Publications by authors named "Zhi-Yuan Song"

30 Publications

  • Page 1 of 1

"One-stop shop": safety and efficacy of combining atrial septal defect occlusion and left atrial appendage closure for patients with atrial septal defect and atrial fibrillation.

BMC Cardiovasc Disord 2020 10 12;20(1):444. Epub 2020 Oct 12.

Department of Cardiology, Southwest Hospital, Army Medical University, Chongqing, China.

Background: One-stop occlusion, which is defined as the combination of atrial septal defect [ASD] or patent foramen ovale [PFO] occlusion and left atrial appendage [LAA] closure, in patients with ASD/PFO and atrial fibrillation (AF) has not yet been investigated systematically. This study aimed to evaluate the safety and efficacy of one-stop occlusion in the treatment of adult patients with ASD/PFO and AF.

Methods: Inpatients with AF and ASD/PFO were recruited between August 2014 and April 2019. Preoperatively, transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) were conducted to identify the ASD/PFO size and margin, presence of thrombus in the LAA, and LAA orifice width and depth at 0°, 45°, 90°, and 135°. After confirmation of the indications of LAA closure (LAAC) and ASD/PFO occlusion, the procedures were performed simultaneously under general anesthesia. Oral anticoagulants were administered for 45-60 days, followed with regular evaluation of TTE and TEE.

Results: Forty-nine patients (age, 65.6 ± 9.6 years) were recruited in this study, including 24 patients with ASD and 25 patients with PFO. They were treated with LAAC and ASD/PFO occlusion successfully. The mean ASD size and mean diameter of the ASD occluders were 14.2 ± 7.7 and 25.4 ± 8.5 mm, respectively. The mean PFO size was 3.5 ± 0.4 mm. The mean maximal LAA orifice width and depth were 20.5 ± 3.4 and 28.3 ± 3.6 mm, respectively. All patients were implanted with a Watchman device (diameter, 27.1 ± 2.9 mm). Postoperatively, all patients took anticoagulants orally for 45-60 days, and their mean postoperative follow-up duration was 29.0 ± 12.1 months. Postoperative TEE showed that all had normal positioning of the LAA and ASD/PFO occluders. At 45-60 days after operation, TEE showed that the LAA and ASD/PFO occluder were in the normal position; however, two patients who took warfarin and novel oral anticoagulants, respectively, have developed occluder thrombosis. After adjusted anticoagulant therapy, TEE showed that the thrombus disappeared at 6 months after operation.

Conclusion: One-stop occlusion is safe and effective for the treatment of adult patients with ASD/PFO and AF. It is also feasible to administer warfarin or novel oral anticoagulants after operation.
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http://dx.doi.org/10.1186/s12872-020-01708-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7552475PMC
October 2020

Exosome Derived from Coronary Serum of Patients with Myocardial Infarction Promotes Angiogenesis Through the miRNA-143/IGF-IR Pathway.

Int J Nanomedicine 2020 21;15:2647-2658. Epub 2020 Apr 21.

Department of Cardiovascular Disease, Cangzhou Central Hospital of Tianjin Medical University, Cangzhou, Hebei Province, People's Republic of China.

Purpose: Myocardial ischemia-reperfusion injury primarily causes myocardial infarction (MI), which is manifested by cell death. Angiogenesis is essential for repair and regeneration in cardiac tissue after MI. In this study, we aimed to investigate the effect of exosomes derived from the serum of MI patients in angiogenesis and its related mechanism.

Patients And Methods: Exosomes, isolated from serum, were collected from MI (MI-exosome) and control (Con-exosome) patients. After coculturing with human umbilical vein endothelial cells, MI-exosome promoted cell proliferation, migration, and tube formation.

Results: The results revealed that the production and release of MI-exosome were associated with cardiomyocytes. Moreover, microarray assays demonstrated that miRNA-143 was significantly decreased in MI-exosome. Meanwhile, the overexpression and knockdown of miRNA-143 could inhibit and enhance angiogenesis, respectively. Furthermore, the effect of exosomal miRNA-143 on angiogenesis was mediated by its targeting gene, insulin-like growth factor 1 receptor (IGF-IR), and was associated with the production of nitric oxide (NO).

Conclusion: Taken together, exosomes derived from the serum of patients with MI promoted angiogenesis through the IGF-IR/NO signaling pathway. The results provide novel understanding of the function of exosomes in MI.
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http://dx.doi.org/10.2147/IJN.S242908DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7183550PMC
July 2020

Physical exercise inhibits atherosclerosis development by regulating the expression of neuropeptide Y in apolipoprotein E-deficient mice.

Life Sci 2019 Nov 9;237:116896. Epub 2019 Oct 9.

Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China. Electronic address:

Aims: Population-based studies have shown that exercise has anti-atherosclerotic effects, but the mechanisms underlying this cardiac protection are poorly understood. The aim of this study was to investigate if the anti-atherosclerotic effects of exercise are associated with changes in neuropeptide Y (NPY) expression in apolipoprotein E-deficient (ApoE) mice.

Main Methods: Thirty-one male ApoE mice were randomly divided into regular exercise (5 days/week), occasional exercise (1-2 days/week), and sedentary groups. After 8 weeks, atherosclerotic burden and plaque stability were measured by histological and morphological analysis. Quantitative real-time PCR and immunohistochemistry were used to measure the expression of NPY and its receptors in the aorta.

Key Findings: Eight weeks of occasional exercise was equally effective as regular exercise at preventing atherosclerotic plaque formation and enhancing atherosclerotic plaque stability. This was shown by increased plaque collagen and smooth muscle cell content and decreased plaque lipid and macrophage content. The expression of NPY and its receptors in the vasculature was decreased in the regular exercise and occasional exercise groups, and this expression was significantly correlated with the progress of atherosclerosis. Moreover, exercise may reduce the activity of macrophages by down-regulating the expression of NPY Y1 receptors, thereby reducing the release of inflammatory cytokines.

