Publications by authors named "Jinggang Xia"

18 Publications

  • Page 1 of 1

Activation of macrophage TBK1-HIF-1α-mediated IL-17/IL-10 signaling by hyperglycemia aggravates the complexity of coronary atherosclerosis: An in vivo and in vitro study.

FASEB J 2021 May;35(5):e21609

Department of Cardiology, Xuanwu Hospital, Capital Medical University, National Clinical Research Centre for Geriatric Diseases, Beijing, China.

Our purpose was to study the effect of hyperglycemia on macrophage TBK1-HIF-1α-mediated IL-17/IL-10 signaling and its correlation with coronary atherosclerosis. A total of 135 patients with coronary heart disease (CHD) were divided into a stable CHD (SCHD) group (n = 30) and an acute myocardial infarction (AMI) group (n = 105) [nondiabetes mellitus (non-DM)-AMI, n = 60; DM-AMI, n = 45] from January to September 2020. The SYNTAX score and metabolic and inflammatory markers were quantified and compared. THP-1 cell studies and an animal study of coronary intimal hyperplasia were also carried out. We found that the DM-AMI group showed a higher SYNTAX score than the non-DM-AMI group (P < .05). The DM-AMI group showed the highest expression levels of TANK-binding kinase 1 (TBK1), hypoxia-inducible factor 1α (HIF-1α), and interleukin (IL)-17 and the lowest expression level of IL-10, followed by the non-DM-AMI group and the SCHD group (P < .05). THP-1 cell studies showed that BAY87-2243 (a HIF-1α inhibitor) reversed the increase in IL-17 and decrease in IL-10 expression induced by hyperglycemia. Amlexanox (a TBK1 inhibitor) reversed the increase in HIF-1α expression induced by hyperglycemia. Amlexanox treatment resulted in lower coronary artery intimal hyperplasia and a larger lumen area in a diabetic swine model. We conclude that hyperglycemia might aggravate the complexity of coronary atherosclerosis through activation of TBK1-HIF-1α-mediated IL-17/IL-10 signaling. Thus, TBK1 may be a novel drug therapy target for CHD complicated with DM.
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http://dx.doi.org/10.1096/fj.202100086RRDOI Listing
May 2021

The effects of glycaemic variability on intimal hyperplasia and plaque stability after stenting via autophagy-mediated G3BP1/NLRP3 inflammasome.

Ann Transl Med 2020 Nov;8(21):1388

Department of Cardiology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Beijing, China.

Background: The objective of this study was to investigate the effects of glycaemic variability (GV) on intimal hyperplasia and plaque stability after coronary stenting via autophagy-mediated G3BP1/NLRP3 inflammasome signalling.

Methods: In the clinical study, between July 2017 and December 2017, 95 patients with acute myocardial infarction (AMI) and diabetes mellitus (DM) comorbidity received stent implantation. The patients were followed up for 2 years after discharge. The patients were divided into a low-GV (n=61) and high-GV (n=34) group, and the incidence of recurrent AMI was measured. In the animal study, thirteen pigs were divided into a sham (n=3), low-GV DM (n=5) and high-GV DM group (n=5). Intima samples were analysed by optical coherence tomography 22 weeks after coronary stenting. Becn1, LC3B, p62, G3BP1 and NLRP3 protein levels in the intima were examined by western blot. experiments with THP-1 cells were also conducted.

Results: In the high-GV group, patients exhibited a higher recurrent AMI, greater neointimal thickness, increased p62 and NLRP3 expression, and decreased Becn1, LC3B and G3BP1 expression compared with the low-GV group (P<0.05). The effects of high GV could be abolished by rapamycin but were aggravated by 3-methyladenine.

Conclusions: GV might impact the intimal hyperplasia and plaque stability via autophagy-mediated G3BP1/NLRP3 inflammasome signalling. GV and the autophagy-mediated G3BP1/NLRP3 inflammasome may be promising targets for the treatment of coronary heart disease.
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http://dx.doi.org/10.21037/atm-20-4818DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723640PMC
November 2020

The impact of hyperglycaemia on PKM2-mediated NLRP3 inflammasome/stress granule signalling in macrophages and its correlation with plaque vulnerability: an in vivo and in vitro study.

