Database : MEDLINE
Search on : myocardial and infarction [Words]
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[PMID]: 29524682
[Au] Autor:Ghosh K; N I
[Ad] Address:Unit of Toxicology, Department of Zoology, School of Life Sciences, Bharathiar University, Coimbatore, 641046, Tamil Nadu, India; Department of Zoology, Annamalai University, Annamalainagar, Chidambaram, 608002, Tamil Nadu, India. Electronic address: kavisa9@gmail.com.
[Ti] Title:Cadmium treatment induces echinocytosis, DNA damage, inflammation, and apoptosis in cardiac tissue of albino Wistar rats.
[So] Source:Environ Toxicol Pharmacol;59:43-52, 2018 Feb 27.
[Is] ISSN:1872-7077
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Cadmium (Cd), a potent carcinogen present in almost all foods, poses a major health risk to humans. Major routes of exposure to Cd for humans are occupation, diet, and tobacco use. Cd elicits various deleterious effects on cellular molecules mainly by causing oxidant-antioxidant imbalance. Cd has been implicated in the pathogenesis of many cancers, Itai-itai disease, diabetic nephropathy, hypertension, peripheral artery disease, and myocardial infarction. This study was designed to investigate the effects of Cd intake on erythrocytes and cardiac tissue in male albino Wistar rats. We treated male albino Wistar rats with cadmium chloride (CdCl ) by intra-gastric administration for 30 days and examined Cd burden and changes in blood constituents and antioxidant status of blood and cardiac tissue. We also studied the structural alterations in the erthrocytes, elemental changes and Cd burden in cardiac tissue using scanning electron microscope (SEM/EDX). Inflammation and apoptosis were analysed in the cardiac tissue by polymerase chain reaction (PCR), western blotting, and DNA fragmentation assay. Cd treatment resulted in echinocytosis of erythrocytes and distorted myofibrils arrangement, vacuolization and congestion in the vessels. Cd administration has also induced inflammation and apoptosis in the cardiac tissue. At molecular level, Cd administration caused oxidative damage to DNA, lipids, and proteins and diminished the activities of various antioxidants. The present study provides a compelling evidence of Cd-induced imbalance in oxidant-antioxidant system with damage to erythrocytes and cardiac tissue that may contribute to various cardiac diseases.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 216867 MEDLINE  
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[PMID]: 29524572
[Au] Autor:Zhang Z; Li Y; Yang X; Wang L; Xu L; Zhang Q
[Ad] Address:Heart Canter, Beijing Chao Yang Hospital, Capital Medical University, Beijing, China.
[Ti] Title:Susceptibility of multiple polymorphisms in ADIPOQ, ADIPOR1 and ADIPOR2 genes to myocardial infarction in Han Chinese.
[So] Source:Gene;, 2018 Mar 07.
[Is] ISSN:1879-0038
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:We aimed to investigate the association of 12 extensively studied polymorphisms in adiponectin (ADIPOQ), adiponectin receptor-1 (ADIPOR1) and adiponectin receptor-2 (ADIPOR2) genes with myocardial infarction in Han Chinese. This is a hospital-based, cross-sectional, case-control study, including 717 myocardial infarction patients and 612 controls. Myocardial infarction was confirmed through electrocardiogram/anatomopathological examinations. All polymorphisms met the Hardy-Weinberg equilibrium (p > 0.05). The genotype/allele counts of ADIPOQ gene rs2241766 (p = 0.001/0.003) and ADIPOR2 gene rs10773989 (p < 0.001/=0.008) differed significantly between patients and controls. Under the recessive model, rs2241766 (odds ratio [OR] = 4.16, 95% confidence interval [CI]: 1.83-9.49, p = 0.001) and rs10773989 (OR = 8.40, 95% CI: 2.54-27.8, p < 0.001) were associated with the significantly increased risk of myocardial infarction. Haplotype analysis revealed none or marginal significance, and there was no likelihood of genetic interaction as indicated by multifactor dimensionality reduction (MDR). Logistic regression analysis indicated that age, total cholesterol, hypertension, rs2241766, rs1342387, rs10773989 and rs1044471 were significant contributors, and a nomogram based on these contributors exhibited a good predictive utility (C-index: 0.795, p < 0.001). Our findings demonstrate that two polymorphisms, rs2241766 in ADIPOQ gene and rs10773989 in ADIPOR2 gene, especially under the recessive model of inheritance, played independent leading roles in susceptibility to myocardial infarction in Han Chinese.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 216867 MEDLINE  
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[PMID]: 29524504
[Au] Autor:Qiu F; Dong C; Liu Y; Shao X; Huang D; Han Y; Wang B; Liu Y; Huo R; Paulo P; Zhang Z; Zhao D; Chu WF
[Ad] Address:Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China, Key Laboratory of Cardiovascular Research, Ministry of Education), College of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, PR China.
