ratio E/E' on the late recurrence of paroxysmal atrial fibrillation in patients after receiving radiofrequency catheter ablation.We retrospectively examined total of 288 paroxysmal atrial fibrillation (PAF) patients that underwent a preliminary radiofrequency catheter ablation (RFCA) in our hospital. During the first phase in this study, the patients were divided into 2 groups upon AF recurrence after RFCA: Recurrent group, n = 67 patients with rapid trial arrhythmia that lasted for more than 30 seconds at 3 months after RFCA and the Nonrecurrent group, n = 221. The clinical conditions were compared between the 2 groups. During the second phase of this study, based on the results in the first phase, the patients were divided into another 2 groups according to whether the ratio of E/E' ≥13 .45: Higher ratio of E/E' group, n = 55 and Lower ratio of E/E' group n = 233. The late AF recurrent rates were also compared between the 2 groups.During the first phase, the univariate analysis indicated that the risk factors(P < .05)for PAF late recurrence included early recurrence, E', and the ratio E/E'. The Cox multivariate analysis showed that the ratio of E/E' and early recurrence were the independent predictors for late PAF recurrence. The ratio of E/E' that was cut off at 13.45 also predicted atrial tachyarrhythmia recurrence with 40.3% sensitivity and 87.3% specificity. In the second phase, after completing the 1:1 matching, the Kaplan-Meier analysis indicated that the ratio of E/E' ≥ 13.45 was associated with further recurrences after RFCA (log-rank P = .009), compared to the patients with a ratio of E/E' < 13.45. The univariate Cox analysis indicated that an elevated ratio of E/E'(≥13.45) was the independent predictor for late PAF recurrence (HR = 3.322, 95%CI: 1.560-7.075, P = .002). However, the ratio of E/E' cut off at 13.25 predicted atrial tachyarrhythmia recurrence with 75% sensitivity and 62.2% specificity.The ratio of E/E' ≥ 13.25 is an important predictor of the late recurrence of paroxysmal atrial fibrillation (PAF) after radiofrequency catheter ablation (RFCA).

Benefit of standard versus low-dose tirofiban for percutaneous coronary intervention in very elderly patients with high-risk acute coronary syndrome.

AIM: 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 (>or=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 microg x kg(-1) x 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 microg x kg(-1) x min(-1) or 0.075 microg x kg(-1) x 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.

Crush versus Culotte stenting techniques for coronary bifurcation lesions: A systematic review and meta-analysis of clinical trials with long-term follow-up.

BACKGROUND: In patients with complex true coronary bifurcation lesions (CBLs), Crush or Culotte stenting has been the commonest approaches of percutaneous coronary intervention (PCI). However, the optimal one remains in debate. METHODS: A systematic review and meta-analysis of cohort studies searched from PubMed, EMBASE, Cochrane Central Register of Controlled Trials (CENTRAL), Chinese National Knowledge Infrastructure (CNKI), VIP information database, and WangFang Data Information Site, to compare the long-term safety and efficacy of PCI with Crush versus Culotte in patients with CBLs. The primary end point was target lesion revascularization (TLR) and secondary end points were a composite of major adverse cardiac events (MACE) including cardiac death (CD), myocardial infarction (MI), stent thrombosis (ST), and target vessel revascularization (TVR) by PCI or bypass surgery, and each individual component at long-term follow-up. Furthermore, omitting each study in turn was used to sensitivity analysis for high heterogeneity of studies. RESULTS: A total of 7 studies were included to perform a meta-analysis, 3 randomized trials and 4 observational studies with 2211 patients, 1281 treated with Crush and 930 with Culotte. There was no significant difference in TLR and MACE between Crush and Culotte [RR 0.76, 95% CI (0.48-1.23), I = 57%; RR 0.78, 95% CI (0.47-1.29), I = 83%, respectively]. ST tended to be lower in patients treated with Crush [RR 0.61, 95% CI (0.37-1.01), I = 23%]. CD and MI were comparable between the 2 groups [RR 0.80, 95% CI (0.43-1.49), I = 0%; RR 0.74, 95% CI (0.49-1.13), I = 32%, respectively]. TVR was also associated with the similar risk [RR 0.76, 95% CI (0.49-1.16), I = 60%]. However, high heterogeneity was detected for TLR, MACE, and TVR, and the source of heterogeneity was DKCRUSH-III study by Chen, SL. CONCLUSIONS: In the treatment of coronary bifurcation lesions, TLR and MACE were not significant difference between the Crush and Culotte groups, but TLR and MACE were also regarded as high heterogeneity mainly due to better outcomes achieved by DK Crush and there was a trend toward lower ST in the Crush group. Crush, particularly DK Crush, may be superior to conventional Culotte for treatment of CBLs. PROSPERO REGISTRATION NUMBER: CRD42018111868.

Higher serum lectin-like oxidized low-density lipoprotein receptor-1 in patients with stable coronary artery disease is associated with major adverse cardiovascular events: A multicentre pilot study.

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.