Metabolism 2020 06 13;107:154231. Epub 2020 Apr 13.

Department of Cardiology, Xuanwu Hospital, Capital Medical University, National Clinical Research Centre for Geriatric Diseases, Beijing 100053, China. Electronic address:

Background: The mechanism of pyruvate kinase M2 (PKM2)-mediated inflammatory signalling in macrophages when plaques rupture and the impact of hyperglycaemia on the signalling are unclear. The present study aimed to explore the impact of hyperglycaemia on PKM2-mediated NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome/stress granule signalling in macrophages and its correlation with plaque vulnerability in vivo and in vitro.

Methods: From July to December 2019, 80 patients with coronary heart disease (CHD) were divided into acute ST-segment elevation myocardial infarction (STEMI) (n = 57) (DM-STEMI, n = 21; non-DM-STEMI, n = 36) and stable CHD (SCHD) groups (n = 23). Circulating mononuclear cells were isolated. The value of peak troponin I (TnI), the Global Registry of Acute Coronary Events (GRACE) risk score, and the expression levels of the related markers were quantified and compared. In vitro studies on the THP-1 cells were also performed.

Results: The DM-STEMI group had a higher value of peak TnI and a higher GRACE risk score than the non-DM-STEMI group (p < 0.05). The highest expression levels of PKM2, NLRP3, interleukin (IL)-1β, and IL-18 and the lowest expression level of GTPase activating protein (SH3 domain)-binding protein 1 (G3BP1) (a stress granule marker protein) were observed in the DM-STEMI group, and they were followed by the non-DM-STEMI group and the SCHD group (p < 0.05). In vitro studies showed similar results and that TEPP-46 (a PKM2 activator) and 2-deoxy-d-glucose (a toxic glucose analogue) reversed the hyperglycaemia-induced increase in the NLRP3 inflammasome and decrease in G3BP1 expression.

Conclusion: Hyperglycaemia might increase the activation of PKM2-mediated NLRP3 inflammasome/stress granule signalling and increase plaque vulnerability, associating it with worse prognosis. PKM2 may be a novel prognostic indicator and a new target for the treatment of patients with CHD and DM.
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http://dx.doi.org/10.1016/j.metabol.2020.154231DOI Listing
June 2020

A GLP-1 Analog Liraglutide Reduces Intimal Hyperplasia After Coronary Stent Implantation Regulation of Glycemic Variability and NLRP3 Inflammasome/IL-10 Signaling in Diabetic Swine.

Front Pharmacol 2020 26;11:372. Epub 2020 Mar 26.

Surgical Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China.

Objective: This study aimed to explore whether treatment with the glucagon-like peptide-1 (GLP-1) analog liraglutide reduces intimal hyperplasia after coronary stent implantation regulation of glycemic variability, the NLRP3 inflammasome, and IL-10 in diabetic swine.

Methods: Fifteen pigs were divided into a diabetes mellitus (DM) group (n = 6), a DM + liraglutide treatment group (L group) (n = 6) and a sham group (n = 3). A total of 24 everolimus-eluting stents were implanted in the left anterior descending and right coronary arteries at 3 weeks. A novel continuous glucose monitoring system (GMS) was used for 2 weeks. The means and standard deviations (SDs) were measured and calculated by the GMS. At 22 weeks, the lumen area (LA), neointimal thickness (NIT), neointimal area (NIA), and percent area stenosis (%AS) were analyzed by optical coherence tomography. Plasma tumor necrosis factor-, interleukin-6, and interleukin-10 were assayed by ELISA. The intima protein expression levels of NLRP3, interleukin-1, interleukin-18 and interleukin-10 were examined using Western blot analysis. Histology was used to evaluate the healing response. In an study, THP-1 cells were divided into control, high glucose (HG), HG + liraglutide, and HG + liraglutide + Exe(9-39) (a GLP-1 receptor inhibitor) groups.

Results: The L group had a lower SD, NIT, NIA, and %AS; a larger LA; reduced inflammation and injury scores; lower expression levels of tumor necrosis factor-, interleukin-6, NLRP3, interleukin-1, and interleukin-18; and higher expression of interleukin-10 compared with those of the DM group ( < 0.05). In the study, similar results were obtained in the HG + liraglutide group, and Exe(9-39) abolished the effect of liraglutide ( < 0.05).

