Publications by authors named "Xiaoyong Qi"

25 Publications

  • Page 1 of 1

Sacubitril/valsartan inhibits ox‑LDL‑induced MALAT1 expression, inflammation and apoptosis by suppressing the TLR4/NF‑κB signaling pathway in HUVECs.

Mol Med Rep 2021 06 31;23(6). Epub 2021 Mar 31.

Department of Cardiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

The therapeutic effect of sacubitril/valsartan (S/V) on heart failure has been confirmed, while its role in atherosclerosis remains largely unexplored. The present study aimed to investigate the effects of S/V on the expression of metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1), inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs) induced by oxidized low‑density lipoprotein (ox‑LDL) and to elucidate its possible mechanism. Cell Counting Kit‑8 assay was used to detect cell viability. Reverse transcription‑quantitative PCR was performed to detect the MALAT1 expression. ELISA was performed to detect the levels of IL‑1β, IL‑6 and TNF‑α. Flow cytometry was conducted to detect the apoptotic rate of cells. A nitric oxide (NO) detection kit was used to determine the concentration of NO. Western blotting analysis was performed to determine the levels of intercellular cell adhesion molecule (ICAM)‑1, vascular cell adhesion molecule (VCAM)‑1, endothelin‑1, caspase‑3, Bax, Bcl‑2, Toll‑like receptor 4 (TLR4), p65 and p‑p65. Compared with the ox‑LDL group, S/V treatment significantly increased the cell viability, NO concentration and Bcl‑2 expression, decreased the levels of IL‑1β, IL‑6 and TNF‑α and reduced the expressions of MALAT1, ICAM‑1, VCAM‑1, cleaved‑caspase‑3, Bax, TLR4 and p‑p65. Overall, the findings suggested that S/V could downregulate the expression of MALAT1, inhibit inflammation and apoptosis and improve endothelial function in ox‑LDL‑induced HUVECs via inactivating the TLR4/NF‑κB signaling pathway. Therefore, S/V might be utilized as a promising therapeutic strategy for the prevention and treatment of atherosclerosis.
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http://dx.doi.org/10.3892/mmr.2021.12041DOI Listing
June 2021

Ginsenoside Rg2 protects cardiomyocytes against trastuzumab-induced toxicity by inducing autophagy.

Exp Ther Med 2021 May 11;21(5):473. Epub 2021 Mar 11.

Department of Cardiovascular Medicine, The Fourth Affiliated Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.

Trastuzumab (TZM) significantly improves the outcomes of patients with breast cancer; however, it is associated with severe cardiotoxicity. Ginsenoside Rg2 was reported to exert protective effects against myocardial injury and apoptosis in human cardiomyocytes (HCMs). However, whether ginsenoside Rg2 protects HCMs against TZM-induced toxicity remains unclear. The present study investigated the proliferation of HCMs using a Cell Counting Kit-8 assay and Ki67 immunofluorescence staining. Apoptotic cells were detected by Annexin V/propidium iodide staining and flow cytometry. Furthermore, monodansylcadaverine staining was performed to detect cell autophagy. In addition, western blotting was used to detect the expression levels of phosphorylated (p)-Akt, p-mTOR, beclin 1, microtubule associated protein 1 light chain 3α (LC3) and autophagy protein 5 (ATG5) in HCMs. Pretreatment with ginsenoside Rg2 significantly protected HCMs against TZM-induced cytotoxicity by inhibiting apoptosis. Furthermore, pretreatment with ginsenoside Rg2 induced autophagy in HCMs by upregulating the expression levels of p-Akt, p-mTOR, beclin 1, LC3 and ATG5. The results obtained in the present study suggested that ginsenoside Rg2 could protect HCMs against TZM-induced cardiotoxicity by activating autophagy. Therefore, ginsenoside Rg2 may serve as a potential therapeutic agent to prevent TZM-related cardiotoxicity in patients with breast cancer.
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http://dx.doi.org/10.3892/etm.2021.9904DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7976377PMC
May 2021

Establishment and validation of a risk model for prediction of in-hospital mortality in patients with acute ST-elevation myocardial infarction after primary PCI.

BMC Cardiovasc Disord 2020 12 9;20(1):513. Epub 2020 Dec 9.

Department of Cardiology, Cangzhou Central Hospital, Cangzhou, Hebei, China.

Background: Currently, how to accurately determine the patient prognosis after a percutaneous coronary intervention (PCI) remains unclear and may vary among populations, hospitals, and datasets. The aim of this study was to establish a prediction model of in-hospital mortality risk after primary PCI in patients with acute ST-elevated myocardial infarction (STEMI).

Methods: This was a multicenter, observational study of patients with acute STEMI who underwent primary PCI. The outcome was in-hospital mortality. The least absolute shrinkage and selection operator (LASSO) method was used to select the features that were the most significantly associated with the outcome. A regression model was built using the selected variables to select the significant predictors of mortality. Receiver operating characteristic (ROC) curve and decision curve analysis (DCA) were used to evaluate the performance of the nomogram.

Results: Totally, 1169 and 316 patients were enrolled in the training and validation sets, respectively. Fourteen predictors were identified by the LASSO analysis: sex, Killip classification, left main coronary artery disease (LMCAD), grading of thrombus, TIMI classification, slow flow, application of IABP, administration of β-blocker, ACEI/ARB, symptom-to-door time (SDT), symptom-to-balloon time (SBT), syntax score, left ventricular ejection fraction (LVEF), and CK-MB peak. The mortality risk prediction nomogram achieved good discrimination for in-hospital mortality (training set: C-statistic = 0.987; model calibration: P = 0.722; validation set: C-statistic = 0.984, model calibration: P = 0.669). Area under the curve (AUC) values for the training and validation sets are 0.987 (95% CI: 0.981-0.994, P = 0.003) and 0.990 (95% CI: 0.987-0.998, P = 0.007), respectively. DCA shows that the nomogram can achieve good net benefit.

Conclusions: A novel nomogram was developed and is a simple and accurate tool for predicting the risk of in-hospital mortality in patients with acute STEMI who underwent primary PCI.
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http://dx.doi.org/10.1186/s12872-020-01804-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7727168PMC
December 2020

Association of -344C/T polymorphism in the aldosterone synthase (CYP11B2) gene with cardiac and cerebrovascular events in Chinese patients with hypertension.

J Int Med Res 2020 Sep;48(9):300060520949409

School of Graduate, Hebei Medical University, Shijiazhuang, Hebei Province, People's Republic of China.

Objective: Several recent studies have shown that the aldosterone synthase gene () -344C/T polymorphism is related to cardiovascular diseases. However, whether the -344C allele influences the incidence of cardiovascular diseases in Chinese patients with hypertension is unclear.