Significance: These results suggest that exercise training can attenuate plaque burden and enhance atherosclerotic plaque stability. The anti-atherosclerotic effect of exercise appears to be, at least in part, dependent on down-regulation of the expression of NPY and its receptors (especially Y1 receptors) in the aorta.
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http://dx.doi.org/10.1016/j.lfs.2019.116896DOI Listing
November 2019

Collagen biomaterial for the treatment of myocardial infarction: an update on cardiac tissue engineering and myocardial regeneration.

Drug Deliv Transl Res 2019 10;9(5):920-934

Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), No. 30 Gaotanyan, Shapingba, Chongqing, 400038, China.

Myocardial infarction (MI) remains one of the leading cause of mortality over the world. However, current treatments are more palliative than curative, which only stall the progression of the disease, but not reverse the disease. While stem cells or bioactive molecules therapy is promising, the limited survival and engraftment of bioactive agent due to a hostile environment is a bottleneck for MI treatment. In order to maximize the utility of stem cells and bioactive molecules for myocardial repair and regeneration, various types of biomaterials have been developed. Among them, collagen-based biomaterial is widely utilized for cardiac tissue engineering and regeneration due to its optimal physical and chemical properties. In this review, we summarize the properties of collagen-based biomaterial. Then, we discuss collagen-based biomaterial currently being applied to treat MI alone, or together with stem cells and/or bioactive molecules. Finally, the delivery system of collagen-based biomaterial will also be discussed.
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http://dx.doi.org/10.1007/s13346-019-00627-0DOI Listing
October 2019

Transcription factor Tbx18 induces the differentiation of c-kit canine mesenchymal stem cells (cMSCs) into SAN-like pacemaker cells in a co-culture model in vitro.

Am J Transl Res 2018 15;10(8):2511-2528. Epub 2018 Aug 15.

Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University) Chongqing 400038, P.R. China.

Bone mesenchymal stem cells (MSCs), as well as cardiomyocytes, are derived from early mesoderm, becoming committed to their fate under the influence of different differentiation factors. We examined whether the overexpression of Tbx18 can induce the differentiation of c-kit cMSCs into a phenotype similar to that of native pacemaker cells and whether these transfected cells can couple to adjacent atrial cells with functional consequences. The c-kit cMSCs were first sorted, then transfected with different lentiviral vectors. Tbx18-c-kit cMSCs represented the experimental group, while EYFP-c-kit cMSCs and canine sinoatrial node (SAN) cells were used as controls. Within days of transfection, the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel HCN4 protein and gap junction protein Connexin 45 (Cx45) expression in Tbx18-c-kit cMSCs were 12-fold and 5.6-fold higher, respectively, than that in EYFP-c-kit cMSCs. After co-culture with canine atrial cells in vitro for three days, the funny currents (I) were recorded in the Tbx18-c-kit cMSCs, but not in EYFP-c-kit cMSCs. The trend of these I currents was highly similar to that of SAN cells, although the current density was smaller. The Tbx18-EYFP-c-kit cMSCs showed responsiveness to β-adrenergic stimulation, and the intracellular cyclic adenosine monophosphate (cAMP) level was higher than that in EYFP-c-kit cMSCs. The Tbx18-EYFP-c-kit cMSCs delivered fluorescent dye to neighboring atrial cells via gap junctions, thus these cell pairs could communicate as a pacemaker unit. We propose that the overexpression of Tbx18 in c-kit cMSCs induces their differentiation to SAN-like pacemaker cells.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6129520PMC
August 2018

Cold exposure promotes obesity and impairs glucose homeostasis in mice subjected to a high‑fat diet.

Mol Med Rep 2018 Oct 10;18(4):3923-3931. Epub 2018 Aug 10.

Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing 400038, P.R. China.

Cold exposure is considered to be a form of stress and has various adverse effects on the body. The present study aimed to investigate the effects of chronic daily cold exposure on food intake, body weight, serum glucose levels and the central energy balance regulatory pathway in mice fed with a high‑fat diet (HFD). C57BL/6 mice were divided into two groups, which were fed with a standard chow or with a HFD. Half of the mice in each group were exposed to ice‑cold water for 1 h/day for 7 weeks, while the controls were exposed to room temperature. Chronic daily cold exposure significantly increased energy intake, body weight and serum glucose levels in HFD‑fed mice compared with the control group. In addition, 1 h after the final cold exposure, c‑fos immunoreactivity was significantly increased in the central amygdala of HFD‑fed mice compared with HFD‑fed mice without cold exposure, indicating neuronal activation in this brain region. Notably, 61% of these c‑fos neurons co‑expressed the neuropeptide Y (NPY), and the orexigenic peptide levels were significantly increased in the central amygdala of cold‑exposed mice compared with control mice. Notably, cold exposure significantly decreased the anorexigenic brain‑derived neurotropic factor (BDNF) messenger RNA (mRNA) levels in the ventromedial hypothalamic nucleus and increased growth hormone releasing hormone (GHRH) mRNA in the paraventricular nucleus. NPY‑ergic neurons in the central amygdala were activated by chronic cold exposure in mice on HFD via neuronal pathways to decrease BDNF and increase GHRH mRNA expression, possibly contributing to the development of obesity and impairment of glucose homeostasis.
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http://dx.doi.org/10.3892/mmr.2018.9382DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6131648PMC
October 2018

Update on glycerol-3-phosphate acyltransferases: the roles in the development of insulin resistance.

Nutr Diabetes 2018 05 25;8(1):34. Epub 2018 May 25.