Conclusions: Liraglutide treatment reduces intimal hyperplasia after stent implantation regulation of glycemic variability, the NLRP3 inflammasome, and IL-10 in diabetic pigs in a GLP-1 receptor-dependent manner. Reducing the inflammation induced by glycemic variability may be one of the cardioprotective mechanisms of liraglutide.
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http://dx.doi.org/10.3389/fphar.2020.00372DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7113385PMC
March 2020

Glycemic variability is associated with vascular calcification by the markers of endoplasmic reticulum stress-related apoptosis, Wnt1, galectin-3 and BMP-2.

Diabetol Metab Syndr 2019 19;11:67. Epub 2019 Aug 19.

3Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing, 100053 China.

Background: The present study identified whether glycemic variability (GV) was associated with vascular calcification and explored the underlying mechanisms.

Methods: Eighty-four consecutive type 2 diabetic patients with unstable angina (UA) were included from January 2018 to June 2018 to calculate calcification scores using computerized tomographic angiography (CTA), and the patients were divided into 2 groups: high calcification score group (HCS group) and low calcification score group (LCS group). Intergroup differences in GV were determined via comparisons of the standard deviation (SD) of blood glucose. Calcification staining, content measurement, apoptosis evaluation and Western blot analysis of endoplasmic reticulum (ER) stress-related apoptosis, Wnt1, galectin-3 and bone morphogenetic protein-2 (BMP-2) were compared in cell cultures from rat vascular smooth muscle cells in the different degrees of GV.

Results: The SD increased significantly with the increases in calcification scores from human studies (HCS group 2.37 ± 0.82 vs. LCS group 1.87 ± 0.78, = 0.007). Multivariate logistic regression analysis suggested that increased SD and serum creatinine were independent predictors of calcification. The high GV group had a higher apoptotic rate, higher calcification content and higher expressions of glucose-regulated protein, caspase-3, Wnt1, galectin-3 and BMP-2 markers compared to the low GV group in the in vitro studies (< 0.001).

Conclusion: We report the novel finding that GV is associated with vascular calcification, and ER stress-related apoptosis, Wnt1, galectin-3 and BMP-2 may be involved in this regulation.
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http://dx.doi.org/10.1186/s13098-019-0464-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6701112PMC
August 2019

Glucose Variability and Coronary Artery Disease.

Heart Lung Circ 2019 Apr 12;28(4):553-559. Epub 2018 Nov 12.

Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing, 100053, China. Electronic address:

Fasting blood glucose, postprandial blood glucose and glycated haemoglobin are considered three important indicators for diabetes treatment. There is increasing evidence that glucose variability has more detrimental effects on the coronary arteries than does chronic sustained hyperglycaemia. This overview summarises recent findings in the field of glucose variability and its possible relationship with coronary artery disease. Glucose variability may be a marker of increased progression of coronary disease and plaque vulnerability. It might be a potential new therapeutic target for secondary prevention of coronary artery disease. Future studies will focus on the early detection and control of glucose variability to improve the clinical outcomes in patients with coronary artery disease.
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http://dx.doi.org/10.1016/j.hlc.2018.10.019DOI Listing
April 2019

Two-year longitudinal evaluation of a second-generation thin-strut sirolimus-eluting bioresorbable coronary scaffold with hybrid cell design in porcine coronary arteries.

Cardiol J 2020 29;27(2):115-125. Epub 2018 Aug 29.

CRF-Skirball Center for Innovation, 8 Corporate Dr., NY, 10965 Orangeburg, United States.

Background: The first commercially available bioresorbable scaffold (BRS) had a strut thickness of 156 microns. As such, it had the potential for delivery challenges and higher thrombogenicity. The aim herein, is to evaluate biomechanical performance, pharmacokinetics and vascular healing of a novel thin strut (100 μm) sirolimus eluting BRS (MeRes-100, Meril Life Sciences, Gujarat, India) against the once clinically used BRS (Absorb BVS, Abbott, Santa Clara, CA) in porcine coronary arteries.

Methods: Following device implantation, angiographic and optical coherence tomography (OCT) evaluation were performed at 45, 90, 180 days, 1 year and 2 years. Histological evaluation was per-formed at 30, 90 and 180 days.