Methods: Chinese patients with essential hypertension were genotyped for the -344C/T polymorphism in (n = 755; CC, n = 112; CT, n = 361; TT, n = 282) and followed for 11 years for major adverse cardiovascular events (MACEs), including stroke, onset of coronary artery disease (CAD), and CAD-related death. Established cardiovascular risk factors were used to adjust the multivariate Cox analysis.

Results: After a mean follow-up period of 7.60 ± 1.12 years, a significantly higher incidence of MACEs was seen in patients with the CC genotype than in those with the CT and TT genotypes. The CC variant was significantly and independently predictive of MACEs (hazard ratio = 2.049), CAD (hazard ratio = 1.754), and stroke (hazard ratio = 2.588), but not CAD-related stroke or death.

Conclusion: The -344 CC genotype is a risk factor for CAD and stroke, independent of other established cardiovascular risk factors in Chinese patients with hypertension.
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http://dx.doi.org/10.1177/0300060520949409DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7503017PMC
September 2020

Effectiveness of Levoamlodipine Maleate for Hypertension Compared with Amlodipine Besylate: a Pragmatic Comparative Effectiveness Study.

Cardiovasc Drugs Ther 2021 02 11;35(1):41-50. Epub 2020 Sep 11.

National Clinical Research Center for Kidney Disease, State Key Laboratory of Organ Failure Research, Department of Biostatistics, School of Public Health, Southern Medical University, Guangzhou, 510515, China.

Purpose: Antihypertensive treatment is the most important method to reduce the risk of cardiovascular events in hypertensive patients. However, there is scant evidence of the benefits of levoamlodipine maleate for antihypertensive treatment using a head-to-head comparison in the real-world. This study aims to examine the effectiveness of levoamlodipine maleate used to treat outpatients with primary hypertension compared with amlodipine besylate in a real-world setting.

Methods: This was a pragmatic comparative effectiveness study carried out at 110 centers across China in outpatients with primary hypertension treated with levoamlodipine maleate or amlodipine besylate, with 24 months of follow-up. The primary outcomes used for evaluating the effectiveness were composite major cardiovascular and cerebrovascular events (MACCE), adverse reactions, and cost-effectiveness.

Results: Among the included 10,031 patients, there were 482 MACCE, 223 (4.4%) in the levoamlodipine maleate group (n = 5018) and 259 (5.2%) in the amlodipine besylate group (n = 5013) (adjusted hazard ratio = 0.90, 95%CI: 0.75-1.08, P = 0.252). The levoamlodipine maleate group had lower overall incidences of any adverse reactions (6.0% vs. 8.4%, P < 0.001), lower extremity edema (1.1% vs. 3.0%, P < 0.001) and headache (0.7% vs. 1.1%, P = 0.045). There was a nearly 100% chance of the levoamlodipine maleate being cost-effective at a willingness to pay threshold of 150,000 Yuan per quality-adjusted life years (QALYs) gained, resulting in more QALYs (incremental QALYs: 0.00392) and cost savings (saving 2725 Yuan or 28.8% reduction in overall costs) per patient.

Conclusion: In conclusion, levoamlodipine maleate could reduce cost by 29% with a similar MACCE incidence rate and lower occurrence of adverse reactions (especially edema and headache) compared with amlodipine besylate.

Trial Registration: Clinicaltrials.gov NCT01844570 registered at May 1, 2013.
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http://dx.doi.org/10.1007/s10557-020-07054-1DOI Listing
February 2021

Cardiac Contractility Modulation Attenuates Chronic Heart Failure in a Rabbit Model via the PI3K/AKT Pathway.

Biomed Res Int 2020 7;2020:1625362. Epub 2020 Jan 7.

School of Graduate, Hebei Medical University, Shijiazhuang, China.

The Akt plays an important role in regulating cardiac growth, myocardial angiogenesis, and cell death in cardiac myocytes. However, there are few studies to focus on the responses of the Akt pathway to cardiac contractility modulation (CCM) in a chronic heart failure (HF) model. In this study, the effects of CCM on the treatment of HF in a rabbit model were investigated. Thirty six-month-old rabbits were randomly separated into control, HF, and CCM groups. The rabbits in HF and CCM groups were pressure uploaded, which can cause an aortic constriction. Then, CCM was gradually injected to the myocardium of rabbits in the CCM group, and this process lasted for four weeks with six hours per day. Rabbit body weight, heart weight, and heart beating rates were recorded during the experiment. To assess the CCM impacts, rabbit myocardial histology was examined as well. Additionally, western blot analysis was employed to measure the protein levels of Akt, FOXO3, Beclin, Pi3k, mTOR, GSK-3, and TORC2 in the myocardial histology of rabbits. Results showed that the body and heart weight of rabbits decreased significantly after suffering HF when compared with those in the control group. However, they gradually recovered after CCM application. The CCM significantly decreased collagen volume fraction in myocardial histology of HF rabbits, indicating that CCM therapy attenuated myocardial fibrosis and collagen deposition. The levels of Akt, FOXO3, Beclin, mTOR, GSK-3, and TORC2 were significantly downregulated, but Pi3k concentration was greatly upregulated after CCM utilization. Based on these findings, it was concluded that CCM could elicit positive effects on HF therapy, which was potentially due to the variation in the Pi3k/Akt signaling pathway.
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http://dx.doi.org/10.1155/2020/1625362DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6973194PMC
September 2020

Serum Levels of Inflammatory Cytokines and Expression of BCL2 and BAX mRNA in Peripheral Blood Mononuclear Cells and in Patients with Chronic Heart Failure.

Med Sci Monit 2019 Apr 10;25:2633-2639. Epub 2019 Apr 10.

Department of Cardiology, Hebei Medical University, Shijiazhuang, Hebei, China (mainland).

