Publications by authors named "Chengzhi Lu"

44 Publications

Corrigendum: Galectin-3 inhibition attenuates doxorubicin-induced cardiac dysfunction by upregulating the expression of peroxiredoxin-4.

Can J Physiol Pharmacol 2021 Mar 9;99(3):348. Epub 2021 Mar 9.

Department of Cardiology, Tongji Hospital of Tongji University, Shanghai 200003, People's Republic of China.

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http://dx.doi.org/10.1139/cjpp-2020-0752DOI Listing
March 2021

Study on Optimal Parameter and Target for Pulsed-Field Ablation of Atrial Fibrillation.

Front Cardiovasc Med 2021 21;8:690092. Epub 2021 Sep 21.

Tianjin Intelligent Health Medical Co., Ltd, Tianjin, China.

Pulsed-field ablation (PFA) had potential advantages in atrial fibrillation ablation, and we aim to confirm the optimal parameter and target of PFA for atrial fibrillation. Two ablation modes of single-cell system (ablation in electrode cup) and monolayer cell system (ablation in inserts with electrode tips) were established to perform PFA for myocardial cell H9C2 and smooth muscle cell A7r5. Ablation effect, calcium ion influx, the expression of Cx45, and surface morphological change were observed. Three Bama minipigs were used to verify the ablation effect of PFA. In monolayer cell system, H9C2 was significantly sensitive to PFA compared with A7r5, with shrinking of the whole monolayer. The ablation effect of bidirectional pulse was weaker than that of the two mono-polar pulses. Expressed Cx45 proteins were increased in H9C2 but decreased in A7r5 cells. Bidirectional PFA performed on Bama minipigs was able to effectively block electrical activity from the pulmonary vein to the atrium with week muscle contraction, not generating pulmonary vein stenosis. Bidirectional PFA was able to significantly ablate myocardial cells, maintain cell-cell connection, and reduce muscle contraction, which was a kind of optimized PFA strategy for atrial fibrillation.
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http://dx.doi.org/10.3389/fcvm.2021.690092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8490619PMC
September 2021

Efficacy and safety of soluble guanylate cyclase stimulators in patients with heart failure: A systematic review and meta-analysis.

Pharmazie 2021 Oct;76(10):488-493

School of Medicine, Nankai University, Tianjin, China; Department of Cardiology, Tianjin First Center Hospital, Tianjin, China;, Email:

To evaluate the efficacy and safety of soluble guanylate cyclase (sGC) stimulators in patients with heart failure (HF). : A systematic literature search from several electronic databases (Web of Science, PubMed, Embase, Medline) was performed up until March 2021. Eligible studies included randomized controlled trials (RCTs) that compared sGC stimulators treatment with placebo. Data extracted from eligible RCTs were pooled using relative risk (RR) and weight mean difference (WMD) on random effect model or fixed effect model. : A total of eight RCTs involving 7225 patients met the inclusion criteria. For the efficacy endpoint, sGC stimulators significantly reduced HF-related hospitalization or cardiovascular (CV) death (RR = 0.92, 95%CI: 0.86-0.99; = 0.03), but no relationship was found for 6-minute walking distance (6MWD) (SMD = 0.04, 95%CI: -0.09-0.17; = 0.55). In addition, compared to control group, the change of NT-proBNP was statistically decreased in the riociguat group (SMD = -0.78, 95%CI: -1.09--0.47; < 0.00), yet not in vericiguat group (SMD = 0.05, 95%CI: -0.19-0.28; = 0.70). For the safety endpoint, there was no significant difference in all-cause mortality (RR = 0.98 95%CI: 0.88-1.09; = 0.69) and serious adverse events (RR = 0.95, 95%CI: 0.892-1.02; = 0.16) between SGC stimulants group and control group. : The oral therapy with sGC stimulators including vericiguat and riociguat decreases the incidence of HF-related hospitalization or CV death with good tolerability and safety. The study did not support improvement in many parameters including 6MWD and NT-proBNP in HF patients.
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http://dx.doi.org/10.1691/ph.2021.1599DOI Listing
October 2021

Targeting mitochondria-inflammation circle by renal denervation reduces atheroprone endothelial phenotypes and atherosclerosis.

Redox Biol 2021 Sep 29;47:102156. Epub 2021 Sep 29.

School of Medicine, Nankai University, Tianjin, 300071, China; Department of Cardiology, Tianjin First Center Hospital, Tianjin, 300192, China. Electronic address:

Objective: The disruption of mitochondrial redox homeostasis in endothelial cells (ECs) can cause chronic inflammation, a substantial contributor to the development of atherosclerosis. Chronic sympathetic hyperactivity can enhance oxidative stress to induce endothelial dysfunction. We determined if renal denervation (RDN), the strategy reducing sympathetic tone, can protect ECs by ameliorating mitochondrial reactive oxygen species (ROS)-induced inflammation to reduce atherosclerosis.

Methods And Results: ApoE deficient (ApoE) mice were conducted RDN or sham operation before 20-week high-fat diet feeding. Atherosclerosis, EC phenotype and mitochondrial morphology were determined. In vitro, human arterial ECs were treated with norepinephrine to determine the mechanisms for RDN-inhibited endothelial inflammation. RDN reduced atherosclerosis, EC mitochondrial oxidative stress and inflammation. Mechanistically, the chronic sympathetic hyperactivity increased circulating norepinephrine and mitochondrial monoamine oxidase A (MAO-A) activity. MAO-A activation-impaired mitochondrial homeostasis resulted in ROS accumulation and NF-κB activation, thereby enhancing expression of atherogenic and proinflammatory molecules in ECs. It also suppressed mitochondrial function regulator PGC-1α, with involvement of NF-κB and oxidative stress. Inactivation of MAO-A by RDN disrupted the positive-feedback regulation between mitochondrial dysfunction and inflammation, thereby inhibiting EC atheroprone phenotypic alterations and atherosclerosis.

Conclusions: The interplay between MAO-A-induced mitochondrial oxidative stress and inflammation in ECs is a key driver in atherogenesis, and it can be reduced by RDN.
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http://dx.doi.org/10.1016/j.redox.2021.102156DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8498003PMC
September 2021

Colchicine-Containing Nanoparticles Attenuates Acute Myocardial Infarction Injury by Inhibiting Inflammation.

Cardiovasc Drugs Ther 2021 Aug 26. Epub 2021 Aug 26.