Results: At 2 years, both lumen (MeRes-100 7.07 ± 1.82 mm² vs. Absorb BVS 7.57 ± 1.39 mm2, p = NS) and scaffold areas (MeRes-100 9.73 ± 1.80 mm² vs. Absorb BVS 9.67 ± 1.25 mm², p = NS) were comparable between tested and control scaffolds. Also, the late lumen area gain at 2 years was similar in both groups tested (MeRes-100 1.03 ± 1.98 mm² vs. Absorb BVS 0.85 ± 1.56 mm², p = NS). Histologic examination up to 6 months showed comparable healing and inflammation profiles for both devices.

Conclusions: The novel sirolimus-eluting BRS with thinner struts and hybrid cell design showed similar biomechanical durability and equivalent inhibition of neointimal proliferation when compared to the first-ever Absorb BVS up to 2 years in normal porcine coronary arteries.
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http://dx.doi.org/10.5603/CJ.a2018.0095DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8016019PMC
August 2018

A 6-Month Follow-Up Study of the Relation between Apolipoprotein E Gene Polymorphism and Major Adverse Cardiovascular Events in Patients with Acute Coronary Syndrome.

Cardiology 2018 21;140(3):187-193. Epub 2018 Aug 21.

Objectives: This study aimed to investigate the relation between ApoE gene polymorphisms and major adverse cardiovascular events (MACE) in patients with acute coronary syndrome (ACS) during a 6-month follow-up.

Methods: From October 2016 to July 2017, 211 patients were admitted to a cardiology clinic with a diagnosis of ACS. Blood samples were obtained from all patients on the first day. The primary end point was a 6-month incidence of MACE. ApoE gene polymorphism was genotyped by real-time PCR using TaqMan® SNP Genotyping Assay.

Results: The patients with the E4 allele were associated with higher low-density lipoprotein (LDL) cholesterol and total cholesterol (TC) levels compared with the patients without the E4 allele (p = 0001 and p = 0.001). The patients with the E4 allele were associated with a higher rate of MACE compared with the patients without the E4 allele (ApoE4 allele(+) 23.1% vs. ApoE4 allele(-) 9.3%; p = 0.03). Multivariable analysis suggested that E4 allele carriers showed an 85% risk increment of 6-month MACE (odds ratio 2.48, 95% confidence interval 2.37-5.95; p = 0.01).

Conclusions: The trial shows that E4 allele carriers were correlated with not only higher LDL cholesterol and TC levels, but also with a higher incidence of MACE during a 6-month follow-up.
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http://dx.doi.org/10.1159/000491597DOI Listing
May 2019

Six-month evaluation of novel bioabsorbable scaffolds composed of poly-L-lactic acid and amorphous calcium phosphate nanoparticles in porcine coronary arteries.

J Biomater Appl 2018 08;33(2):227-233

1 Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Objective Using coronary angiography and intravascular ultrasound methods to evaluate the performance of the novel fully bioabsorbable scaffold (NFBS) composed of poly-L-lactic acid/amorphous calcium phosphate (PLLA/ACP) at six-month follow-up by comparing with PLLA scaffolds Methods Twelve PLLA/ACP scaffolds and 12 PLLA scaffolds were implanted into the coronary arteries of 12 miniature pigs. Quantitative coronary angiography (QCA) was used to measure the reference vessel diameter (RVD), mean lumen diameter (MLD) and late lumen loss (LLL). According to IVUS images, we calculated the strut malapposition rate (SMR) at post implantation, strut overlap rate (SOR), reference vessel area (RVA), mean stent area (MSA), mean lumen area (MLA) and luminal patency rate (LPR) at six-month follow-up. The radial strength of the scaffold was evaluated using a catheter tensile testing machine. Results QCA results indicated that, at six month, MLD of PLLA/ACP scaffolds was greater than those of PLLA scaffolds (2.47 ± 0.22 mm vs. 2.08 ± 0.25 mm, P < 0.05); LLL of PLLA/ACP scaffolds was less than those of PLLA scaffolds (0.42 ± 0.20 mm vs. 0.75 ± 0.22 mm, P < 0.05). IVUS results showed the SMR and SOR were all significantly less with the PLLA/ACP scaffolds than the PLLA scaffolds (5.84% ± 3.56% vs. 17.72% ± 4.86%, P < 0.05) (6.17% ± 4.63% vs. 17.65% ± 4.29%, P < 0.05). MSA, MLA and LPR of the PLLA/ACP scaffolds were all greater than those of PLLA scaffolds (6.35 ± 0.45 mm vs. 5.35 ± 0.51 mm, P < 0.05) (4.76 ± 0.46 mm vs. 3.77 ± 0.46 mm, P < 0.05) (78.01% ± 12.29% vs. 61.69% ± 9.76%, P < 0.05). Radial strength of PLLA/ACP scaffold at six month was greater than that of PLLA scaffold (76.33 ± 3.14 N vs. 67.67 ± 3.63 N). Conclusion The NFBS had less stent recoil, better lumen patency rate and greater radial strength than PLLA scaffolds. The results suggest the NFBS scaffolds can maintain the structural strength and functional performance, which are effective for up to six months when implanted in porcine coronary arteries.
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http://dx.doi.org/10.1177/0885328218790332DOI Listing
August 2018