Department of Cardiology, Southwest Hospital, Third Military Medical University (Army Medical University), Chongqing, China.

Glycerol-3-phosphate acyltransferase (GPAT) is the rate-limiting enzyme in the de novo pathway of glycerolipid synthesis. It catalyzes the conversion of glycerol-3-phosphate and long-chain acyl-CoA to lysophosphatidic acid. In mammals, four isoforms of GPATs have been identified based on subcellular localization, substrate preferences, and NEM sensitivity, and they have been classified into two groups, one including GPAT1 and GPAT2, which are localized in the mitochondrial outer membrane, and the other including GPAT3 and GPAT4, which are localized in the endoplasmic reticulum membrane. GPATs play a pivotal role in the regulation of triglyceride and phospholipid synthesis. Through gain-of-function and loss-of-function experiments, it has been confirmed that GPATs play a critical role in the development of obesity, hepatic steatosis, and insulin resistance. In line with this, the role of GPATs in metabolism was supported by studies using a GPAT inhibitor, FSG67. Additionally, the functional characteristics of GPATs and the relation between three isoforms (GPAT1, 3, and 4) and insulin resistance has been described in this review.
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http://dx.doi.org/10.1038/s41387-018-0045-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5968029PMC
May 2018

Effects of Neuropeptide Y on Stem Cells and Their Potential Applications in Disease Therapy.

Stem Cells Int 2017 3;2017:6823917. Epub 2017 Oct 3.

Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.

Neuropeptide Y (NPY), a 36-amino acid peptide, is widely distributed in the central and peripheral nervous systems and other peripheral tissues. It takes part in regulating various biological processes including food intake, circadian rhythm, energy metabolism, and neuroendocrine secretion. Increasing evidence indicates that NPY exerts multiple regulatory effects on stem cells. As a kind of primitive and undifferentiated cells, stem cells have the therapeutic potential to replace damaged cells, secret paracrine molecules, promote angiogenesis, and modulate immunity. Stem cell-based therapy has been demonstrated effective and considered as one of the most promising treatments for specific diseases. However, several limitations still hamper its application, such as poor survival and low differentiation and integration rates of transplanted stem cells. The regulatory effects of NPY on stem cell survival, proliferation, and differentiation may be helpful to overcome these limitations and facilitate the application of stem cell-based therapy. In this review, we summarized the regulatory effects of NPY on stem cells and discussed their potential applications in disease therapy.
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http://dx.doi.org/10.1155/2017/6823917DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5646323PMC
October 2017

Supraventricular tachycardia with alternating QRS morphology and cycle length.

Chronic Dis Transl Med 2016 Sep 14;2(3):189-192. Epub 2016 Dec 14.

Southwest Hospital of the Third Military Medical University, Chongqing 400038, China.

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http://dx.doi.org/10.1016/j.cdtm.2016.11.010DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5643769PMC
September 2016

Current views on neuropeptide Y and diabetes-related atherosclerosis.

Diab Vasc Dis Res 2017 07 20;14(4):277-284. Epub 2017 Apr 20.

1 Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.

Diabetes-induced atherosclerotic cardiovascular disease is the leading cause of death of diabetic patients. Neuronal regulation plays a critical role in glucose metabolism and cardiovascular function under physiological and pathological conditions, among which, neurotransmitter neuropeptide Y has been shown to be closely involved in these two processes. Elevated central neuropeptide Y level promotes food intake and reduces energy expenditure, thereby increasing adiposity. Neuropeptide Y is co-localized with noradrenaline in central and sympathetic nervous systems. As a major peripheral vascular contractive neurotransmitter, through interactions with its receptors, neuropeptide Y has been implicated in the pathology and progression of diabetes, by promoting the proliferation of endothelial cells and vascular fibrosis, which may contribute to diabetes-induced cardiovascular disease. Neuropeptide Y also participates in the pathogenesis of atherosclerosis, the major form of cardiovascular disease, via aggravating endothelial dysfunction, growth of vascular smooth muscle cells, formation of foam cells and platelets aggregation. This review highlights the causal role of neuropeptide Y and its receptor system in the development of diabetes mellitus and one of its complications: atherosclerotic cardiovascular disease. The information from this review provides both critical insights onto the mechanisms underlying the pathogenesis of atherosclerosis and evidence for the development of therapeutic strategies.
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http://dx.doi.org/10.1177/1479164117704380DOI Listing
July 2017

The central mechanism of risperidone-induced hyperprolactinemia.

Prog Neuropsychopharmacol Biol Psychiatry 2017 06 20;76:134-139. Epub 2017 Mar 20.

Department of Cardiology, Southwest Hospital, Third Military Medical University, PR China; School of Medicine, Illawarra Health and Medical Research Institute, University of Wollongong, NSW 2522, Australia. Electronic address:

Risperidone is known to increase prolactin secretion in treating mental illness patients. This side-effect is thought to be mediated via central signaling pathway. However, the exact pathway involved between risperidone and hyperprolactinemia are still unknown. Therefore, we have treated mice with risperidone and investigated the central mechanisms. The present study showed that in risperidone treated group, the level of the serum prolactin significantly increased, which was consistent with increased positive prolactin staining in pituitary gland. Elevated c-fos expression was observed in the arcuate hypothalamic nucleus (Arc) where we found 65% c-fos positive neurons co-localised with neuropeptide Y (NPY) in mice treated with risperidone. In addition, the results from in situ hybridization showed that the NPY mRNA in the Arc was significantly increased, whereas the tyrosine hydroxylase (TH) mRNA dramatically decreased compared with control group in the paraventricular hypothalamic nucleus (PVN). These findings revealed that risperidone may mediate the transcriptional regulation of Arc NPY and TH in the PVN. Furthermore, risperidone induced a decreased dopamine synthesis in the PVN and thus reduced the dopamine-induced inhibition of prolactin release, ultimately lead to hyperprolactinemia. Therefore, insights into these neuronal mechanisms open up potential new ways to treat schizophrenia patients in order to ameliorate hyperprolactinemia.
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http://dx.doi.org/10.1016/j.pnpbp.2017.03.009DOI Listing
June 2017

Reduced serum levels of oestradiol and brain derived neurotrophic factor in both diabetic women and HFD-feeding female mice.