Key Laboratory of Bioactive Materials, Ministry of Education, College of Life Sciences, Nankai University, Tianjin, 300071, China.

Purpose: Anti-inflammatory therapy is important for reducing myocardial injury after acute myocardial infarction (MI). New anti-inflammatory drugs and their mechanism are necessary to be explored to improve clinical efficacy. We aimed to improve the efficacy of colchicine on attenuating MI injury by nano-drug delivery systems and to investigate the mechanism of anti-inflammatory.

Methods: A colchicine-containing delivery system based on calcium carbonate nanoparticles (ColCaNPs) was synthesized. The protection against MI by ColCaNPs was evaluated using an in vivo rat model established by ligating the left anterior descending coronary artery. Macrophage polarization and the levels of inflammatory cytokines were determined using immunohistochemistry, Western blot, and ELISA analysis.

Results: ColCaNP treatment showed about a 45% reduction in myocardial infarct size and attenuating myocardial fibrosis compared with groups without drug intervention after MI. Furthermore, ColCaNPs significantly decreased the levels of CRP, TNF-α, and IL-1β in serum and the expression of proinflammatory cytokine in myocardial tissues after MI (p < 0.05). We also found that ColCaNPs notably restrained pyroptosis and inhibited inflammatory response by modulating on M1/M2 macrophage polarization and suppressing TLR4/NFκB/NLRP3 signal pathway.

Conclusion: Colchicine-containing nanoparticles can protect against MI injury in a clinically relevant rat model by reducing inflammation. In addition, calcium carbonate nanoparticles can increase the cardioprotective effects of colchicine.
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http://dx.doi.org/10.1007/s10557-021-07239-2DOI Listing
August 2021

Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction.

Front Physiol 2021 3;12:717187. Epub 2021 Aug 3.

Department of Cardiology, Tianjin First Central Hospital, Tianjin, China.

Myocardial infarction is characterized by cardiomyocyte death, and can be exacerbated by mitochondrial damage and endoplasmic reticulum injury. In the present study, we investigated whether communication between mitochondria and the endoplasmic reticulum contributes to cardiomyocyte death after myocardial infarction. Our data demonstrated that hypoxia treatment (mimicking myocardial infarction) promoted cardiomyocyte death by inducing the c-Jun N-terminal kinase (JNK) pathway. The activation of JNK under hypoxic conditions was dependent on overproduction of mitochondrial reactive oxygen species (mtROS) in cardiomyocytes, and mitochondrial division was identified as the upstream inducer of mtROS overproduction. Silencing mitochondrial division activators, such as B cell receptor associated protein 31 () and mitochondrial fission 1 (), repressed mitochondrial division, thereby inhibiting mtROS overproduction and preventing JNK-induced cardiomyocyte death under hypoxic conditions. These data revealed that a novel death-inducing mechanism involving the BAP31/Fis1/mtROS/JNK axis promotes hypoxia-induced cardiomyocyte damage. Considering that BAP31 is localized within the endoplasmic reticulum and Fis1 is localized in mitochondria, abnormal mitochondria-endoplasmic reticulum communication may be a useful therapeutic target after myocardial infarction.
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http://dx.doi.org/10.3389/fphys.2021.717187DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369510PMC
August 2021

Study of SARS-CoV-2 transmission in urban environment by questionnaire and modeling for sustainable risk control.

J Hazard Mater 2021 10 10;420:126621. Epub 2021 Jul 10.

Department of Cardiology, Tianjin First Central Hospital, Tianjin 300190, PR China.

Caused by SARS-CoV-2, COVID-19 has become a severe threaten to society and human health, its epidemic control emerges as long-term issue. A sustainable epidemic and environmental transmission risk control (SEERC) in urban area is urgently needed. This work aims to conduct a new investigation on the transmission risk of SARS-COV-2 as virus/hazardous material through various environmental medias, routes and regions in the entirely urban area for guiding the SEERC. Specifically, 5 routes in 28 regions (totally 140 scenarios) are considered. For a new perspective, the risk evaluation is conducted by the quantification of frontline medicals staffs' valuable experience in this work. 207 specialists responsible for the treatment of over 9000 infected patients are involved. The result showed that degree of risk was in the order of breath>contact-to-object>contact-to-human>intake>unknown. The modeling suggested source control as the prior measure for epidemic control. The combination of source control & mask wearing showed high efficiency in SEERC. The homeworking policy needed to cooperate with activity limitation to perform its efficiency. Subsequently, a new plan for SEERC was discussed. This work delivered significant information to researchers and decision makers for the further development of sustainable control for SARS-COV-2 spreading and COVID-19 epidemic.
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http://dx.doi.org/10.1016/j.jhazmat.2021.126621DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8270745PMC
October 2021

PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β signaling pathway in mice model.

J Renin Angiotensin Aldosterone Syst 2021 Jan-Dec;22(1):14703203211003786

First Center Clinic College of Tianjin Medical University, Tianjin First Center Hospital, Tianjin, China.

Objects: To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.

Methods: PM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β was examined by Western Blotting (WB) and Real time PCR (RT-PCR).

Results: The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β was increased in higher dose groups in protein and mRNA level.

Conclusion: 1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.
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http://dx.doi.org/10.1177/14703203211003786DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7983242PMC
March 2021

Involvement of non‑coding RNAs in the pathogenesis of myocardial ischemia/reperfusion injury (Review).

Int J Mol Med 2021 04 12;47(4). Epub 2021 Feb 12.

School of Medicine, Nankai University, Tianjin 300071, P.R. China.