Effect of novel bioresorbable scaffold composed of poly-L-lactic acid and amorphous calcium phosphate nanoparticles on inflammation and calcification of surrounding tissues after implantation.

J Mater Sci Mater Med 2018 Jul 17;29(8):112. Epub 2018 Jul 17.

Department of Cardiology, Renmin Hospital of Wuhan University, 430060, Wuhan, China.

To study the effect of novel bioresorbable scaffold composed of poly-L-lactic acid (PLLA) and amorphous calcium phosphate (ACP) nanoparticles on inflammation and calcification of surrounding tissues after implantation. Ninety six PLLA/ACP scaffolds and 96 PLLA scaffolds were randomly implanted in the back muscle tissue of 48 SD rats. At the 1st, 2nd, 4th, and 12th weeks after implantation, the calcium, phosphorus, and alkaline phosphatase levels in the blood serum and the contents of calcium and alkaline phosphatase in the tissue surrounding the scaffolds were measured. Hematoxylin-eosin staining was performed to count the inflammatory cells. Von kossa staining was performed to observe calcification of the surrounding tissue around the scaffold. NF-κB staining was performed by immunohistochemistry to calculate the positive expression index of inflammatory cells. Western blot was used to detect the expression of IL-6 and BMP-2 in the tissues surrounding the scaffolds. At the 1st, 2nd, 4th, and 12th weeks after scaffold implantation, there were no significant difference in the serum concentration of calcium, phosphorus, alkaline phosphatase and in the tissue homogenate concentration of alkaline phosphatase between the two groups (P > 0.05). The level of calcium in tissue homogenates was lower in the PLLA/ACP group than in the PLLA group at 12-week (P < 0.05). The hematoxylin-eosin staining results showed that the inflammatory cell count in the PLLA/ACP group was lower than the PLLA group at 4-week and 12-week (P < 0.05). The results of NF-kB positive expression index showed that the PLLA group was significantly more than the PLLA/ACP group at 4-week and 12-week (P < 0.01). Western blot results showed that IL-6 expression levels in the PLLA/ACP group scaffolds were significantly lower than those in the control group at the 2-week, 4-week and 12-week (P < 0.05). The expression of BMP-2 in the PLLA group was significantly lower than that in the control group at 4-week and 12-week (P < 0.05). The PLLA/ACP composite material has good histocompatibility. The integration of nanoscale ACPs reduces the inflammatory response induced by acidic metabolites of PLLA material and may inhibit tissue calcification by reducing the amount of calcification factors in the body.
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http://dx.doi.org/10.1007/s10856-018-6125-6DOI Listing
July 2018

The correlation between glucose fluctuation from self-monitored blood glucose and the major adverse cardiac events in diabetic patients with acute coronary syndrome during a 6-month follow-up by WeChat application.

Clin Chem Lab Med 2018 11;56(12):2119-2124

Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing, P.R.China.