Endocrine 2017 Apr 16;56(1):65-72. Epub 2016 Dec 16.

Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, China.

The estrogen levels in the pre and post menstrual phases interact with brain-derived neurotrophic factor in a complex manner, which influences the overall state of the body. To study the role of oestradiol and brain-derived neurotrophic factor in modulating obesity related type 2 diabetes and the interactions between two factors, we enrolled 15 diabetic premenopausal women and 15 diabetic postmenopausal women respectively, the same number of healthy pre and postmenopausal women were recruited as two control groups. The fasting blood glucose, insulin, lipids, estrogen, and brain-derived neurotrophic factor levels were measured through clinical tests. Additionally, we set up obese female mouse model to mimic human trial stated above, to verify the relationship between estrogen and brain-derived neurotrophic factor. Our findings revealed that there is a moderately positive correlation between brain-derived neurotrophic factor and oestradiol in females, and decreased brain-derived neurotrophic factor may worsen impaired insulin function. The results further confirmed that high fat diet-fed mice which exhibited impaired glucose tolerance, showed lower levels of oestradiol and decreased expression of brain-derived neurotrophic factor mRNA in the ventromedial hypothalamus. The level of brain-derived neurotrophic factor reduced on condition that the level of oestradiol is sufficiently low, such as women in postmenopausal period, which aggravates diabetes through feeding-related pathways. Increasing the level of brain-derived neurotrophic factor may help to alleviate the progression of the disease in postmenopausal women with diabetes.
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http://dx.doi.org/10.1007/s12020-016-1197-xDOI Listing
April 2017

Elevated Type II Secretory Phospholipase A2 Increases the Risk of Early Atherosclerosis in Patients with Newly Diagnosed Metabolic Syndrome.

Sci Rep 2016 12 12;6:34929. Epub 2016 Dec 12.

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, 400038, China.

A critical association between type II secretory phospholipase A2 (sPLA2-IIa) and established atherosclerotic cardiovascular disease has been demonstrated. However, the contribution of sPLA2-IIa to early atherosclerosis remains unknown. This study investigated the association between early-stage atherosclerosis and sPLA2-IIa in metabolic syndrome (MetS) patients. One hundred and thirty-six MetS patients and 120 age- and gender-matched subjects without MetS were included. Serum sPLA2-IIa protein levels and activity were measured using commercial kits. Circulating endothelial activation molecules (vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), E-selectin, and P-selectin), and carotid intima-media thickness (cIMT), were measured as parameters of vascular endothelial dysfunction and early atherosclerosis. MetS patients exhibited significantly higher sPLA2-IIa protein and activity levels than the controls. Both correlated positively with fasting blood glucose and waist circumference in MetS patients. Additionally, MetS patients exhibited strikingly higher levels of endothelial activation molecules and increased cIMT than controls. These levels correlated positively with serum sPLA2-IIa protein levels and activity. Moreover, multivariate analysis showed that high sPLA2-IIa protein and activity levels were independent risk factors of early atherosclerosis in MetS patients. This study demonstrates an independent association between early-stage atherosclerosis and increased levels of sPLA2-IIa, implying that increased sPLA2-IIa may predict early-stage atherosclerosis in MetS patients.
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http://dx.doi.org/10.1038/srep34929DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5150250PMC
December 2016

Microbiota prevents cholesterol loss from the body by regulating host gene expression in mice.

Sci Rep 2015 May 27;5:10512. Epub 2015 May 27.

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, 400038, China.

We have previously observed that knockout of Niemann-Pick C1-Like 1 (NPC1L1), a cholesterol transporter essential for intestinal cholesterol absorption, reduces the output of dry stool in mice. As the food intake remains unaltered in NPC1L1-knockout (L1-KO) mice, we hypothesized that NPC1L1 deficiency may alter the gut microbiome to reduce stool output. Consistently, here we demonstrate that the phyla of fecal microbiota differ substantially between L1-KO mice and their wild-type controls. Germ-free (GF) mice have reduced stool output. Inhibition of NPC1L1 by its inhibitor ezetimibe reduces stool output in specific pathogen-free (SPF), but not GF mice. In addition, we show that GF versus SPF mice have reduced intestinal absorption and increased fecal excretion of cholesterol, particularly after treatment with ezetimibe. This negative balance of cholesterol in GF mice is associated with reduced plasma and hepatic cholesterol, and likely caused by reduced expression of NPC1L1 and increased expression of ABCG5 and ABCG8 in small intestine. Expression levels of other genes in intestine and liver largely reflect a state of cholesterol depletion and a decrease in intestinal sensing of bile acids. Altogether, our findings reveal a broad role of microbiota in regulating whole-body cholesterol homeostasis and its response to a cholesterol-lowering drug, ezetimibe.
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http://dx.doi.org/10.1038/srep10512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444975PMC
May 2015

Nifedipine inhibits ox-LDL-induced lipid accumulation in human blood-derived macrophages.

Biochem Biophys Res Commun 2015 Feb 12;457(3):440-4. Epub 2015 Jan 12.