Myocardial ischemia/reperfusion injury (MIRI) may cause myocardial stunning, reperfusion arrhythmia, no‑reflow phenomenon and lethal reperfusion injury, which has a significant effect on the prognosis of patients undergoing thrombolytic agent therapy and percutaneous coronary intervention. Increasing evidence suggests that apoptosis, innate inflammation, oxidative stress, calcium overload and autophagy are involved in the pathogenesis of MIRI. Recent advancements in RNA sequencing technologies and genome‑wide analyses led to the finding of small non‑coding RNAs (ncRNAs). ncRNAs modulate cellular processes such as signal transduction, transcription, chromatin remodeling and post‑transcriptional modification. The effects of ncRNAs on cellular biology is more considerable than initially expected, and thus ncRNAs have gained increasing attention and focus in modern medical research. There are several types of ncRNAs, such as microRNAs (miRNAs), long non‑coding RNAs (lncRNAs) and circular RNAs (circRNAs), which have been shown to regulate gene expression at the transcription, post‑transcription and epigenetic levels. Dysregulation of ncRNAs, including miRNAs, lncRNAs and circRNAs, may participate in the molecular mechanisms of MIRI. The present review summarizes the characteristics and biological roles of miRNAs, lncRNAs and circRNAs, with particular emphasis on their role in MIRI, which show the novel complexity of ischemic hearts and may offer valuable insights into the pathogenesis of MIRI.
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http://dx.doi.org/10.3892/ijmm.2021.4875DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7895537PMC
April 2021

Oxidized LDL Causes Endothelial Apoptosis by Inhibiting Mitochondrial Fusion and Mitochondria Autophagy.

Front Cell Dev Biol 2020 11;8:600950. Epub 2020 Nov 11.

Department of Cardiology, Tianjin First Center Hospital, Tianjin, China.

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction is an initial step toward atherosclerosis development. Mitochondria damage correlates with ox-LDL-induced endothelial injury through an undefined mechanism. We explored the role of optic atrophy 1 (Opa1)-related mitochondrial fusion and mitophagy in ox-LDL-treated endothelial cells, focusing on mitochondrial damage and cell apoptosis. Oxidized low-density lipoprotein treatment reduced endothelial cell viability by increasing apoptosis. Endothelial cell proliferation and migration were also impaired by ox-LDL. At the molecular level, mitochondrial dysfunction was induced by ox-LDL, as demonstrated by decreased mitochondrial membrane potential, increased mitochondrial reactive oxygen species production, augmented mitochondrial permeability transition pore openings, and elevated caspase-3/9 activity. Mitophagy and mitochondrial fusion were also impaired by ox-LDL. Opa1 overexpression reversed this effect by increasing endothelial cell viability and decreasing apoptosis. Interestingly, inhibition of mitophagy or mitochondrial fusion through transfection of siRNAs against Atg5 or Mfn2, respectively, abolished the protective effects of Opa1. Our results illustrate the role of Opa1-related mitochondrial fusion and mitophagy in sustaining endothelial cell viability and mitochondrial homeostasis under ox-LDL stress.
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http://dx.doi.org/10.3389/fcell.2020.600950DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7686653PMC
November 2020

Oxidized LDL Disrupts Metabolism and Inhibits Macrophage Survival by Activating a miR-9/Drp1/Mitochondrial Fission Signaling Pathway.

Oxid Med Cell Longev 2020 1;2020:8848930. Epub 2020 Nov 1.

Department of Cardiology, Tianjin First Center Hospital, Tianjin, China.

Mitochondrial dysfunction is associated with macrophage damage, but the role of mitochondrial fission in macrophage cholesterol metabolism is not fully understood. In this study, we explored the influences of miR-9 and mitochondrial fission on macrophage viability and cholesterol metabolism. Macrophages were incubated with oxidized low-density lipoprotein (ox-LDL) , after which mitochondrial fission, cell viability, and cholesterol metabolism were examined using qPCR, ELISAs, and immunofluorescence. ox-LDL treatment significantly increased Drp1-associated mitochondrial fission. Transfection of Drp1 siRNA significantly reduced cell death, attenuated oxidative stress, and inhibited inflammatory responses in ox-LDL-treated macrophages. Interestingly, inhibition of Drp1-related mitochondrial fission also improved cholesterol metabolism by balancing the transcription of cholesterol influx/efflux enzymes. We also found that miR-9 was downregulated in ox-LDL-treated macrophages, and administration of a miR-9 mimic decreased Drp1 transcription and mitochondrial fission, as well as its effects. These results indicate that signaling via the novel miR-9/Drp1/mitochondrial fission axis is a key determinant of macrophage viability and cholesterol metabolism.
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http://dx.doi.org/10.1155/2020/8848930DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7655251PMC
June 2021

Effect of Renal Denervation on Cardiac Function and Inflammatory Factors in Heart Failure After Myocardial Infarction.

J Cardiovasc Pharmacol 2020 11;76(5):602-609

Department of Cardiology, Tianjin First Central Hospital, Tianjin, China.

Heart failure (HF) affects around 100 million people and is a staggering burden for health care system worldwide. Rapid and sustained activation of inflammatory response is an important feature of HF after myocardial infarction. Sympathetic overactivation is also an important factor in the occurrence and progression of HF. The beneficial effect of renal denervation (RDN) has been demonstrated in HF. In the current study, we hypothesized that RDN improves cardiac function in HF canine models due to acute myocardial infarction (AMI) and reduced inflammation might be involved. Twenty-four beagles were randomized into the control (n = 8), HF (n = 8), and HF + RDN group (n = 8). The HF model after AMI was established by embolization the anterior descending distal artery with anhydrous ethanol in the HF and HF + RDN group. Bilateral renal artery ablation was performed in the HF + RDN group. Cardiac function, serum creatine kinase, creatine kinase-MB and NT-Pro BNP level, and expression of inflammation-related proteins in myocardial were examined. Because the paraventricular nucleus of the hypothalamus might be involved in inflammation-induced central neural excitation in HF and plays an important role in regulating extracellular fluid volume and sympathetic activity, expression of inflammation-related proteins in hypothalamus was also examined. AMI and post-AMI HF model was created successfully. Compared with the HF group, dogs in the HF + RDN group showed better cardiac function 4 weeks after AMI: lower left ventricular end-diastolic pressure, left ventricular end-diastolic dimension, and left ventricular end-systolic dimension and higher LEVF and left ventricular systolic pressure (P < 0.05 for all) were observed in the HF + RDN group. In addition, dogs in the HF + RDN group had slightly less ventricular fibrosis. Interestingly, RDN had lower expression of inflammation-related proteins including interleukin-6, tumor necrosis factors-α, nuclear factor κB, and monocyte chemotactic protein 1 (P < 0.05 for all) in both myocardial tissue and hypothalamus. RDN can improve cardiac function in dogs with HF after myocardial infarction. Our results suggested that RDN might affect cytokine-induced central neural excitation in HF and later affect sympathetic activity. Our results suggested a potential beneficial mechanism of RDN independent of mechanism involving renal afferent and efferent sympathetic nerves.
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http://dx.doi.org/10.1097/FJC.0000000000000899DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7641177PMC
November 2020

The relationship between serum uric acid and cognitive function in patients with chronic heart failure.