Background This study aimed to investigate the correlation between glucose fluctuation from self-monitored blood glucose (SMBG) and the major adverse cardiac events (MACE) in diabetic patients with acute coronary syndrome (ACS) during a 6-month follow-up period using the WeChat application. Methods From November 2016 to June 2017, 262 patients with ACS were discharged in a stable condition and completed a 6-month follow-up period. SMBG was recorded using the WeChat application. The patients were divided to a high glucose fluctuation group (H group; n=92) and a low glucose fluctuation group (L group; n=170). The 6-month incidence of MACE, lost-to-follow-up rate and satisfaction rate were measured through the WeChat follow-up. Results MACE occurred in 17.4% of patients in the H group and in 8.2% of patients in the L group (p=0.04). Multivariable analysis suggested that high glucose fluctuation conferred an 87% risk increment of MACE in the 6-month follow-up period (odds ratio: 2.1, 95% confidence interval 1.95-4.85; p=0.03). The lost-to-follow-up rate was lower and the satisfaction rate was higher in the patients using the WeChat application during follow-up than those of the regular outpatient follow-up during the same period (p<0.05). Conclusions The trial demonstrates that higher glucose fluctuation from SMBG after discharge was correlated with a higher incidence of MACE in diabetic patients with ACS. WeChat follow-up might have the potential to promote a good physician-patient relationship.
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http://dx.doi.org/10.1515/cclm-2018-0220DOI Listing
November 2018

Optical Coherence Tomography Assessment of Glucose Fluctuation Impact on the Neointimal Proliferation After Stent Implantation in a Diabetic/Hypercholesterolemic Swine Model.

Int Heart J 2017 Aug 10;58(4):608-614. Epub 2017 Jul 10.

Department of Cardiology, Xuanwu Hospital, Capital Medical University.

The aim of the present study was to investigate the effects of glucose fluctuation on neointimal proliferation after stent implantation by optical coherence tomography (OCT) in a diabetic/hypercholesterolemic (DM/HC) swine model.A total of 24 everolimus-eluting stents (EES) were implanted in the right coronary artery (RCA) of the animals using a 20% overstretch ratio. The 24 swines were divided into a DM-high glucose fluctuation (HGF) group (n = 8), DMlow glucose fluctuation (LGF) group (n = 8), and a control group (n = 8). Percent diameter stenosis (%DS), late loss (LL), percent area stenosis (%AS), and neointimal thickness (NIT) were analyzed. The differences in neointimal characteristics and circulating oxidative stress and inflammation biomarkers were assessed and measured.At 28 days, the highest values of %DS, LL, %AS, and NIT were achieved in the HGF group followed by the LGF group (P < 0.05) and the control group (P < 0.05). The highest frequency of the heterogeneous pattern was in the HGF group followed by the LGF group (P < 0.05) and the control group (P < 0.05). This was also the case for the oxidative stress and inflammation biomarkers.DM might have a deleterious impact on neointimal proliferation after EES implantation in this DM/HC swine model. The extent of glucose fluctuation may be related to the degree of neointimal proliferation and this needs to be further confirmed by long-term follow-up and histology.
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http://dx.doi.org/10.1536/ihj.16-574DOI Listing
August 2017

Impact of glycemic variability on the occurrence of periprocedural myocardial infarction and major adverse cardiovascular events (MACE) after coronary intervention in patients with stable angina pectoris at 6months follow-up.

Clin Chim Acta 2017 Aug 15;471:196-200. Epub 2017 Jun 15.

Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. Electronic address:

Background: We explored the impact of glycemic variability on the occurrence of periprocedural myocardial infarction and major adverse cardiovascular events (MACE) after coronary intervention in patients with stable angina pectoris (SAP) at 6months follow-up.

Methods: From May 2015 to April 2016, a total of 746 patients with SAP were divided to high glycemic variability group (H group) (n=261) and low glycemic variability group (L group) (n=485). The primary end point was incidence of periprocedural myocardial infarction and MACE at 6months follow-up.

Results: The occurrence of periprocedural myocardial infarction occurred in 18.8% of patients in H group and in 12.4% in L group (P=0.03). The incidence of MACE at 6months follow-up was 9.6% in H group and 4.5% in L group (P=0.01). Multivariable analysis suggested that high glycemic variability conferred a 53% risk increment of 6months follow-up MACE (odds ratio 2.13, 95% confidence interval 1.85-5.38; P=0.01).