BACKGROUND This study investigated the expression of the BCL2 and BAX mRNA, inflammatory cytokines, interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-alpha (TNF-alpha), and cardiac function in patients with chronic heart failure (CHF). The New York Heart Association (NYHA) Functional Classification and measurement of the left ventricular ejection fraction (LVEF) evaluated cardiac function. MATERIAL AND METHODS Patients with CHF (n=60) due to coronary heart disease, hypertensive heart disease, and cardiomyopathy, and healthy controls (n=30) were studied. Enzyme-linked immunosorbent assay (ELISA) measured serum levels of IL-1ß, IL-6, and TNF-alpha. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) detected mRNA expression of BCL2 and BAX in peripheral blood mononuclear cells (PBMCs). Color Doppler ultrasound measured the LVEF, and the NYHA classification of CHF was used. RESULTS In patients with CHF, levels of IL-1ß, IL-6 and TNF-alpha, and mRNA expression of BAX were significantly increased compared with the control group (p<0.01); BCL2 mRNA level was significantly lower (p<0.01). There were no significant differences in the expression levels of inflammatory cytokines, or BCL2 or BAX mRNA in patients with CHF due to coronary heart disease, hypertensive heart disease, or cardiomyopathy. Expression levels of IL-1ß, IL-6, TNF-alpha, and BAX mRNA were significantly associated with the degree of CHF. Cardiac function was negatively correlated with LVEF (p<0.05). Expression levels of BCL2 mRNA level were negatively correlated with cardiac function (p<0.05), and positively correlated with LVEF (p<0.05). CONCLUSIONS Levels of IL-1ß, IL-6, TNF-alpha, and BAX mRNA were negatively correlated with cardiac function, and BCL2 mRNA expression was positively associated with CHF.
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http://dx.doi.org/10.12659/MSM.912457DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6474297PMC
April 2019

Effect of Different Methods of Administration of Diltiazem on Clinical Efficacy in Patients with Acute ST-Segment Elevation Myocardial Infarction.

Med Sci Monit 2018 Sep 17;24:6544-6550. Epub 2018 Sep 17.

Department of Cardiology, Affiliated Hospital of Hebei University, Baoding, Hebei, China (mainland).

BACKGROUND The aim of this study was to investigate the optimal route of administration of diltiazem in emergency PCI and to provide the best clinical treatment for ASTEMI patients. MATERIAL AND METHODS A total of 90 patients with ASTEMI treated in our hospital from January 2015 to January 2016 were selected. Prior to thrombus aspiration, a thrombus aspiration catheter was used to perform diltiazem injection at the distal end of the infarct-related artery (IRA). We chose the acute ST-elevation myocardial infarction (ASTEMI) patients treated with direct PCI to compare different administration routes of diltiazem. The occurrence of major adverse cardiac events (MACEs) was closely observed during hospitalization and was obtained through outpatient visits or telephone follow-ups over the next 6 months. RESULTS Intracoronary infusion of diltiazem at the distal end of the culprit vessel, compared to conventional coronary mouth and intravenous injection, was significantly improved in thrombolysis in myocardial infarction (TIMI) frame count immediately after PCI stent implantation, ST-segment drop rate after 90 min, and left ventricular ejection fraction (LVEF) after 1 week. Furthermore, the peak value of high-sensitivity cardiac troponin I (hs-cTnI), a marker for myocardial injury, was the lowest. White blood cell count, neutrophil count, mean platelet volume (MPV), and high-sensitivity C-reactive protein (hs-CRP) were significantly lower than with the other 2 administration routes, and there was no effect on intracoronary pressure or heart rate. CONCLUSIONS Patients with ASTEMI who underwent emergency PCI treatment had good clinical outcomes using intracoronary diltiazem at the distal end of the culprit vessel.
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http://dx.doi.org/10.12659/MSM.912576DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6149237PMC
September 2018

Inhibition of SETD7 protects cardiomyocytes against hypoxia/reoxygenation-induced injury through regulating Keap1/Nrf2 signaling.

Biomed Pharmacother 2018 Oct 11;106:842-849. Epub 2018 Jul 11.

Department of Cardiology, Hebei General Hospital, No.348 West Heping Road, Shijiazhuang, Hebei 050051, China. Electronic address:

The protein SET domain-containing lysine methyltransferase 7 (SETD7) has recently been shown to regulate apoptosis in various cells. However, the role of SETD7 on cardiomyocyte apoptosis during myocardial ischemia/reperfusion injury remains unclear. This study aimed to investigate the potential role of SETD7 in hypoxia/reoxygenation (H/R)-induced apoptosis of rat cardiomyocytes and reveal the underlying mechanism. Our results demonstrated that SETD7 expression was significantly up-regulated in cardiomyocytes in response to H/R injury. The inhibition of SETD7 by siRNA-mediated gene silencing significantly suppressed H/R-induced apoptosis and decreased the production of reactive oxygen species (ROS). The overexpression of SETD7 markedly enhanced H/R-induced apoptosis and ROS production. Moreover, the knockdown of SETD7 reduced the expression of Keap1 and promoted the expression of Nrf2. In addition, the knockdown of SETD7 increased the activity of antioxidant response element and promoted the expression of heme oxygenase-1 and NADPH-quinone oxidoreductase 1. However, the knockdown of Nrf2 partially abrogated the SETD7 inhibition-mediated protective effect against H/R injury. Taken together, these results indicate that the inhibition of SETD7 attenuates H/R-induced injury of cardiomyocytes via the down-regulation of Keap1 and promotion of the Nrf2-mediated anti-oxidation signaling pathway.
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http://dx.doi.org/10.1016/j.biopha.2018.07.007DOI Listing
October 2018

Evaluation of the therapeutic effects of QuickOpt optimization in Chinese patients with chronic heart failure treated by cardiac resynchronization.

Sci Rep 2018 03 9;8(1):4259. Epub 2018 Mar 9.

Department of Cardiology, Xiangya Hospital Central South University, No. 87 xiangya Road, Changsha, 410008, China.

In this trial, long-term therapeutic effects and clinical improvements in Chinese chronic heart failure patients optimized by QuickOpt or echocardiography were compared for atrioventricular (AV) and interventricular (VV) delay optimizations after cardiac resynchronization therapy (CRT) with pacing (CRT-P) or with pacing and defibrillator (CRT-D) therapy. One hundred and ninety-six subjects (50%) had dilated cardiomyopathy, 108 (27.6%) had ischemic heart disease and 112 (28.6%) were hypertensive and were randomized into QuickOpt (198) or echocardiographic optimization (control) (194) groups at ≤2-weeks post-implantation. Programmed AV/VV delay was optimized at baseline and at 3 and 6 months. Left ventricular end-systolic volume (LVESV), New York Heart Association (NYHA) class, specific activity scale (SAS), and the six-minute walk tests (6MWT) were evaluated by blinded researchers at 12 months. Of the QuickOpt group, LVESV decreased significantly by 24.7% ± 33.9% compared with baseline, while LVESV of Controls decreased by 25.1% ± 36.1% (P = 0.924). NYHA class, SAS and 6MWT also improved similarly in both groups at 12 months. Mortality in both groups was not significantly different (11.0% vs 7.6%, P = 0.289). However, there was a significant difference in the time required for optimization by QuickOpt compared with echocardiography (3.33 ± 3.11 vs 58.79 ± 27.03 minutes, P < 0.000).
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http://dx.doi.org/10.1038/s41598-018-22525-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5844885PMC
March 2018

Effect of miR-23a on anoxia-induced phenotypic transformation of smooth muscle cells of rat pulmonary arteries and regulatory mechanism.