BMC Cardiovasc Disord 2020 08 20;20(1):381. Epub 2020 Aug 20.

Department of Cardiology, Tianjin First Central Hospital, No 24 Fukang Road, Nankai District, Tianjin, 300192, China.

Background: Evidence has shown that serum uric acid (UA) is associated with cognitive function, but this finding remains debatable. Serum UA is commonly elevated in patients with chronic heart failure (CHF), especially in men. However, the relationship between serum UA and cognitive function in CHF populations and stratified by sex are unclear. We aimed to examine whether serum UA was independently associated with cognitive function in CHF populations after controlling for demographic, medical and psychological variables and whether there was a sex difference in the association between serum UA and cognitive function among male and female CHF patients.

Methods: One hundred ninety-two hospitalized patients with CHF underwent an assessment of cognitive function using the Montreal Cognitive Assessment (MoCA) and the determination of serum UA. Hyperuricemia was defined as serum UA ≥7 mg/dl in men and ≥ 6 mg/dl in women. Multiple linear hierarchical regression analyses were conducted to examine the independent association between serum UA and cognitive function in CHF populations and stratified by sex.

Results: The mean serum UA concentration of participants was 7.3 ± 2.6 mg/dL. The prevalence of hyperuricemia was 54.7% (105 of 192) in CHF patients, 52.9% (64 of 121) in men, and 57.7% (41 of 71) in women. In the total sample, higher serum UA was associated with poorer cognitive function independent of demographic, medical and psychological variables (β = - 0.130, ΔR = 0.014, p = 0.015). In sex-stratified groups, elevated serum UA was independently associated with worse cognitive function in men (β = - 0.247, ΔR = 0.049, p = 0.001) but not in women (β = - 0.005, ΔR = 0.000, p = 0.955).

Conclusions: Higher serum UA is independently associated with poorer cognitive function in CHF populations after adjusting for confounding variables. Furthermore, elevated serum UA is independently related to worse performance on cognitive function in men but not in women. More longitudinal studies are needed to examine the association between serum UA and cognitive function in CHF populations and stratified by sex.
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http://dx.doi.org/10.1186/s12872-020-01666-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7441639PMC
August 2020

SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury.

Aging (Albany NY) 2020 07 28;12(16):16224-16237. Epub 2020 Jul 28.

Department of Cardiology, Tianjin First Central Hospital, Tianjing 300192, P.R. China.

Sirtuin-3 (SirT3) and AMPK stimulate mitochondrial biogenesis, which increases mitochondrial turnover and cardiomyocyte regeneration. We studied the effects of SirT3, AMPK, and mitochondrial biogenesis on sepsis-induced myocardial injury. Our data showed that after treating cardiomyocytes with lipopolysaccharide, SirT3 and AMPK levels decreased, and this was followed by mitochondrial dysfunction and cardiomyocyte death. Overexpression of SirT3 activated the AMPK pathway and improved mitochondrial biogenesis, which is required to sustain mitochondrial redox balance, maintain mitochondrial respiration, and suppress mitochondrial apoptosis. Inhibition of mitochondrial biogenesis abolished SirT3/AMPK-induced cardioprotection by causing mitochondrial damage. These findings indicate that SirT3 reduces sepsis-induced myocardial injury by activating AMPK-related mitochondrial biogenesis.
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http://dx.doi.org/10.18632/aging.103644DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485737PMC
July 2020

Recurrent Type III Kounis Syndrome: Will Anti-Immunoglobulin E Drug Be Another Option?

Can J Cardiol 2020 06 10;36(6):966.e5-966.e6. Epub 2019 Dec 10.

Division of Cardiology, Tianjin 1st Central Hospital, Tianjin, China. Electronic address:

Kounis syndrome was recognized as the concurrence of acute cardiovascular events with hypersensitivity reactions. We report a case of Kounis syndrome type III (coronary thrombosis) variant in a 48-year-old man who had experienced recurrent acute myocardial infarctions after scallion-induced hypersensitivity reactions. After appropriate antithrombotic, antihistamine, and reperfusion strategies, the patient was found to have elevated levels of immunoglobulin E and chronic urticaria. Upon administration of omalizumab, there was an improvement of chronic urticaria, a decrease in immunoglobulin E levels, and resolution of the ischemic attacks.
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http://dx.doi.org/10.1016/j.cjca.2019.12.007DOI Listing
June 2020

Galectin-3 inhibition attenuates doxorubicin-induced cardiac dysfunction by upregulating the expression of peroxiredoxin-4.

Can J Physiol Pharmacol 2020 Oct 9;98(10):700-707. Epub 2020 Jun 9.

Department of Cardiology, Tongji Hospital of Tongji University, Shanghai 200003, People's Republic of China.

Doxorubicin (DOX) is a highly efficient chemotherapeutic drug limited by its cardiotoxicity. Galectin-3 (Gal-3) overexpression is associated with several cardiovascular diseases. In this study, the in vivo models of DOX-treated rats and the in vitro model of DOX-treated H9C2 cells were used. DOX induced cardiac injury and dysfunction accompanied with the upregulation of Gal-3 at the end of the experiment, while inhibition of Gal-3 with modified citrus pectin (MCP) exhibited a dramatic improvement in cardiac function of the DOX-treated rats, as manifested by increased left ventricular systolic pressure and ±d/d and decreased left ventricular end-diastolic pressure. The plasma levels of myocardial injury markers such as lactate dehydrogenase, creatine kinase, creatine kinase-MB, and cardiac troponin I were decreased after MCP treatment. In parallel, MCP attenuated myocardial tissue markers of oxidative stress such as hydrogen peroxide and malondialdehyde restored the activities of superoxide dismutase, catalase, and glutathione peroxidase and upregulated antioxidant peroxiredoxin-4 (Prx-4). To further verify the role of Prx-4, it was downregulated by siRNA-mediated knockdown in H9C2 cells. MCP could not reverse DOX-induced oxidative stress in Prx-4-knock-down cells. In conclusion, Gal-3 mediated DOX-induced cardiotoxicity and Gal-3 inhibition attenuated DOX-induced cardiac dysfunction by upregulating the expression of Prx-4 to reduce myocardial oxidative stress.
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http://dx.doi.org/10.1139/cjpp-2019-0700DOI Listing
October 2020

Renal denervation improves vascular endothelial dysfunction by inducing autophagy via AMPK/mTOR signaling activation in a rat model of type 2 diabetes mellitus with insulin resistance.