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing 400038, China. Electronic address:

Studies have shown that nifedipine, an anti-hypertensive drug, protects against atherosclerotic progression, but the underlying mechanisms remain elusive. Oxidized low-density lipoprotein (ox-LDL) is critically implicated in macrophage lipid deposition seen in atherosclerosis. In this study, we examined the effects of nifedipine on some ox-LDL-associated changes in human blood-derived macrophages. We isolated monocytes from normal human blood and differentiated them into macrophages. We then treated these human macrophages with ox-LDL and/or nifedipine, and examined lipid accumulation and expression levels of two scavenge receptors CD36 and SR-A as well as a protein kinase PKC-θ. Nifedipine treatment substantially reduced lipid accumulation and the expression of CD36, SR-A, and protein kinase C (PKC)-θ in human macrophages treated with ox-LDL. Silencing of PKC-θ using siRNA also reduced the expression of CD36 and SR-A in these cells. Our results thus suggest that nifedipine may inhibit atherosclerosis by reducing ox-LDL-induced lipid deposition through suppression of the CD36/SR-A-mediated uptake of ox-LDL by macrophages via a PKC-θ-dependent mechanism.
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http://dx.doi.org/10.1016/j.bbrc.2015.01.010DOI Listing
February 2015

Cholesterol efflux is LXRα isoform-dependent in human macrophages.

BMC Cardiovasc Disord 2014 Jul 4;14:80. Epub 2014 Jul 4.

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, China.

Background: The nuclear receptor liver X receptor (LXR) has two isoforms: LXRα and LXRβ. LXR activation promotes cholesterol efflux in macrophages, but the relative importance of each LXR isoform in mediating cholesterol efflux remains elusive.

Methods: We evaluated the ability of different doses of LXRs agonist T0901317 to affect cholesterol efflux in human macrophages and its relationship with mRNA and protein levels of several well-characterized proteins involved in cholesterol efflux, including ABCA1, ABCG1, SR-BI, LXRβ and LXRα, using quantitative real-time PCR, Western blotting, and siRNA techniques.

Results: Here we show that LXRα rather than LXRβ sustains baseline cholesterol efflux in human blood-derived macrophages. Treatment of human macrophages with a non-isoform-specific LXR agonist T0901317 substantially increased HDL- and apoA-I-mediated cholesterol efflux, which was associated with increased mRNA and protein expression levels of ABCA1, ABCG1, SR-BI, LXRα and LXRβ. The siRNA- mediated silencing of LXRα, but not LXRβ significantly reduced the protein levels of ABCA1,ABCG1, and SR-BI as wellas HDL- and ApoA1-mediated cholesterol in human macrophages.

Conclusions: These findings imply that LXRα- rather than LXRβ- specific agonists may promote reverse cholesterol transport in humans.
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http://dx.doi.org/10.1186/1471-2261-14-80DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4107624PMC
July 2014

Clinical efficacy and safety of transcatheter closure of ruptured sinus of valsalva aneurysm.

Catheter Cardiovasc Interv 2014 Dec 6;84(7):1184-9. Epub 2014 Jan 6.

Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, 400038, China.

Objectives: To evaluate the clinical efficacy and safety of transcatheter closure (TCC) in patients with ruptured sinus of Valsalva aneurysm (RSVA).

Background: RSVA is a rare cardiovascular disease with a varied clinical presentation. The clinical efficacy and safety of TCC for RSVA still remain an ongoing concern.

Methods: From January 2009 to March 2013, 22 patients with RSVA were selected for TCC. Intracardiac pressure and size of cardiac chamber were measured before and post TCC. All patients were followed up by transthoracic echocardiography at 1, 3, 6, 12 months after procedure.

Results: RSVA was successfully occluded in 20 patients (19 cases with Amplatzer duct occluder and one with muscular ventricular septal defect occluder). Aortic root angiography showed no shunt in 18 cases and a small residual shunt in two cases. The pressures in the right atrium, right ventricle, and pulmonary artery were significantly decreased after the procedure (P < 0.01), and the aortic pressure was elevated (P < 0.001). The internal diameters of the right atrium, left atrium, and left ventricle were also significantly declined after the procedure (P < 0.05). No complications were found after 18.5 ± 6.5 (range 3-35) months follow-up. Two patients underwent acute surgical aortic valve replacement because of procedure-related aortic valve regurgitation.

Conclusions: Our results indicate that TCC is a promising alternative therapy to surgery in appropriate patients with RSVA. However, rare but severe procedure-related complications should be considered in the risk assessment.
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http://dx.doi.org/10.1002/ccd.25323DOI Listing
December 2014

Relative efficacy of catheter ablation vs antiarrhythmic drugs in treating premature ventricular contractions: a single-center retrospective study.

Heart Rhythm 2014 Feb 22;11(2):187-93. Epub 2013 Oct 22.

Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota. Electronic address:

Background: It is unknown whether radiofrequency ablation (RFA) or antiarrhythmic therapy is superior when treating patients with symptomatic premature ventricular contractions (PVCs).

Objective: To determine the relative efficacy of RFA and antiarrhythmic drugs (AADs) on PVC burden reduction and increasing left ventricular systolic function.

Methods: Patients with frequent PVCs (>1000/24 h) were treated either by RFA or with AADs from January 2005 through December 2010. Data from 24-hour Holter monitoring and echocardiography before and 6-12 months after treatment were compared between the 2 groups.

Results: Of 510 patients identified, 215 (40%) underwent RFA and 295 (60%) received AADs. The reduction in PVC frequency was greater by RFA than with AADs (-21,799/24 h vs -8,376/24 h; P < .001). The left ventricular ejection fraction (LVEF) was increased significantly after RFA (53%-56%; P < .001) but not after AAD (52%- 52%; P = .6) therapy. Of 121 (24%) patients with reduced LVEF, 39 (32%) had LVEF normalization to 50% or greater. LVEF was restored in 25 of 53 (47%) patients in the RFA group compared with 14 of 68 (21%) patients in the AAD group (P = .003). PVC coupling interval less than 450 ms, less impaired left ventricular function, and RFA were independent predictors of LVEF normalization performed by using multivariate analysis.