Oncol Lett 2017 Jan 28;13(1):89-98. Epub 2016 Nov 28.

Department of Internal Medicine, Hebei Medical University, Shijiazhuang, Hebei 050017, P.R. China; Department of Heart Disease Center, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

We investigated the possible implication of miR-23a in anoxia-induced phenotypic transformation of the pulmonary arterial smooth muscle and studied the mechanism of upregulation of miR-23a expression in anoxia. The collagenase digestion method was used for preparing rat primary pulmonary artery smooth muscle cell (PASMC) culture. SM-MHC, SM-α-actin, calponin-1 and SM22α protein expression levels were evaluated using western blot analysis after the ASMCs were subjected to anoxia treatment (3% O). Transfection with miR-23a mimics were conducted when PASMCs were under normoxia and anoxia conditions. EdU staining was used to detect the proliferative activity of PASMCs. Cells were transfected with HIF-1α specific siRNA under anoxia condition. RT-qPCR was used to detect miR-23a expression in PASMCs. Chromatin immunoprecipitation method was employed to verify the binding sites of HIF-1α. The dual-luciferase reporter gene was used to study the role of HIF-1 and its binding sites. Rat hypoxic pulmonary hypertension models were established to study the expression of miR-23a using RT-qPCR method and to verify the expression of miR-23a in the arteriole of the rat pulmonary. Our results showed that compared with normoxia condition, under anoxia condition (3% O), the expression levels of the contractile phenotype marker proteins decreased significantly after 24 and 48 h. The positive rate of the EdU staining increased significantly and the expression of miR-23a increased. Transfection with miR-23a-mimic downregulated the expression of contractile marker proteins and improved the positive rate of the EdU staining under normoxia. Anoxia and transfection with HIF-1α enhanced the activity of the wild-type Luc-miR-23a-1 (WT) reporter gene. We concluded that miR-23a participated in the anoxia-induced phenotypic transformation of PASMCs. Increased expression of miR-23a under anoxia may primarily be due to miR-23a-1 and miR-23a-3 upregulation. The anoxia-induced upregulation of miR-23a was regulated by HIF-1.
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http://dx.doi.org/10.3892/ol.2016.5440DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5245139PMC
January 2017

Expression of miRNA-26a in platelets is associated with clopidogrel resistance following coronary stenting.

Exp Ther Med 2016 Jul 20;12(1):518-524. Epub 2016 Apr 20.

Department of Cardiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.

The present study aimed to evaluate the association between platelet microRNA (miRNA)-26a expression and clopidogrel resistance in patients who underwent coronary stenting. Between September 2013 and August 2014, 43 patients with coronary heart disease underwent percutaneous coronary intervention at Heibei General Hospital (Shijiazhuang, China). In the same period, 20 healthy volunteers without any history of cardiovascular disease were enrolled in the present study as the control group. Flow cytometry was used to measure the phosphorylation levels of vasodilator-stimulated phosphoprotein (VASP), and to calculate the platelet reactivity index (PRI). Low response to clopidogrel was defined as PRI ≥50% on day 7 following clopidogrel administration. Western blotting was used to measure protein expression of VASP and reverse transcription-quantitative polymerase chain reaction analysis was performed to determine the expression levels of mRNA and miRNAs. Bioinformatics tools were employed to predict that miR-26a, miR-199 and miR-23a may target VASP mRNA. The results of the present study demonstrated that the activity of platelets in patients with low or high clopidogrel response was increased, as compared with healthy subjects. No differences in platelet VASP protein expression levels were detected between patients with high clopidogrel response and healthy subjects; whereas VASP protein expression was elevated in patients with low clopidogrel response. Furthermore VASP gene transcription was maintained at low levels in healthy subjects and patients with high clopidogrel response, whereas patients with low clopidogrel response exhibited increased VASP mRNA expression levels. Platelet expression of miRNA-26a, but not miRNA-199 or miRNA-23a, was associated with high platelet reactivity. Serum miRNA-26a, miRNA-199 and miRNA-23a were not demonstrated to be involved in clopidogrel resistance. Therefore, the present study demonstrated that platelet miRNA-26a has an important role in clopidogrel resistance. Combined miRNA and VASP PRI tests may aid the early diagnosis and prediction of clopidogrel resistance.
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http://dx.doi.org/10.3892/etm.2016.3278DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4907078PMC
July 2016

Cardiac Contractility Modulation Attenuate Myocardial Fibrosis by Inhibiting TGF-β1/Smad3 Signaling Pathway in a Rabbit Model of Chronic Heart Failure.

Cell Physiol Biochem 2016 27;39(1):294-302. Epub 2016 Jun 27.

School of Graduate, Hebei Medical University, Shijiazhuang, China.

Unlabelled: Backgroun/Aims: To explore the effect of cardiac contractility modulation (CCM) on myocardial fibrosis in heart failure and to investigate the underlying mechanism.

Methods: Rabbits were randomly divided into sham group, HF group and CCM group. A rabbit model of chronic heart failure (CHF) was induced 12 weeks after aortic constriction by pressure unloading. Then cardiac contractility modulation was delivered to the myocardium lasting six hours per day for 4 weeks. Histology examination was carried out to evaluate the myocardial pathological changes. Protein levels of collagen I, collagen III, α-SMA, MMP2, MMP9, TIMP1, TGF-β1 and Smad3 were measured by western blot analysis.

Results: Histology examination results showed that CCM therapy attenuated myocardial fibrosis and collagen deposition in rabbits with CHF. In addition, protein levels of collagen I, collagen III, α-SMA, MMP2, MMP9, TIMP1, TGF-β1 and Smad3 were down regulated.

Conclusion: CCM therapy exerted protective effects against myocardial fibrosis potentially by inhibiting TGF-β1/Smad3 signaling pathway in CHF rabbits.
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http://dx.doi.org/10.1159/000445624DOI Listing
February 2017

Effects of atorvastatin on atrial remodeling in a rabbit model of atrial fibrillation produced by rapid atrial pacing.

BMC Cardiovasc Disord 2016 06 24;16(1):142. Epub 2016 Jun 24.

Department of Cardiology, Hebei General Hospital, Shijiazhuang, Hebei Province, People's Republic of China.

Background: Accumulating evidence suggests that myeloperoxidase (MPO) is involved in atrial remodeling of atrial fibrillation (AF). Statins could reduce the MPO levels in patients with cardiovascular diseases. This study evaluated the effects of atorvastatin on MPO level and atrial remodeling in a rabbit model of pacing-induced AF.