Acta Diabetol 2020 Oct 1;57(10):1227-1243. Epub 2020 Jun 1.

Department of Cardiology, Tianjin First Central Hospital, Tianjin, China.

Background: Recent clinical and animal studies have shown that renal denervation (RDN) improves insulin sensitivity and endothelial dysfunction. However, the specific mechanism remains incompletely understood. The purpose of this study is to investigate the effects of RDN on endothelial dysfunction of type 2 diabetes mellitus (TDM) rat models with insulin resistance and to explore the underlying molecular mechanisms.

Methods: Male Sprague-Dawley rats were fed with or without high-fat diet allocated in different groups, combined with low-dose streptozotocin which induces a rat model to develop TDM with insulin resistance. RDN was conducted 1 week after the rat models fully developed TDM. The animals were sub-divided into four groups randomly: control group (CON, n = 6), diabetic group (TDM, n = 6), diabetic with sham surgery group (Sham, n = 6) and diabetic with RDN group (RDN, n = 6). Rats in all groups were studied at baseline, both preoperatively and 4 weeks after RDN, respectively. Western blot was used to detect the expression of angiotensin-converting enzyme 2 (ACE2) protein and the expression of autophagy-related proteins Beclin1, LC3 and p62 and autophagy signaling pathway AMPK/mTOR proteins and apoptosis-related protein caspase-3 in the aorta endothelial cells. In addition, the effects of ACE2 on autophagy of human umbilical vein insulin resistance endothelial cell culture in vitro were also studied.

Results: RDN decreased plasma and renal tissue norepinephrine levels. The Von Willebrand factor level was also decreased, while the plasma level of nitric oxide (NO) was significantly increased after RDN. Compared with the TDM group and the Sham group, the endothelium-dependent and endothelium-independent diastolic function of the RDN group was improved significantly, the expression of Beclin1, LC3, ACE2 and eNOS proteins was higher, and the level of p62 protein was decreased. Furthermore, we found that RDN can activate the expression of p-AMPK and inhibit the expression of p-mTOR. In cell culture experiment, ACE2 activated p-AMPK and inhibited p-mTOR, thus promoting autophagy.

Conclusions: RDN may not only increase the expression of ACE2 in the vascular endothelium, but also can via ACE2 activate p-AMPK and inhibit p-mTOR, thus promoting autophagy and improving endothelial dysfunction.
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http://dx.doi.org/10.1007/s00592-020-01532-6DOI Listing
October 2020

Inhibition of HES-1 might play a protective role in endothelial cells under cholesterol stimulation via PI3K/AKT signaling pathway.

Gen Physiol Biophys 2020 Mar;39(2):145-155

The Fourth Center Clinical College of Tianjin Medical University, Tianjin, China.

The occurrence of atherosclerotic cardiovascular disease (ASCVD) was closely related to low-density lipoprotein (LDL) cholesterol. HES-1 is critical for maintains of stem cells, quiescent cells or cancer cells, and contributes to drug resistance and metastasis of tumor cells. In this study, we established a cell model of HES-1 inhibition and overexpression in Ea.hy 926 cells, and firstly detected the proliferation rete of Ea.hy 926 cells under cholesterol stimulation using MTT assay, and apoptosis of Ea.hy 926 cells were detected using flow cytometry. Expression of HES-1, apoptosis related proteins and phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway were detected using Western blotting analysis. The expression of apoptotis related genes were detected using polymerase chain reaction (PCR) method. The concentration of angiogenesis cytokines was detected using enzyme-linked immunosorbent assay (ELISA) method. We found that proliferation of Ea.hy 926 cells was inhibited after stimulation of cholesterol, inhibition of HES-1 expression would reduce this effect. We also found that expression of apoptosis related molecules was increased and expressions of angiogenesis factors were decreased after cholesterol treatment. Besides, we revealed that these effects were mediated via PI3K/AKT signaling pathway, and HES-1 inhibition could increase the activity of this signaling pathway.
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http://dx.doi.org/10.4149/gpb_2019052DOI Listing
March 2020

High blood pressure as the first manifestation and multiple organ dysfunction in primary hyperparathyroidism: a case report.

Hypertens Res 2020 10 16;43(10):1125-1127. Epub 2020 Apr 16.

Department of Anesthesiology, Tianjin First Center Hospital, No. 24, Fukang Road, Nankai District, Tianjin, 300192, China.

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http://dx.doi.org/10.1038/s41440-020-0447-8DOI Listing
October 2020

Irisin activates Opa1-induced mitophagy to protect cardiomyocytes against apoptosis following myocardial infarction.

Aging (Albany NY) 2020 03 10;12(5):4474-4488. Epub 2020 Mar 10.

Department of Cardiology, Tianjin First Center Hospital, Tianjin, China.

Myocardial infarction is characterized by sudden ischemia and cardiomyocyte death. Mitochondria have critical roles in regulating cardiomyocyte viability and can sustain damage under ischemic conditions. Mitophagy is a mechanism by which damaged mitochondria are removed by autophagy to maintain mitochondrial structure and function. We investigated the role of the dynamin-like GTPase optic atrophy 1 (Opa1) in mitophagy following myocardial infarction. Opa1 expression was downregulated in infarcted hearts and in hypoxia-treated cardiomyocytes . We found that Opa1 overexpression protected cardiomyocytes against hypoxia-induced damage and enhanced cell viability by inducing mitophagy. Opa1-induced mitophagy was activated by treatment with irisin, which protected cardiomyocytes from further damage following myocardial infarction. Opa1 knockdown abolished the cardioprotective effects of irisin resulting in an enhanced inflammatory response, increased oxidative stress, and mitochondrial dysfunction in cardiomyocytes. Our data indicate that Opa1 plays an important role in maintaining cardiomyocyte viability and mitochondrial function following myocardial infarction by inducing mitophagy. Irisin can activate Opa1-induced mitophagy and protect against cardiomyocyte injury following myocardial infarction.
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http://dx.doi.org/10.18632/aging.102899DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093202PMC
March 2020

Naringin protects endothelial cells from apoptosis and inflammation by regulating the Hippo-YAP Pathway.