[Ti] Title:Pharmacological inhibition of SUMO-1 with ginkgolic acid alleviates cardiac fibrosis induced by myocardial infarction in mice.
[So] Source:Toxicol Appl Pharmacol;, 2018 Mar 07.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND AND PURPOSE: Protein modification by small ubiquitin-like modifier (SUMO) plays a critical role in the pathogenesis of heart diseases. The present study was designed to determine whether ginkgolic acid (GA) as a SUMO-1 inhibitor exerts an inhibitory effect on cardiac fibrosis induced by myocardial infarction (MI). EXPERIMENTAL APPROACH: GA was delivered by osmotic pumps in MI mice. Masson staining, electron microscopy (EM) and echocardiography were used to assess cardiac fibrosis, ultrastructure and function. Expression of SUMO-1, PML, TGF-1 and Pin1 was measured with Western blot or Real-time PCR. Collagen content, cell viability and myofibroblast transformation were measured in neonatal mouse cardiac fibroblasts (NMCFs). Promyelocytic leukemia (PML) protein was over-expressed by plasmid transfection. KEY RESULTS: GA improved cardiac fibrosis and dysfunction, and decreased SUMO-1 expression in MI mice. GA (>20 M) inhibited NMCF viability in a dose-dependent manner. Nontoxic GA (10 M) restrained angiotensin II (Ang II)-induced myofibroblast transformation and collagen production. GA also inhibited expression of TGF-1 mRNA and protein in vitro and in vivo. GA suppressed PML SUMOylation and PML nuclear body (PML-NB) organization, and disrupted expression and recruitment of Pin1 (a positive regulator of TGF-1 mRNA), whereas over-expression of PML reversed that. CONCLUSIONS AND IMPLICATIONS: Inhibition of SUMO-1 by GA alleviated MI-induced heart dysfunction and fibrosis, and the SUMOylated PML/Pin1/TGF-1 pathway is crucial for GA-inhibited cardiac fibrosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  4 / 216867 MEDLINE  
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[PMID]: 29524460
[Au] Autor:Gupta K; Phan N; Wang Q; Liu B
[Ad] Address:Department of Surgery, School of Medicine and Public Health, University of Wisconsin, Madison, WI, USA.
[Ti] Title:Necroptosis in cardiovascular disease - a new therapeutic target.
[So] Source:J Mol Cell Cardiol;, 2018 Mar 07.
[Is] ISSN:1095-8584
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Contrary to the apoptosis-necrosis binary view of cell death, recent experimental evidence demonstrates that several forms of necrosis, represented by necroptosis, are regulated or programmed in nature. Multiple death stimuli known to be associated with cardiovascular disease are capable of causing either apoptosis or necroptosis. Whether a cell dies from apoptosis or necroptosis has distinct consequences on inflammation. It is known that apoptosis, a non-lytic form of death mediated by the caspase family of proteases, does not generally evoke an immune response. Necroptosis, on the other hand, is a lytic form of cell death. Due to the rapid loss of plasma membrane integrity, cells dying from necroptosis release proinflammatory intracellular contents and subsequently cause inflammation. Our review delineates various genetic and biochemical evidence that demonstrates a compelling role of necroptosis in the pathogenesis and/or progression of cardiovascular disease including myocardial infarction, atherosclerosis, and aortic aneurysm. Through recent studies of necroptosis in cardiovascular diseases, we attempt to discuss the role of necroptosis in vascular inflammation as well as the potential of necroptosis inhibitors in future clinical management of cardiovascular events. Inhibiting necroptosis in the vasculature has an overall protective role and necroptosis may represent a new therapeutic target to prevent the development and progression of cardiovascular diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 216867 MEDLINE  
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[PMID]: 29520182
[Au] Autor:Wang L; Chen Y; Zhang B; Chen W; Wang C; Song L; Xu Z; Zheng J; Gao F
[Ad] Address:Molecular Imaging Center, West China Hospital of Sichuan University, Chengdu 610041, China.