Methods: Eighteen rabbits were randomly divided into sham, control and atorvastatin groups. Rabbits in the control and atorvastatin groups were subjected to rapid atrial pacing (RAP) at 600 bpm for 3 weeks, and treated with placebo or atorvastatin (2.5 mg/kg/d), respectively. Rabbits in the sham group did not receive RAP. After 3 weeks of pacing, atrial structural and functional changes were assessed by echocardiography, atrial effective refractory period (AERP) and AF inducibility were measured by atrial electrophysiological examination, and histological changes were evaluated by Masson trichrome-staining. The L-type calcium channel α1c (Cav1.2), collagen I and III, MPO, matrix metalloproteinase (MMP)-2 and MMP-9 were analyzed by real time polymerase chain reaction and/or western blot.

Results: All rabbits were found to have maintained sinus rhythm after 3 weeks of RAP. Atrial burst stimulation induced sustained AF (>30 min) in 5, 4, and no rabbits in the control, atorvastatin, and sham groups, respectively. The AERP shortened and Cav1.2 mRNA level decreased in the control group, but these changes were suppressed in the atorvastatin group. Obvious left atrial enlargement and dysfunction was found in both control and atorvastatin groups. Compared with the control group, these echocardiograhic indices of left atrium did not differ in the atorvastatin group. Prominent atrial fibrosis and increased levels of collagen I and III were observed in the control group but not in the atorvastatin group. The mRNA and protein levels of MPO, MMP-2 and MMP-9 significantly increased in the control group, but these changes were prevented in the atorvastatin group.

Conclusion: Treatment with atorvastatin prevented atrial remodeling in a rabbit model of RAP-induced AF. The reduction of levels of atrial MPO, MMP-2 and MMP-9 may contribute to the prevention of atorvastatin on atrial remodeling.
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http://dx.doi.org/10.1186/s12872-016-0301-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4921022PMC
June 2016

[Impact of statin therapy on recurrence of persistent atrial fibrillation after electrical cardioversion: a meta-analysis].

Zhonghua Xin Xue Guan Bing Za Zhi 2015 Nov;43(11):994-8

Heart Center, Hebei General Hospital, Shijiazhuang 050051, China.

Objective: To evaluate the impact of statin therapy on the recurrence rate in patients with persistent atrial fibrillation (AF) after electrical cardioversion.

Methods: PubMed, EMBbase, Cochrane central register of controlled trials were searched up to February 2015 to identify randomized controlled trials, which reported the effect of statin therapy on AF recurrence after electrical cardioversion. The data were analyzed by RevMan 5.3 and Stata 12.0 software.

Results: Six trials with 572 patients were included. The result showed that statin therapy had no effect on the recurrence rate in patients with persistent AF after electrical cardioversion (OR=0.60, 95%CI: 0.32-1.11, P>0.05) compared with controls. Four out of the six trials investigated the effect of atorvastatin on the recurrence rate of AF after electrical cardioversion, subgroup analysis of these trials showed that compared with controls, atorvastatin had no effect on the recurrence of AF after electrical cardioversion (OR=0.59, 95%CI: 0.25-1.39, P>0.05). Three out of the six trials had high quality (Jadad score≥3), subgroup analysis of these trials also showed that statins did not affect the recurrence rate of AF after electrical cardioversion (OR=0.76, 95%CI: 0.49-1.16, P>0.05).

Conclusion: This analysis suggested that statin therapy had no effect on the recurrence rate in patients with persistent AF after electrical cardioversion.
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November 2015

Association of systolic blood pressure levels with cardiovascular and cerebrovascular events and all-cause mortality: a result from the Kailuan study.

Blood Press Monit 2016 Jun;21(3):149-54

aGraduate School, Hebei Medical University, Shijiazhuang bDepartment of Cardiology, Kailuan Hospital, Hebei United University cDepartment of Cardiology, Tangshan People's Hospital, Tangshan, China.

Objective: We aimed to examine the impact of different levels of systolic blood pressure (SBP) on the incidence of cardiovascular and cerebrovascular events and all-cause death in Chinese adults.

Patients And Methods: A total of 97 013 Chinese men and women from the Kailuan study were followed up with the incidence of cardiovascular and cerebrovascular events and all-cause death. The participants were categorized into nine groups on the basis of the different SBP levels (mmHg) (groups 1-9): SBP<110, 110≤SBP<120, 120≤SBP<130, 130≤SBP<140, 140≤SBP<150, 150≤SBP<160, 160≤SBP<170, 170≤SBP<180, and SBP≥180. Hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated from Cox regression models.

Results: During a mean follow-up of 4.02 years, a total of 2043 cardiovascular and cerebrovascular events and 1686 of all-cause deaths occurred. After adjustments for potential confounding factors and using group 1 as a reference, HRs (95% CIs) of total cardiovascular and cerebrovascular events for groups 2-9 were 1.35 (1.00-1.82), 1.61 (1.22-2.12), 1.54 (1.16-2.04), 2.05 (1.55-2.72), 2.47 (1.86-3.29), 3.04 (2.28-4.06), 3.93 (2.89-5.36), and 4.56 (3.39-6.15), respectively. HRs (95% CIs) of all-cause death for groups 2-9 were 0.92 (0.71-1.20), 0.95 (0.75-1.20), 1.06 (0.83-1.34), 1.18 (0.93-1.50), 1.16 (0.90-1.49), 1.39 (1.07-1.81), 1.74 (1.29-2.33), and 2.06 (1.56-2.72), respectively.

Conclusion: An increase in the SBP levels is significantly associated with an increased risk of cardiovascular and cerebrovascular events and all-cause death.
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http://dx.doi.org/10.1097/MBP.0000000000000181DOI Listing
June 2016

Dexrazoxane protects breast cancer patients with diabetes from chemotherapy-induced cardiotoxicity.

Am J Med Sci 2015 May;349(5):406-12

Department of Internal Medicine, Hebei Medical University, Shijiazhuang, P. R. China (FS, XL), Department of Cardiology, Hebei General Hospital, Shijiazhuang, P. R. China (XQ), Department of surgical medicine, Fourth Hospital of Hebei Medical University, Shijiazhuang, P. R. China (CG), Fourth Hospital of Hebei Medical University, Shijiazhuang, China.

Background: To evaluate the cardioprotective effect of dexrazoxane (DEX) on chemotherapy in patients with breast cancer with concurrent type 2 diabetes mellitus (DM2).

Methods: Eighty female patients with breast cancer with DM2 were randomly assigned to receive chemotherapy only or chemotherapy plus DEX. All patients received 80 mg/m epirubicin and 500 mg/m cyclophosphamide by intravenous infusion every 3 weeks for a total of 6 cycles. The group assigned to receive chemotherapy alone received placebo 30 minutes before epirubicin administration. The group assigned to receive chemotherapy plus DEX received 800 mg/m DEX 30 minutes before epirubicin administration. Cardiac function and hematology before and after 6 cycles of chemotherapy were analyzed.