Biosci Rep 2020 03;40(3)

Department of Cardiology, First Center Clinic College of Tianjin Medical University, Tianjin 300192, China.

Atherosclerosis is the primary cause of several cardiovascular diseases. Oxidized low-density lipoprotein (ox-LDL)-induced apoptosis, endothelial-mesenchymal transition (EndMT), and inflammation are crucial for the progression of cardiovascular diseases, including atherosclerosis. Naringin, a major compound from tomatoes, grapefruits, and related citrus, reportedly exhibits potential protective effects during atherosclerosis development; however, its effect on ox-LDL-induced human umbilical vein endothelial cell (HUVEC) damage remains unknown. In the present study, we investigated the anti-apoptotic and anti-inflammatory activities of naringin against ox-LDL-induced endothelial cells, and the underlying mechanism. Naringin pretreatment significantly and concentration-dependently inhibited ox-LDL-induced cell injury and apoptosis. Additionally, naringin restored endothelial barrier integrity by preventing VE-cadherin disassembly and F-actin remodeling, and down-regulated pro-inflammatory factors like IL-1β, IL-6, and IL-18, in the HUVECs. We also demonstrated that naringin treatment restored ox-LDL-induced YAP (yes-associated protein) down-regulation, given the YAP-shRNA attenuated cytoprotective effect of naringin on ox-LDL-induced endothelial cell injury and apoptosis. Collectively, our data indicate that naringin reversed ox-LDL-triggered HUVEC apoptosis, EndMT, and inflammation by inhibiting the YAP pathway. Therefore, naringin may have a therapeutic effect on endothelial injury-related disorders.
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http://dx.doi.org/10.1042/BSR20193431DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7056449PMC
March 2020

LATS2 promotes cardiomyocyte H9C2 cells apoptosis via the Prx3-Mfn2-mitophagy pathways.

J Recept Signal Transduct Res 2019 Oct-Dec;39(5-6):470-478. Epub 2019 Dec 12.

Department of Cardiology, Shanghai Tongji Hospital, Shanghai, China.

The pathogenesis of cardiomyocyte death is closely associated with mitochondrial homeostasis poorly understood mechanisms. The aim of our study is to explore the contribution of large tumor suppressor kinase 2 (LATS2) to the apoptosis of cardiomyocyte H9C2 cells. Adenovirus-mediated LATS2 overexpression was carried out in H9C2 cells. The cell viability and apoptosis rate were measured an MTT assay, TUNEL staining, western blotting, an ELISA, and an LDH release assay. Mitophagy was quantified using immunofluorescence and western blotting. The overexpression of LATS2 in H9C2 cells drastically promoted cell death. Molecular investigations showed that LATS2 overexpression was associated with mitochondrial injury, as evidenced by increased mitochondrial ROS production, reduced antioxidant factor levels, increased cyt-c liberation into the nucleus and activated mitochondrial caspase-9-dependent apoptotic pathway activity. Furthermore, our results demonstrated that LATS2-mediated mitochondrial malfunction by repressing mitophagy and that the reactivation of mitophagy could sustain mitochondrial integrity and homeostasis in response to LATS2 overexpression. Furthermore, we found that LATS2 inhibited mitophagy by inactivating the Prx3-Mfn2 axis. The reactivation of Prx3-Mfn2 pathways abrogated the LATS2-mediated inhibition of mitochondrial apoptosis in H9C2 cells. The overexpression of LATS2 induces mitochondrial stress by repressing protective mitophagy in a manner dependent on Prx3-Mfn2 pathways, thus reducing the survival of H9C2 cells.
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http://dx.doi.org/10.1080/10799893.2019.1701031DOI Listing
June 2020

Early Renal-Protective Effects of Remote Ischemic Preconditioning in Elderly Patients with Non-ST-Elevation Myocardial Infarction (NSTEMI).

Med Sci Monit 2019 Nov 15;25:8602-8609. Epub 2019 Nov 15.

Department of Cardiology, Tianjin First Central Hospital, Tianjin, China (mainland).

BACKGROUND With the wide clinical application of angiography, contrast-enhanced nephropathy (CIN) has become the third-leading cause of acute kidney injury (AKI). Remote ischemic preconditioning (RIPC) is a non-fatal ischemia-reperfusion injury that can provide protection against lethal ischemia-reperfusion. This study aimed to assess the effect of RIPC on CIN in elderly patients with non-ST-elevation myocardial infarction (NSTEMI). MATERIAL AND METHODS Patients were randomly divided into 2 groups with 119 patients in each group treated with interventional therapy. Patients in the RIPC group received distal ischemic preconditioning 2 h before contrast exposure, while patients in the control group received a sham RIPC procedure. Incidence of CIN was the primary outcome. Changes in creatinine, NGAL, and KIM-1 after contrast administration were secondary outcomes. RESULTS CIN occurred in a total of 27 (12.3%) patients, including 12 (10.1%) in the RIPC group and 15 (15.1%) in the control group (P=0.329). RIPC treatment significantly reduced the levels of NGAL (P=0.024) and KIM-1 (P=0.007) at 12 h after contrast administration, suggesting RIPC treatment reduces sub-clinical renal damage. Subgroup analysis revealed that significant reduction of KIM-1 and NGAL by RIPC, mainly occurring in patients with a Mehran risk score of 6-10. CONCLUSIONS Although RIPC did not significantly reduce CIN incidence in elderly patients with NSTEMI, the application of more sensitive biomarkers - NGAL and KIM-1 - indicated a reduction of sub-clinical renal damage by RIPC, especially in the early stage of injury. As a simple and well-tolerated method, RIPC may be a potentially feasible option to prevent CIN.
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http://dx.doi.org/10.12659/MSM.917442DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6873631PMC
November 2019

MiR-495 regulates macrophage M1/M2 polarization and insulin resistance in high-fat diet-fed mice via targeting FTO.

Pflugers Arch 2019 12 11;471(11-12):1529-1537. Epub 2019 Nov 11.

Department of Cardiology, Tianjin First Central Hospital, No. 24 Fukang Road, Tianjin, 300192, Nankai District, China.