Conclusions: The trial shows that higher blood glucose variability was correlated with higher incidence of periprocedural myocardial infarction and MACE at 6months follow-up.
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http://dx.doi.org/10.1016/j.cca.2017.06.014DOI Listing
August 2017

Association between glycemic variability and major adverse cardiovascular and cerebrovascular events (MACCE) in patients with acute coronary syndrome during 30-day follow-up.

Clin Chim Acta 2017 Mar 19;466:162-166. Epub 2017 Jan 19.

Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.. Electronic address:

Background: We explored the association between glycemic variability and major adverse cardiovascular and cerebrovascular events (MACCE) in patients with acute coronary syndrome (ACS) during 30-day follow-up.

Methods: From May 2013 to April 2015, a total of 864 patients with ACS were divided to high glycemic variability group (H group) (n=285) and low glycemic variability group (L group) (n=579). The primary end point was a 30-day incidence of MACCE. Secondary end points were the incidence of atrial fibrillation (AF) during hospitalization and length of hospital stay.

Results: The primary end point occurred in 15.2% of patients in H group and in 9.7% in L group (p=0.03). The incidence of AF during hospitalization was 14.5% in H group and 8.9% in L group (p=0.02). Compared with the L group, the H group extended the length of hospital stay. Multivariable analysis suggested that high glycemic variability conferred a 57% risk increment of 30-day MACCE (odds ratio 1.97, 95% confidence interval 1.32-6.86; p=0.02).

Conclusion: The trial shows that higher blood glucose variability was correlated with higher incidence of MACCE, AF and longer length of stay.
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http://dx.doi.org/10.1016/j.cca.2017.01.022DOI Listing
March 2017

Preliminary study of beta-blocker therapy on modulation of interleukin-33/ST2 signaling during ventricular remodeling after acute myocardial infarction.

Cardiol J 2017 17;24(2):188-194. Epub 2016 Oct 17.

Xuanwu Hospital, Capital Medical University.

Background: This study aimed to evaluate the role of b-blocker therapy on modulating interleukin (IL)-33/ST2 (interleukin-1 receptor-like 1) signaling during ventricular remodeling related to heart failure (HF) after acute myocardial infarction (AMI).

Methods: Sprague-Dawley rats that survived surgery to induce AMI were randomly divided into the placebo group and the b-blocker treatment group. A sham group was used as a control. Left ventricular (LV) function variables, the myocardial infarct size, fibrosis and IL-33/ST2 protein expression was measured.

Results: Compared with the placebo group, b-blocker treatment significantly improved LV function and reduced infarct size (p < 0.05). There was higher protein expression of IL-33 (p < 0.05) and sST2 (p < 0.05), as well as higher expression of fibrosis (p < 0.05), compared to the sham group. Notably, the high expression of cardioprotective IL-33 was not affected by b-blocker treatment (p > 0.05), however, treatment with b-blocker enhanced IL-33/ST2 signaling, with lower expression of sST2 (p < 0.05) and significantly attenuated fibrosis (p < 0.05).

Conclusions: Our study suggested that b-blocker therapy might play a beneficial role in the modula-tion of IL-33/ST2 signaling during ventricular remodeling. These results may be helpful in identifying IL-33/ST2 systems as putative b-blocker targets at an early stage after AMI. (Cardiol J 2017; 24, 2: 188-194).
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http://dx.doi.org/10.5603/CJ.a2016.0096DOI Listing
June 2017

Efficacy of High-Intensity Atorvastatin for Asian Patients Undergoing Percutaneous Coronary Intervention.

Ann Pharmacother 2016 09 15;50(9):725-33. Epub 2016 Jun 15.

Xuanwu Hospital Capital Medical University, Beijing, China

Background: Statins have proven cardioprotective effects, but higher doses are accompanied by various concerns and may not lead to superior clinical outcomes in Chinese/Asian populations.

Objective: We designed a trial to test the efficacy of high-intensity statin therapy for the reduction of periprocedural myocardial infarction (MI) and 1-year major adverse cardiovascular events (MACEs, including cardiovascular death, spontaneous MI, unplanned revascularization) in an Asian population.