Results: There was no difference in baseline systole or diastole function between the 2 DM2 groups. Patients receiving chemotherapy alone experienced significantly greater reductions in Ea and significantly greater elevations in E/Ea and Tei index in comparison with patients receiving chemotherapy plus DEX. After chemotherapy, superoxide dismutase was significantly reduced, and serum malondialdehyde (MDA) was significantly increased in patients with DM2. Serum superoxide dismutase levels were comparable between the 2 groups before and after chemotherapy, MDA levels were comparable between the 2 groups before chemotherapy, whereas serum MDA was significantly higher after chemotherapy in the chemotherapy alone group in comparison with the group that received DEX.

Conculsions: DEX protects against cardiotoxicity induced by chemotherapy in patients with breast cancer with concurrent DM2.
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http://dx.doi.org/10.1097/MAJ.0000000000000432DOI Listing
May 2015

The preventive effect of atorvastatin on atrial fibrillation: a meta-analysis of randomized controlled trials.

BMC Cardiovasc Disord 2014 Aug 13;14:99. Epub 2014 Aug 13.

Department of Cardiology, Hebei General Hospital, Shijiazhuang, Hebei, People's Republic of China.

Background: A number of clinical and experimental studies have investigated the effect of atorvastatin on atrial fibrillation (AF), but the results are equivocal. This meta-analysis was performed to evaluate whether atorvastatin can reduce the risk of AF in different populations.

Methods: We searched PubMed, EMBASE and the Cochrane Database for all published studies that examined the effect of atorvastatin therapy on AF up to April 2014. A random effects model was used when there was substantial heterogeneity and a fixed effects model when there was negligible heterogeneity.

Results: Eighteen published studies including 9952 patients with sinus rhythm were identified for inclusion in the analysis. Ten studies investigated primary prevention of AF by atorvastatin in patients without AF, seven studies investigated secondary prevention of atorvastatin in patients with AF, and one study investigated mixed populations of patients. Overall, atorvastatin was associated with a decreased risk of AF (odds ratio (OR) 0.51, 95% confidence interval (CI) 0.36-0.70, P < 0.0001). However, subgroup analyses showed that in the primary prevention subgroup (OR 0.55, 95% CI 0.38-0.81, P = 0.002), atorvastatin reduced the risk of new-onset AF in patients after coronary surgery (OR 0.44, 95% CI 0.29-0.68, P = 0.0002), but had no beneficial effect in patients without coronary surgery (OR 0.97, 95% CI 0.59-1.58, P = 0.89); in the secondary prevention subgroup, atorvastatin had no beneficial effect on AF recurrence in patients with electrical cardioversion (EC) (OR 0.57, 95% CI 0.25-1.32, P = 0.19) or without EC (OR 0.38, 95% CI 0.14-1.06, P = 0.06).

Conclusions: This meta-analysis suggests that atorvastatin has an overall protective effect against AF. However, this preventive effect was not seen in all types of AF. Atorvastatin was significantly associated with a decreased risk of new-onset AF in patients after coronary surgery. Moreover, atorvastatin did not prove to exert a significant protective effect against the AF recurrences in both patients who had experienced sinus rhythm restoration by means of EC and those who had obtained cardioversion by means of drug therapy. Thus, further prospective studies are warranted.
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http://dx.doi.org/10.1186/1471-2261-14-99DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135360PMC
August 2014

Biventricular pacing cardiac contractility modulation improves cardiac contractile function via upregulating SERCA2 and miR-133 in a rabbit model of congestive heart failure.

Cell Physiol Biochem 2014 5;33(5):1389-99. Epub 2014 May 5.

School of Graduate, HeBei Medical University, Shi Jia Zhuang, China.

Objective: To compare the effects of biventricular electrical pacing and conventional single-ventricular pacing for cardiac contractility modulation (CCM) on cardiac contractile function and to delineate the underlying molecular mechanisms.

Methods: Forty rabbits were divided into four groups before surgery: healthy control, HF sham, HF left ventricular pacing CCM (LVP-CCM), and HF biventricular pacing CCM (BVP-CCM) groups with n=10 for each group. A rabbit model of chronic heart failure was established by ligating ascending aortic root of rabbits. Then electrical stimulations during the absolute refractory period were delivered to the anterior wall of left ventricle in the LVP-CCM group and on the anterior wall of both left and right ventricles in the BVP-CCM group lasting six hours per day for seven days. Changes in ventricular structure, cardiac function and electrocardiogram were monitored before and after CCM stimulation.

Results: Compared with the sham-operated group, heart weight, heart weight index, LV end-systolic diameter (LVESD), LV end-diastolic diameter (LVEDD) in the LVP-CCM and BVP-CCM groups were significantly decreased (p<0.05), while LV ejection fraction (LVEF) and fractional shortening fraction (FS) were increased (p<0.05). Notably all these changes were consistently found to be greater in BVP-CCM than in LVP-CCM. Moreover, plasma BNP levels were highest in the HF sham-control group, followed by the LVP-CCM group, and lowest in the BVP-CCM group (p<0.05). Furthermore, sarco/endoplasmic reticulum Ca(2+)-ATPase (SERCA2a) protein levels were upregulated by 1.7 and 2.4 fold, along with simultaneous upregulation of a cardiac-enriched microRNA miR-133 levels by 2.6 and 3.3 fold, in LVP-CCM and BVP-CCM, respectively, compared to sham.

Conclusions: Biventricular pacing CCM is superior to conventional monoventricular pacing CCM, producing greater improvement cardiac contractile function. Greater upregulation of SERCA2 and miR-133 may account, at least partially, for the improvement by BVP-CCM.
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http://dx.doi.org/10.1159/000358705DOI Listing
April 2015

Regulation of the catecholamine beta-adrenergic system in ventricular remodeling of hypertension.