Conclusion: RFA appears to be more effective than AADs in PVC reduction and LVEF normalization.
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http://dx.doi.org/10.1016/j.hrthm.2013.10.033DOI Listing
February 2014

TNFa alter cholesterol metabolism in human macrophages via PKC-θ-dependent pathway.

BMC Biochem 2013 Aug 3;14:20. Epub 2013 Aug 3.

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, China.

Background: Studies have shown that inflammation promoted atherosclerotic progression; however, it remains unclear whether inflammation promoted atherosclerotic progression properties by altering cholesterol metabolism in human macrophages. In the present study, we evaluated a potential mechanism of inflammation on atherogenic effects. We evaluated the ability of TNFa to affect Reverse cholesterol transport (RCT) and cholesterol uptake and its mechanism(s) of action in human macrophages.

Results: We initially determined the potential effects of TNFa on cholesterol efflux in the human macrophages. We also determined alterations in mRNA and protein levels of ABCA1, ABCG1, LXRa, CD-36, SR-A in human macrophages using quantitative real-time polymerase chain reaction (PCR) and Western immunoblot analyses. The cholesterol efflux rate and protein expression of ABCA1, ABCG1, LXRa, CD-36, SR-A were quantified in human macrophages under PKC-θ inhibition using PKC-θ siRNA. Our results showed that TNFa inhibited the rate of cholesterol efflux and down-regulation the expression levels of ABCA1, ABCG1 and LXRa and up-regulation the expression levels of CD-36, SR-A in human macrophages; PKC-θ inhibition by PKC-θ siRNA attenuated the effect of TNFa on ABCA1, ABCG1, LXRa, SR-A, CD-36 expression.

Conclusions: Our results suggest TNFa alter cholesterol metabolism in human macrophages through the inhibition of Reverse cholesterol transport and enhancing cholesterol uptake via PKC-θ-dependent pathway, implicating a potential mechanism of inflammation on atherogenic effects.
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http://dx.doi.org/10.1186/1471-2091-14-20DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751201PMC
August 2013

Nifedipine enhances cholesterol efflux in RAW264.7 macrophages.

Cardiovasc Drugs Ther 2013 Oct;27(5):425-31

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, China.

Purpose: Studies have shown that nifedipine protects against atherosclerotic progression, but its underlying mechanisms remain unclear. In this study, we examined if nifedipine increases macrophage cholesterol efflux, a pathway known to inhibit atherogenesis.

Methods: We evaluated the ability of different doses of nifedipine to affect cholesterol efflux in RAW264.7 macrophages and its relationship with mRNA and protein levels of several well-characterized proteins involved in cholesterol efflux, including ABCA1, ABCG1, SR-BI and LXRα, using quantitative real-time PCR, Western blotting, and siRNA techniques.

Results: Nifedipne at 1, 10, and 100 nmol/L increased apoA-I-mediated cholesterol efflux from 2.55 % to 5.65 %, 6.20 %, and 6.10 %, as well as HDL-mediated cholesterol efflux from 31.0 % to 42.5 %, 46.0 %, and 43.5 %, respectively, in RAW264.7 macrophages (p < 0.05), which was associated with increased mRNA expression levels of ABCA1, ABCG1, SR-BI, and LXRα (405 %, 381 %, 336 %; 890 %, 960 %, 1002 %; 285 %, 325 %, 336 %; 482 %, 445 %, 405 %, respectively, p < 0.05), and with increased protein levels of ABCA1, ABCG1, SR-BI, and LXRα (428 %, 492 %, 361 %; 288 %, 331 %, 365 %; 283 %, 320 %, 505 %; 581 %, 678 %, 608 %, respectively, p < 0.05). SiRNA-mediated silencing of LXRα revealed that LXRα was involved in these increases and the enhanced cholesterol efflux.

Conclusion: Nifedipine may protect against atherosclerosis partly by promoting macrophage cholesterol efflux through the stimulation of LXRα-dependent expression of ABCA1, ABCG1, and SR-BI.
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http://dx.doi.org/10.1007/s10557-013-6472-yDOI Listing
October 2013

Glycemic load, glycemic index and risk of cardiovascular diseases: meta-analyses of prospective studies.

Atherosclerosis 2012 Aug 6;223(2):491-6. Epub 2012 Jun 6.

Department of Cardiology, Southwest Hospital, Third Military Medical University, Gaotanyan Street 30, Chongqing 400038, China.

Objective: The objective of this study was to assess the relations between glycemic load (GL), glycemic index (GI) and the risk of fatal or nonfatal cardiovascular diseases (CVDs).

Methods: Prospective studies were identified by a comprehensive search of Pubmed, ISI web of Science, the Cochrane Library and EMBASE database, supplemented with manual searches through the reference lists of original publications and review articles. Relative risks (RRs) and 95% confidence intervals (CIs) were extracted and pooled using a random-effect model, and dose-response meta-analysis was performed by the method of generalized least-squares.

Results: Fourteen studies were identified, involving 229,213 participants and more than 11,363 cases. The pooled RRs of CVDs risk for the highest vs lowest categories of GL and GI were 1.23 (95% CI: 1.11-1.36) and 1.13 (95% CI: 1.04-1.22) respectively. Both the risk estimates of GL and GI for women (GL: RR = 1.35, 95% CI: 1.18-1.55; GI: RR = 1.19, 95% CI: 1.06-1.34) were higher than men (GL: RR = 1.10, 95% CI: 0.95-1.28; GI: RR = 1.05, 95% CI: 0.94-1.17). No heterogeneity or publication bias was detected. Dose-response meta-analysis found an increased RR of 1.18 (95% CI: 1.01-1.38, P = 0.033) per 50 unit increment of GL with cardiac event risk in Caucasians.