MicroRNA 495 (miR-495) has been discovered to be involved in the metabolism and immune response in human body. The purpose of this study was to investigate the effect of miR-495 on macrophage M1/M2 polarization and insulin resistance in type 2 diabetes (T2D). A T2D mouse model was established by feeding C57BL/6 mice with a high-fat diet (HFD). The expressions of M1/M2 polarization markers and miR-495 in peritoneal macrophages were determined by qRT-PCR or Western blot. Mouse insulin tolerance test (ITT) and glucose tolerance test (GTT) were performed, and the targeted binding effect between miR-495, fat mass, and obesity-associated gene (FTO) was verified by double luciferase gene reporter assay. The body weight, blood glucose content, and miR-495 expression in macrophages of the HFD group were remarkably higher than those of the normal diet (ND) group. Besides, miR-495 induced the transformation of macrophages into M1-type pro-inflammatory macrophages and enhanced the insulin resistance of T2D mice. More importantly, FTO was proved to be a direct target gene of miR-495 and silencing FTO could induce the transformation of macrophages into M1-type pro-inflammatory macrophages. These results demonstrated that miR-495 could promote the transformation of macrophages into M1-type pro-inflammatory macrophages by inhibiting the expression of its target gene FTO, and aggravate the insulin resistance and adipose tissue inflammation in T2D mice, which provided a certain theoretical basis for the targeted treatment of T2D.
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http://dx.doi.org/10.1007/s00424-019-02316-wDOI Listing
December 2019

LncRNA MEG3-derived miR-361-5p regulate vascular smooth muscle cells proliferation and apoptosis by targeting ABCA1.

Am J Transl Res 2019 15;11(6):3600-3609. Epub 2019 Jun 15.

Department of Cardiology, Tianjin First Center Hospital Tianjin 300192, China.

Background: Atherosclerosis remains a leading cause of cardiology disease worldwide, which vascular smooth muscle cells (VSMCs) proliferation and apoptosis are involved. Increasing evidences have revealed that long non-coding RNAs (lncRNAs) considered to be critical regulatory factors of VSMCs function. However, the molecular mechanism is not fully understood.

Methods: First, we establish the ox-LDL induced VSMC model. We conducted RT-PCR to measure MEG3 expression and miR-361-5p expression in this model. The proliferation and apoptosis of VSMCs were measured via CCK-8 proliferative assay and flow cytometry respectively. We used knockdown and overexpression system to identify the molecular mechanism. In addition, luciferase report assay and bioinformatics analysis were used to confirm the bio-target of different factors.

Results: LncRNA MEG3 was down-regulated and related with miR-361-5p expression in ox-LDL injured VSMCs. Inhibition of lncRNA MEG3 promotes the proliferation and decelerates apoptosis of VSMCs. Moreover, MEG3 acts as a competing endogenous RNA (ceRNA) for miR-361-5p and further regulate ABCA1 expression regulate proliferation and apoptosis in ox-LDL injured VSMCs.

Conclusion: These results suggest that LncRNA MEG3 regulate proliferation and apoptosis in ox-LDL injured VSMCs and function as a ceRNA for miR-361-5p to modulate ABCA1 expression.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6614649PMC
June 2019

Effects of probucol on contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention.

Medicine (Baltimore) 2019 Jun;98(25):e16049

Department of Cardiology, Tianjin First Center Hospital, Tianjin, China.

Objective: This study was performed to explore the effects of probucol on contrast-induced acute kidney injury (CIAKI) in patients with coronary heart disease undergoing percutaneous coronary intervention (PCI).

Methods: In total, 220 patients undergoing PCI were randomly assigned to either the control group (hydration from 12 hours before to 12 hours after contrast administration; n = 110) or the probucol group (hydration plus probucol 500 mg twice daily 1 day before and 3 days after the operation; n = 110). The primary endpoint was the occurrence of serum creatinine (Scr)-based CIAKI, defined as an absolute increase in Scr by 0.5 mg/dl (44.2 μmol/L) or a relative 25% increase from baseline within 48 to 72 hours after exposure to contrast medium. The secondary outcomes were composite variations in Scr, blood urea nitrogen (BUN), creatinine clearance rate (Ccr) within 48 to 72 hours, and major adverse events during hospitalization or the 7-day follow-up period after PCI.

Results: The overall incidence of Scr-based CIAKI was 7.3% (16/220): 5.5% (6/110) in the control group and 9.1% (10/110) in the probucol group (χ = 1.078, P = .298). There were no significant differences in the occurrence rate of major adverse events during hospitalization or the 7-day follow-up period after PCI between the groups. Multivariate logistic regression analysis showed that probucol was not an independent protective factor for CIAKI (odds ratio, 1.825; 95% confidence interval, 0.639-5.212; P = .261). However, hydration was an independent protective factor (odds ratio, 0.997; 95% confidence interval, 0.995-0.999; P = .004).

Conclusion: Probucol cannot effectively reduce the incidence of CIAKI through its anti-inflammatory and antioxidative stress effects.
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http://dx.doi.org/10.1097/MD.0000000000016049DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6636920PMC
June 2019

Long noncoding RNA OIP5-AS1 accelerates the ox-LDL mediated vascular endothelial cells apoptosis through targeting GSK-3β via recruiting EZH2.

Am J Transl Res 2019 15;11(3):1827-1834. Epub 2019 Mar 15.

Department of Cardiology, Tianjin First Center Hospital Tianjin 300192, China.

An increasing amount of research is demonstrating the role of long noncoding RNAs (lncRNAs) in human cardiovascular disease, and in particular, atherosclerosis. To date, the mechanism through which lncRNA OIP5-AS1 regulates the oxidative low-density lipoprotein (ox-LDL)-mediated endothelial cell apoptosis is still unclear. Results from this study found that lncRNA OIP5-AS1 was significantly over-expressed in the human umbilical vein endothelial cells (HUVECs) administered with ox-LDL. The silencing of OIP5-AS1 inhibited apoptosis and promoted proliferation via inducing G0/G1 cycle arrest. Chromatin immunoprecipitate (ChIP) revealed that lncRNA OIP5-AS1 reduced GSK-3β expression through recruiting EZH2, a critical element of the Polycomb Repressive Complex 2 (PRC2) complex that directly bind with the GSK-3β promoter region. Rescue experiments validated that GSK-3β could eliminate the effect of OIP5-AS1 on HUVECs. Overall, these findings suggest that lncRNA OIP5-AS1 accelerates ox-LDL mediated vascular endothelial cell apoptosis through targeting GSK-3β via recruiting EZH2, providing potential therapeutic strategies for atherosclerosis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6456540PMC
March 2019

Impact of Optimal Medical Therapy at Discharge on One-year Direct Medical Costs in Patients with Acute Coronary Syndromes: A Retrospective, Observational Database Analysis in China.