Jpn Heart J 2004 Mar;45(2):285-96

Department of Cardiology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

Differences in structural remodeling are believed to be influenced by hormonal systems in hypertension. The objective of the present study was to investigate the change in the circulating catecholamine beta-adrenergic system in the left ventricle remodeling process in hypertensives. One hundred and thirty-four men (mean age, 53 years) had essential hypertension and underwent echocardiography before treatment. Normal morphology (n = 26) and concentric remodeling (n = 41) were defined by a relative wall thickness at diastole (RWT) of < 0.44 and > or = 0.44, respectively, and concentric hypertrophy (n = 28) and eccentric hypertrophy (n = 39) by a left ventricular mass index (LVMI) of < 150 g/m(2) and > or = 150 g/m(2), respectively. Forty healthy males were studied as normal controls. Plasma levels of norepinephrine (NE) and epinephrine (E) were measured by high performance liquid chromatography. The density of lymphocyte beta-adrenoceptors (beta-AR) and the content of intralymphocyte cyclic AMP (cAMP) in peripheral blood were measured using (3)H-dihydroalpneol as a ligand and protein binding assay, respectively. The plasma levels of NE and E in the 4 groups of patients with essential hypertension were significantly increased compared with the control group. The density of lymphocyte beta-AR and the content of intralymphocyte cAMP of peripheral blood in the normal morphology, concentric remodeling, and concentric hypertrophy groups were significantly higher than those in the control group, while the values in the eccentric hypertrophy group were significantly lower than those in the control group. Among the 4 groups, the plasma levels of NE and E had increased the most in the normal morphology group, followed in decreasing order by the concentric remodeling, concentric hypertrophy, and eccentric hypertrophy groups; the density of lymphocyte beta-AR and the content of intralymphocyte cAMP of peripheral blood in the normal morphology, concentric remodeling, and concentric hypertrophy groups increased while they decreased in the eccentric hypertrophy group in patients with essential hypertension. The catecholamine beta-adrenergic system appears to be related to left ventricular remodeling of hypertension. In this process, catecholamines increased continually. The density of beta-AR and the content of cAMP in peripheral lymphocytes increased at first and then decreased.
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http://dx.doi.org/10.1536/jhj.45.285DOI Listing
March 2004

Changes and significance of subtype function of beta-adrenoreceptors in left ventricular remodeling of hypertension.

Jpn Heart J 2003 Nov;44(6):933-42

Zhejiang University, Hangzhou, China.

Changes in the density of myocardium and blood lymphocyte beta-adrenoceptors (beta-AR) in left ventricular (LV) geometry have been found in patients with essential hypertension (EH). However, it is not known whether intrinsic beta-AR subtype function changes during left ventricular remodeling of hypertension. The purpose of this study was to further investigate the changes and clinical significance of beta-AR subtype function in LV remodeling in patients with EH. One hundred and thirty-four men (mean age, 53 years) with EH as defined in the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure grades 1 to 2 and 40 normotensives were studied. Based on the echocardiographic LV mass index and relative wall thickness, four patterns of LV geometry, ie, normal left ventricle, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy were identilied. beta-Adrenoreceptor subtype responsiveness was measured by a treadmill exercise test (to measure cardiac beta1-adrenoreceptor responsiveness) and by Salbutamol injection test (to measure cardiac beta2-adrenoreceptor responsiveness) in 134 male patients with EH. Forty normotension subjects were also studied as controls. In patients with EH in the groups of concentric remodeling, concentric hypertrophy, and eccentric hypertrophy, heart rate in response to the treadmill test (peak exercise-resting rate) was significantly higher (P < 0.05, P < 0.01. P < 0.01, respectively) than that in the control group. In the concentric remodeling and concentric hypertrophy group, the chronotropic doses of salbutamol required to increase the heart rate by 30 beats/min (CD30) were significantly lower (P < 0.05, P < 0.01, respectively) than that in the control group. However, in the eccentric hypertrophy group. CD30 was higher significantly (P < 0.01) than that in the control group. In the concentric remodeling, concentric hypertrophy, and eccentric hypertrophy groups, beta1-AR responsiveness significantly increased them in the normotensive group, whereas beta2-AR responsiveness significantly increased in the concentric remodeling and concentric hypertrophy groups them in the normotensive group, and significantly decreased in the eccentric hypertrophy them in the normotensive group. The results suggest that non-beta-selective blocker may be beneficial for normal morphology, concentric remodeling and concentric hypertrophy, while beta1-selective blockers may be beneficial for eccentric hypertrophy in patients with EH.
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http://dx.doi.org/10.1536/jhj.44.933DOI Listing
November 2003

The prognostic value of IL-8 for cardiac events and restenosis in patients with coronary heart diseases after percutaneous coronary intervention.

Jpn Heart J 2003 Sep;44(5):623-32

Cardiac Center of Hebei Provincial Pecople's Hospital, Shijiazhuang, China.

The objective of the present study was to investigate the prognostic value of plasma interleukin-8 (IL-8) for adverse cardiac events and restenosis in patients with percutaneous coronary intervention (PCI). The pre- and post-procedural peak plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, while adverse cardiae events and restenosis within one year follow-up were observed in 134 consecutive patients who underwent PCI. Angiography revealed that 23.88% (32/134) of the patients had adverse cardiac events and 29.41% (35/119) of the patients had restenosis. Preprocedural levels of IL-8 and CRP and post-procedural peak levels of IL-8 in patients with adverse cardiac events were higher than those without adverse cardiac events (all P < 0.05). The incidence of adverse cardiac events increased from 6.67% in the bottom tertile to 31.82% in the top tertile of IL-8 levels (P = 0.001): a similar trend was observed for restenosis from 10% in low tertile to 51.28% in high tertile of IL-8 levels to 51.8% (P = 0.012). The preprocedural levels of IL-8 (RR = 5.539, CI = 1.720-17.887, P = 0.001) and CRP (RR = 2.031, CI = 1.132-2.049, P = 0.003) were the only independent predictors of adverse cardiac events. The post-procedure peak level of IL-8 (RR = 3.766, CI = 2.990-5.904, P = 0.002) and stent length (RR = 1.468, CI = 1.161-2.022. P = 0.021) were the independent predictors of restenosis. The results demonstrate that the release of IL-8 after PCI is a powerful prognostic factor for cardiac events and restenosis. The higher the peak level of post-procedure IL-8, the lower the event-free survival observed.
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http://dx.doi.org/10.1536/jhj.44.623DOI Listing
September 2003

Effects of catecholamine-beta-adrenoceptor-cAMP system on severe patients with heart failure.

Chin Med J (Engl) 2003 Oct;116(10):1459-63

Cardiac Center, Hebei Provincial People's Hospital, Shijiazhuang 050051, China.

Objective: To investigate the association between catecholamine-beta-adrenoceptor (beta-AR)-adenosine 3', 5'-monophosphate (cAMP) system and long-term prognosis in patients with chronic heart failure (CHF).

Methods: The study population comprised 73 patients with CHF (EF: 23% +/- 10%) with a mean follow-up of 3.8 +/- 1.9 years. Plasma levels of norepinephrine (NE) were measured using high performance lipid chromatography, beta-adrenergic receptor density (Bmax) and the content of cAMP in peripheral lymphocytes were calculated using 3H-dihydroalpneolo as ligand and competitive immunoassay, respectively. Deaths due to cardiovascular events within the follow-up period were registered.