Methods: A total of 798 Chinese patients with stable angina or acute coronary syndrome (ACS) were randomized to high-intensity atorvastatin (80 mg/d before percutaneous coronary intervention [PCI] and 40 mg/d thereafter for 1 year, n = 400) or moderate-intensity atorvastatin (20 mg/d for 1 year, n = 398). The primary end point was 1-year incidence of MACEs.

Result: In patients with stable angina, 1-year MACE rates were not significantly different between moderate- and high-intensity groups (7.6% vs 5.7%, P = 0.53). In contrast, in patients with ACS, the 1-year MACE rate was significantly higher in the moderate- than in the high-intensity atorvastatin group (16.8% vs 10.1%, P = 0.021; adjusted hazard ratio = 1.71, 95% CI = 1.08 to 2.77, P = 0.021).

Conclusions: Whereas stable angina patients derive similar benefit from moderate- and high-intensity atorvastatin therapy over the duration of 1 year after PCI, high-intensity statin therapy is superior in ACS patients.
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http://dx.doi.org/10.1177/1060028016654722DOI Listing
September 2016

Preoperative rosuvastatin protects patients with coronary artery disease undergoing noncardiac surgery.

Cardiology 2015 27;131(1):30-7. Epub 2015 Mar 27.

Department of Cardiology, Xuanwu Hospital, Capital Medical University, Beijing, PR China.

Objectives: We explored whether preoperative rosuvastatin could protect the cardiac health of patients with coronary artery disease undergoing emergency, noncardiac surgery.

Methods: We randomized 550 noncardiac emergency surgery patients with stable coronary artery disease on long-term statin therapy to treatment with and without preoperative rosuvastatin. All patients received rosuvastatin after surgery. We evaluated the incidence of myocardial necrosis and major adverse cardiovascular and cerebrovascular events (MACCE) 30 days and 6 months after surgery.

Results: Creatinine kinase-myocardial band (CK-MB) isoform elevations occurred less frequently 12 and 24 h after noncardiac emergency surgery in the experimental group than in the control group (p = 0.029). After surgery, the incidence of MACCE was also lower in the experimental group than in the control group (p = 0.019). The difference was mainly due to the incidence of perioperative myocardial infarction (p = 0.029). Multivariable analysis found that rosuvastatin reload reduced the incidence of MACCE 52% 6 months after surgery (p = 0.03).

Conclusions: Preoperative rosuvastatin reload therapy decreases the incidence of myocardial necrosis and MACCE after noncardiac emergency surgery in patients with stable coronary artery disease on long-term statin therapy.
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http://dx.doi.org/10.1159/000371872DOI Listing
July 2015

Patients with stable coronary artery disease receiving chronic statin treatment who are undergoing noncardiac emergency surgery benefit from acute atorvastatin reload.

Cardiology 2014 28;128(3):285-92. Epub 2014 May 28.

Medical School of Chinese People's Liberation Army, Beijing, PR China.

Objective: This study was designed to investigate whether patients with stable coronary artery disease (CAD) receiving chronic statin treatment who are undergoing noncardiac emergency surgery benefit from acute atorvastatin reload.

Methods: A total of 500 patients with stable CAD and regular administration of statin before noncardiac emergency surgery were randomized to atorvastatin reload (n = 250) or placebo (n = 250). All patients received atorvastatin treatment thereafter. The primary end point was a 30-day incidence of major adverse cardiac events (MACE). Secondary end points were the incidence of atrial fibrillation (AF) during hospitalization and length of hospital stay.

Results: The primary end point occurred in 2.4% of patients treated with atorvastatin reload and in 8% in the placebo arm (p = 0.0088). The incidence of AF during hospitalization was 6.8% in patients treated with atorvastatin reload and 17% in the placebo arm (p = 0.0003). Compared with the placebo arm, the atorvastatin reload arm shortened the length of stay (9.8 ± 3.3 vs. 10.6 ± 3.5 days, p = 0.009). Multivariable analysis suggested that atorvastatin reload conferred a 65% risk reduction of 30-day MACE (odds ratio 0.35, 95% confidence interval 0.18-0.86; p = 0.005).

Conclusion: The trial suggests that atorvastatin reload may improve the clinical outcome of patients with stable CAD receiving chronic statin treatment who are undergoing noncardiac emergency surgery.
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http://dx.doi.org/10.1159/000362593DOI Listing
February 2015