Conclusions: High GL and GI were associated with significant increased risk of CVDs, specifically for women.
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http://dx.doi.org/10.1016/j.atherosclerosis.2012.05.028DOI Listing
August 2012

Associations of the ATP-binding cassette transporter A1 R219K polymorphism with HDL-C level and coronary artery disease risk: a meta-analysis.

Atherosclerosis 2011 Apr 21;215(2):428-34. Epub 2011 Jan 21.

Department of Cardiology, Southwest Hospital, Third Military Medical University, Gaotanyan Street 30, Chongqing 400038, China.

Objective: Previous studies have evaluated the associations of the ATP-binding cassette transporter A1 (ABCA1) R219K polymorphism (rs2230806) with the level of high-density lipoprotein cholesterol (HDL-C) and the risk of developing coronary artery disease (CAD), but results from many small, underpowered studies are conflicting. The objective of this study was to overcome the limitations of individual study and provide solid epidemiologic evidence.

Methods: We conducted a systematic review and meta-analysis of available studies to clarify the associations of the ABCA1 R219K polymorphism with HDL-C level and CAD risk.

Results: Through retrieving PubMed, Embase, Web of Science, CBM and CNKI, we identified a total of 22 studies with 6597 cases and 15,369 controls for the association between the ABCA1 R219K polymorphism and CAD risk. The carriers of allele 219K were found to have a lower risk of CAD than the non-carriers: OR=0.76, 95% CI=0.68-0.85, P=3.78E-07, P(heterogeneity)=3.59E-08; meanwhile, 18 studies from 17 papers with 12,869 subjects were included in the association between the ABCA1 R219K polymorphism and the level of HDL-C. It was suggested that the carriers of KK genotype had higher level of HDL-C than those of RR genotype: SMD=0.19, 95% CI=0.06-0.32, P=0.005, P(heterogeneity)=3.19E-09. Subgroup analyzes by ethnicity certified that the effect on HDL level was just significant in Asians. Exclusion of the outlier studies effectively removed the heterogeneity and confirmed the total results. No publication bias was detected in this meta-analysis.

Conclusions: The synthesis of available evidence demonstrates that the ABCA1 R219K polymorphism is associated with a higher HDL-C level in Asians and a protective role for CAD risk both in Asians and Caucasians.
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http://dx.doi.org/10.1016/j.atherosclerosis.2011.01.008DOI Listing
April 2011

[Brief history of percutaneous coronary intervention].

Zhonghua Yi Shi Za Zhi 2010 May;40(3):180-3

Department of Cardiology, Cangzhou Center Hospital, Cangzhou 061001, China.

Percutaneous coronary intervention (PCI) is that delivering balloon catheter and/or equipment such as a stent to the target coronary artery bypass peripheral artery, at the same time, expanding and opening the stenosis of coronary artery. Through several decades of development, PCI has become a most effective way to rescue patients with coronary heart disease and become one of the biggest advances in the field of heart disease. Because of the development of PCI, more lives have been saved in patients with coronary heart disease. However, PCI does not meet the point of perfection, still has a lot of issues remain to be further resolved. Through a review the development of PCI, we may be able to get some insights to perfect the treatment technique for the patients of coronary heart disease.
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May 2010

[Prognostic impact of heart block during transcatheter closure of ventricular septal defect].

Zhonghua Xin Xue Guan Bing Za Zhi 2009 Nov;37(11):990-3

Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing 400038, China.

Objective: To investigate the prognostic impact of heart block during the transcatheter closure of ventricular septal defect (VSD).

Methods: Forty three patients developed complete left or right bundle branch block (CLBBB, CRBBB), incomplete left or right bundle branch block (ILBBB, IRBBB), and atrioventricular block (AVB) during and within 1 week post procedure were followuped at 1, 6, 12, 24, 36, 48 and 60 months post procedure. Electrocardiogram, dynamic electrocardiogram and transthoracic echocardiography were made.

Results: Bundle branch block and atrioventricular block were detected in 26 patients (CLBBB n = 4, CRBBB n = 5, ILBBB n = 2, IRBBB n = 10 and third-degree AVB n = 5) during the transcatheter closure of VSD, and in 17 patients (CLBBB n = 5, CRBBB n = 2, first-degree AVB n = 3, second-degree I-type AVB n = 1 and third-degree AVB n = 6) within 1 week post procedure. Heart block disappeared in 33 patients (76.7%) before discharge, in 37 patients (86.1%) at 1 month and in 41 patients (95.4%) at 6 months post procedure. CLBBB or CRBBB was seen in two cases at 24 months after closure. There was no heart failure and serious cardiac dilatation during follow up.

Conclusion: The heart block occurred during the periprocedure period of transcatheter closure of VSD was a benign phenomenon without prognostic importance.
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November 2009

Clinical efficiency and safety analysis of transcatheter closure of multiple atrial septal defects in adults.

Clin Cardiol 2009 Mar;32(3):130-4

Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing, People's Republic of China.

Background: Transcatheter closure of atrial septal defects (ASDs) is currently a reliable alternative to surgery, even though challenging in patients with multiple ASDs.

Hypothesis: The aim of this study was to evaluate the clinical efficiency and safety of transcatheter closure in multiple ASDs.

Methods: Multiple ASDs were diagnosed by transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE). The occlusive condition and distance between 2 adjacent ASDs were measured by TTE examination. Then, the number and size of the occluder(s) was determined. TTE examinations were performed after transcatheter closure as follow-up.