Results: The total mortality was 64.7%, 57.4% of which was for cardiogenic (worsening heart failure: 32.4%; sudden death: 25.0%). In the cardiogenic death group, plasma levels of NE and epinephrine (E) (3.74 nmol/L +/- 0.09 nmol/L and 3.17 nmol/L +/- 1.0 nmol/L) and the contents of peripheral lymphocyte cAMP (3.64 pmol/mg protein +/- 1.4 pmol/mg protein) were significantly increased as compared with the survival group (2.68 nmol/L +/- 0.07 nmol/L, 2.41 nmol/L +/- 0.24 nmol/L and 2.73 pmol/mg protein +/- 0.9 pmol/mg protein, respectively, all P < 0.01). In the sudden death group, plasma levels of NE and E (5.01 nmol/L +/- 0.06 nmol/L and 4.13 nmol/L +/- 0.08 nmol/L) were significantly increased as compared with the worsening heart failure group (2.49 nmol/L +/- 0.07 nmol/L and 2.33 nmol/L +/- 0.8 nmol/L, all P < 0.001) and to the survival group (2.68 nmol/L +/- 0.07 nmol/L and 2.41 nmol/L +/- 0.14 nmol/L, all P < 0.01). The incidences of sudden death were 0%, 75%, and 100% (chi(2) = 16.018, P < 0.01) in patients with plasma NE < 2.5 nmol/L, NE 2.5 nmol/L - 4.5 nmol/L, and NE > 4.5 nmol/L, respectively. In the worsening heart failure group, the content of peripheral lymphocyte cAMP (4.46 pmol/mg protein +/- 0.18 pmol/mg protein) was significantly increased compared with the sudden death group (2.39 pmol/mg protein +/- 0.9 pmol/mg protein, P < 0.001) and to the survival group (2.73 pmol/mg protein +/- 1.1 pmol/mg protein, P < 0.001). The worsening heart failure death occurences were 5.0%, 72.2%, and 100% (chi(2) = 14.26, P < 0.01) in patients with a content of peripheral lymphocyte cAMP < 2.5 nmol/L, cAMP 2.5 nmol/L - 4.5 nmol/L, and cAMP > 4.5 nmol/L, respectively. Bmax in peripheral lymphocyte was not significantly different (P > 0.05) among the sudden death, worsening heart failure, and survival groups in CHF patients.

Conclusions: Plasma levels of catecholamine increase significantly, and Bmax and the contents of cAMP in peripheral lymphocytes decrease significantly in patients with CHF. High plasma catecholamine levels may be associated with sudden death, and high intralymphocyte cAMP content may be associated with worsening heart failure in CHF patients.
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October 2003

Plasma levels of IL-8 predict early complications in patients with coronary heart disease after percutaneous coronary intervention.

Jpn Heart J 2003 Jul;44(4):451-61

Cardiac Center of Hebei Provincial People's Hospital, Shijiazhuang, China.

The aim of the present study was to investigate the prognostic value of plasma interleukin-8 (IL-8) for early complications after percutaneous coronary intervention (PCI). The pre- and postprocedural plasma levels of IL-8 and serum C-reactive protein (CRP) were examined by immunoassay, and the expression of CD11b/CD18 on neutrophils was assessed by flow cytometry. Early complications (abrupt occlusion, threatened abrupt occlusion, early recurrence of ischemia, myocardial infarction, cardiac sudden death, and target vessel revascularization) occurred intra-procedure and 30 days after PCI and were observed in 121 consecutive patients with coronary heart disease. Sixteen patients with early complications had high preprocedural levels and high postprocedural differentials of IL-8, CRP, and CD11b/CD18 compared to those without complications (all P < 0.05). The occurrence of complications showed a significant increase in the patients according to the tertiles of IL-8, CRP, and CD11b/CD18. Preprocedural levels of IL-8 (RR = 5.864, CI = 1.658-20.734, P = 0.006) and diabetes (RR = 1.587, CI = 1.246-2.132, P = 0.038) were independent predictors of early complications. There were significant correlations in the postprocedural differential between IL-8 and CD11b/CD18 (r = 0.776, P = 0.002) in patients with complications. The results reveal that the early complications after PCI contribute to preprocedural inflammatory responses. Normal levels of IL-8 may be powerful negative predictors of early complications in patients with CHD following PCI.
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http://dx.doi.org/10.1536/jhj.44.451DOI Listing
July 2003

Inflammatory cytokine release in patients with unstable angina after coronary angioplasty.

Jpn Heart J 2002 Mar;43(2):103-15

Cardiac Center, Hebei Provincial People's Hospital of Hebei Medical University, Shijiazhuang, China.

The aim of the present study was to investigate inflammatory cytokine release and the interaction with platelets in patients with unstable angina (UA) after coronary angioplasty. In 50 patients with stable angina (SA) and 58 patients with UA, serial venous blood samples were obtained immediately before, and 30 minutes, 4, 12, 24, 48 and 72 hours, and 7 days after coronary angioplasty. Plasma concentrations of IL-8 and vWF were determined by immunoassay, while the expression of CD11 b/CD18 on monocytes and the expression of CD41 on platelets were assessed by flow cytometry. Differences in the baseline plasma concentrations of IL-8, vWF and CD11b/CD18, CD41 were found in the UA and SA groups before angioplasty (101.1 +/- 31.28 pg/mL to 55.8 +/- 17.24 pg/mL, 137.67 +/- 38.14% to 107.40 +/- 28.67% and 318.67 +/- 36.85 MFI to 240.72 +/- 28.43 MFI, 147.5 +/- 23.18 MFI to 104.43 +/- 26.68 MFI all p < 0.05). The peak plasma levels of IL-8 (172.24 +/- 37.82 pg/mL at 12 hours) and vWF (256 +/- 42.32% at 4 hours) significantly increased after coronary angioplasty (both p < 0.01), and were associated with significant time course increases in surface expression of CD11b/CD18 (p < 0.01) and CD41 (p < 0.01). The levels of plasma IL-8 and vWF were significantly higher pre- and post-procedure in UA patients with lesion type C compared to types A or B (p < 0.05), but there were no differences for pre-procedure in the SA group patients with different lesion types (p > 0.05). There were significant correlations between plasma IL-8 and monocyte CD11b/CD18, vWF and CD41 in the UA group (r = 0.5248, r = 0.6240 both p < 0.01, respectively). The findings demonstrate increases in plasma IL-8 and CD11b/CD18 as inflammatory mediators, vWF and CD41 as the abnormal coagulation activity may therefore yield a rationale for pharmacological anticytokines in patients with UA after coronary angioplasty.
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http://dx.doi.org/10.1536/jhj.43.103DOI Listing
March 2002
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