Clin Ther 2019 03 13;41(3):456-465.e2. Epub 2019 Feb 13.

School of Pharmaceutical Science and Technology, Tianjin University, Tianjin, China. Electronic address:

Purpose: This study was conducted to examine the use of optimal medical therapy (OMT), consisting of an antiplatelet, a β-blocker, an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB), and a statin combined, after hospital discharge and its relationship with direct medical costs in patients with acute coronary syndromes (ACS) in Tianjin, China.

Methods: Data were obtained from the Tianjin Urban Employee Basic Medical Insurance database (2011-2015). Data from adult patients with ≥1 hospitalization for ACS between January 2012 and December 2014 were included. Medications including antiplatelets, β-blockers, ACEIs/ARBs, and statins at discharge were recorded, with OMT defined as the use of all 4 indicated medications. Propensity-score matching was conducted to form matched OMT and non-OMT cohorts based on baseline differences. All-cause and ACS-related health care resource utilization and direct medical costs during a 12-month follow-up period were assessed and compared between cohorts. Generalized linear modeling was conducted to assess the association between OMT at discharge and direct medical costs.

Findings: A total of 22,041 patients were identified (mean age, 64.7 [10.7] years; 45.6% female), of whom 15.1% (3336) received OMT at discharge. The OMT cohort had fewer patients hospitalized for any cause during follow-up compared with the matched non-OMT cohort (38.1% vs 43.2%; P < 0.001), which was further associated with fewer hospitalizations (1.55 vs 1.64; P = 0.019) and shorter annualized length of stay (15.9 vs 17.2 d; P = 0.041). Despite higher costs of outpatient services (9958 vs 10,060 Chinese yuan [CNY] [P = 0.006]; adjusted difference, +456 CNY [P = 0.004]) (year-2014 1 USD = 6.20 CNY), the OMT cohort had significantly lower all-cause total costs (20,771 vs 22,877 CNY [P = 0.174]; adjusted difference, -2089 CNY [P = 0.006]), driven by lower costs of inpatient services (10,813 vs 12,817 CNY [P < 0.001]; adjusted difference, -2184 CNY [P = 0.001]). The difference in ACS-related total costs between the 2 cohorts was not statistically significant (8535 vs 9304 CNY [P = 0.128]; adjusted difference, -558 CNY [P = 0.214]).

Implications: Receiving OMT at discharge was associated with fewer hospitalizations and lower all-cause direct medical costs in these patients with ACS in China. Strategies are needed to improve OMT prescribing rates at discharge, which would lead to better clinical prognosis and total cost-savings among patients with ACS in China.
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http://dx.doi.org/10.1016/j.clinthera.2019.01.005DOI Listing
March 2019

The prognostic value of mean platelet volume to platelet count ratio in older patients with non-ST elevation acute coronary syndrome receiving primary percutaneous coronary intervention: a retrospective study.

Minerva Cardioangiol 2019 Apr 4;67(2):102-108. Epub 2019 Jan 4.

Cardiovascular Department, The First Center Clinic College of Tianjin Medical University, Tianjin, China -

Background: The aim of this study was to investigate the value of the mean platelet volume to platelet count (MPV/P) ratio for predicting in-hospital and long-term cardiac mortality in older non-ST elevation-acute coronary syndrome (NSTE-ACS) patients after primary percutaneous coronary intervention (PCI).

Methods: We retrospectively reviewed 452 older NSTE-ACS patients who received primary PCI. The patients were divided into two groups based on MPV/P ratios: high MPV/P group (N.=150) defined as a value in the third tertile (>0.056628) and low MPV/P group (N.=302) in the lower two tertiles (≤0.056628). Clinical outcomes included non-fatal reinfarction, heart failure, and cardiac mortality.

Results: Multivariate analyses showed that high MPV/P and MPV values were independent predictors of cardiac mortality. The in-hospital cardiac mortality of the high MPV/P group was higher than the low MPV/P group (1.3% vs. 14.7%, P<0.001). The rates of heart failure and cardiac mortality in one year were significantly higher in the high MPV/P group compared to the low MPV/P group (P<0.05). The cut-off value of MPV/P for predicting cardiac death was 0.067107, with a sensitivity of 0.707 and a specificity of 0.868. MPV/P was superior to MPV (z=9.235, P<0.001) for predicting cardiac mortality.

Conclusions: High MPV/P and MPV values are independent predictors of cardiac mortality in older patients with NSTE-ACS receive primary PCI. Moreover, MPV/P is better than MPV for predicting cardiac mortality.
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http://dx.doi.org/10.23736/S0026-4725.18.04836-3DOI Listing
April 2019

Aconitine-induced cardiac arrhythmia in human induced pluripotent stem cell-derived cardiomyocytes.

Exp Ther Med 2018 Oct 22;16(4):3497-3503. Epub 2018 Aug 22.

Department of Cardiology, Tianjin First Central Hospital, Tianjin 300192, P.R. China.

Pre-clinical evaluation of cardiac dysfunction is important for assessing the safety of traditional or novel medicines due to the universality of potential drug-induced heart failure and irreversible arrhythmia. Aconitine (ACO), a traditionally used anti-pyretic, analgesic and anti-rheumatic drug, has been reported to have arrhythmogenic effects. In the present study, the Real-Time Cellular Analysis Cardio system was applied to evaluate the arrhythmogenic effects of ACO in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). The results indicated that ACO is capable of increasing the frequency and decreasing the amplitude of hiPSC-CM contraction in a dose- and time-dependent manner. ACO at 0.25 µM increased the beating rate of hiPSC-CMs by 3.7-fold within 30 min, while 3.0 µM of ACO increased the beating rate by 7.3-fold. The present study also evaluated the potential pro-apoptotic effects of ACO by using caspase-3 and caspase-9 kits. To the best of our knowledge, the present study was the first to record the ACO-induced cardiac arrhythmia of hiPSC-CMsin real-time. The results also indicate that ACO-induced cell death is mediated, at least in part, by caspase-dependent apoptotic pathways.
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http://dx.doi.org/10.3892/etm.2018.6644DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143858PMC
October 2018
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