Results: The transcatheter procedure was successful in 15 patients with multiple ASDs, using a single occluder in 9 patients and 2 occluders in the remaining 6 patients. Overall, 21 ASD occluders were implanted. During a follow-up period of 6 mo to 5 y, a slight residual shunt was found in 1 patient without any symptoms; a moderate residual shunt was identified at the inferior vena cava and the occluder was removed by surgery 1 mo after procedure. Other complications, including endocarditis, arrhythmia, thromboembolism, and atrioventricular valve damage were not recorded in any of the 15 patients during the follow-up period.

Conclusion: Transcatheter closure of multiple ASDs is safe and efficient. Two occluders are necessary for the distance of 2 ASDs more than 7 mm, and a single occluder is sufficient for those 7 mm or less.
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http://dx.doi.org/10.1002/clc.20450DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6653734PMC
March 2009

Relationship among soluble CD105, hypersensitive C-reactive protein and coronary plaque morphology: an intravascular ultrasound study.

Chin Med J (Engl) 2008 Jan;121(2):128-32

Department of Cardiology, Anzhen Hospital Affiliated to Capital Medical University, Beijing 100029, China.

Background: Rupture of unstable plaque with subsequent thrombus formation is the common pathophysiological substrate of acute coronary syndrome (ACS). It is of potential significance to explore the blood indexes predicting plaque characteristics. We investigated the relationship among soluble CD105, hypersensitive C-reactive protein (hs-CRP), and coronary plaque morphology.

Methods: A clinical study from April 2004 to December 2006 was conducted in 130 patients who were divided into 3 groups: 56 patients (43.1%) in stable angina (SA) group, 52 patients (40.0%) in unstable angina (UA) group and 22 patients (16.9%) in acute myocardial infarction group. The concentrations of soluble CD105 and hs-CRP were measured in all of the patients by cardioangiography (CAG). Plasma samples of arterial blood were collected prior to the procedure. The levels of soluble CD105 and hs-CRP were measured by enzyme-linked immunosorbent assay (ELISA).

Results: Unstable and ruptured plaque was found more frequently in patients with acute myocardial infarction and UA. External elastic membrane cross-sectional area (EEM CSA), plaque area, lipid pool area and plaque burden were significantly larger in the ruptured and unstable plaque group. Positive remodeling, thinner fabric-cap, smaller minimal lumen cross-sectional area (MLA), dissection and thrombus were significantly more frequent in the ruptured and unstable plaque group. Remodeling index (RI) was positively correlated with the levels of soluble CD105 in the UA group (r = 0.628, P < 0.01) and the acute myocardial infarction group (r = 0.639, P < 0.01). The levels of soluble CD105 and hs-CRP were higher in the ruptured plaque group. Soluble CD105 > 4.3 ng/ml was used to predict ruptured plaque with a receiver operating characteristic (ROC) curve area of 0.77 (95% confidence interval (CI), 66.8% - 87.2%), a sensitivity of 72.8%, a specificity of 78.0% and an accuracy of 70.2% (P < 0.01), similarly for hs-CRP > 5.0 mg/ml with a ROC curve area of 0.70 (95% CI, 59.2% - 80.2%), a sensitivity of 70.2%, a specificity of 76.2% and an accuracy of 67.2% (P < 0.01).

Conclusions: The plaque characteristics correlate with the clinical presentation. The elevation of soluble CD105 and hs-CRP is related to the plaque instability and rupture.
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January 2008

Clinical efficiency and safety analysis of transcatheter interventional therapy for compound congenital cardiovascular abnormalities.

Clin Cardiol 2007 Oct;30(10):518-21

Department of Cardiology, Southwest Hospital, The Third Military Medical University, Chongqing, China.

Objective: To investigate the efficiency and safety of transcatheter interventional therapy for compound congenital cardiovascular abnormalities.

Methods: From Nov 2001 to Jun 2006, a total of 36 patients (17 male, 19 female), aged 17.20 +/- 10.52, with compound congenital cardiovascular abnormalities underwent transcatheter interventional procedure. These patients included 11 with perimembranous ventricular septal defect (PVSD) and patent ductus arteriosus (PDA), 8 patients with PVSD and atrial septal defect (ASD), 8 patients with ASD and PDA, 7 patients with ASD and pulmonary stenosis (PS), 1 patient with ASD and mitral stenosis(MS), 1 patient with coarctation of aorta (COA) and PDA. According to the principle of "easy first, hard second," balloon valvuloplasties of PS or MS were performed before the closure of PVSD, and of PDA and ASD. Electrocardiogram and transthoracic echocardiogram were examined at 4 days, 1, 2, 6 and 12 months, respectively, after each procedure.

Results: Transcatheter interventional therapy for compound congenital cardiovascular abnormalities was successful in all patients. Among these, 2 occluders were planted in each of 27 patients, 7 patients with ASD combined with PS and 1 patient with ASD combined with MS underwent successfully performed balloon valvuloplasty and ASD closure, 1 patient with COA combined with PDA underwent successfully performed balloon valvuloplasty and subsequent covered stent implantation. No patient encountered serious adverse events during the (30.5 +/- 14.6) months of follow-up.

Conclusions: Transcatheter interventional therapy for compound congenital cardiovascular abnormalities could obtain satisfactory results with technical feasibility.
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http://dx.doi.org/10.1002/clc.20149DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6653647PMC
October 2007

Relationship between intravascular ultrasound imaging features of coronary plaques and soluble CD105 level in patients with coronary heart disease.

Chin Med J (Engl) 2007 Apr;120(7):595-7

Department of Cardiology, Anzhen Hospital Affiliated to Capital Medical University, Beijing 100029, China.

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April 2007