[Ti] Title:Self-Gated Late Gadolinium Enhancement at 7T to Image Rats with Reperfused Acute Myocardial Infarction.
[So] Source:Korean J Radiol;19(2):247-255, 2018 Mar-Apr.
[Is] ISSN:2005-8330
[Cp] Country of publication:Korea (South)
[La] Language:eng
[Ab] Abstract:Objective: A failed electrocardiography (ECG)-trigger often leads to a long acquisition time (TA) and deterioration in image quality. The purpose of this study was to evaluate and optimize the technique of self-gated (SG) cardiovascular magnetic resonance (CMR) for cardiac late gadolinium enhancement (LGE) imaging of rats with myocardial infarction/reperfusion. Materials and Methods: Cardiovascular magnetic resonance images of 10 rats were obtained using SG-LGE or ECG with respiration double-gating (ECG-RESP-gating) method at 7T to compare differences in image interference and TA between the two methods. A variety of flip angles (FA: 10-80) and the number of repetitions (NR: 40, 80, 150, and 300) were investigated to determine optimal scan parameters of SG-LGE technique based on image quality score and contrast-to-noise ratio (CNR). Results: Self-gated late gadolinium enhancement allowed successful scan in 10 (100%) rats. However, only 4 (40%) rats were successfully scanned with the ECG-RESP-gating method. TAs with SG-LGE varied depending on NR used (TA: 41, 82, 154, and 307 seconds, corresponding to NR of 40, 80, 150, and 300, respectively). For the ECG-RESP-gating method, the average TA was 220 seconds. For SG-LGE images, CNR (42.5 5.5, 43.5 7.5, 54 9, 59.5 8.5, 56 13, 54 8, and 41 9) and image quality score (1.85 0.75, 2.20 0.83, 2.85 0.37, 3.85 0.52, 2.8 0.51, 2.45 0.76, and 1.95 0.60) were achieved with different FAs (10, 15, 20, 25, 30, 35, and 40, respectively). Optimal FAs of 20-30 and NR of 80 were recommended. Conclusion: Self-gated technique can improve image quality of LGE without irregular ECG or respiration gating. Therefore, SG-LGE can be used an alternative method of ECG-RESP-gating.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.3348/kjr.2018.19.2.247

  6 / 216867 MEDLINE  
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[PMID]: 29510122
[Au] Autor:Wei J; Yang RX; Ye Q; Xiao XL; Zang XL; Zhao ZJ; Cai ZZ; Wang M; Xu J; Jiang L
[Ad] Address:Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
[Ti] Title:Higher risk of myocardial injury in chest pain patients with elevated red blood cell distribution width.
[So] Source:Clin Chim Acta;481:121-125, 2018 Mar 03.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: High level of red blood cell distribution width (RDW) has been associated with adverse outcomes in coronary artery disease patients. We aimed to investigate the relationship between RDW and the risk of myocardial injury in chest pain patients. METHODS AND RESULTS: We retrospectively reviewed 2078 chest pain patients with suspected acute myocardial infarction. Myocardial injury was defined as high-sensitivity cardiac troponin T (hs-cTnT) >14 ng/L. RDW was associated with hs-cTnT (r = 0.607) and the risk of myocardial injury stepwise increased across increasing RDW quartiles in all subgroups based on age and sex. The receiver operating characteristic curve analysis was calculated to assess the elevated RDW to predict myocardial injury, with the cutoff value of 13.25%. RDW had a high sensitivity (78.10%), specificity (87.44%), as well as positive predictive value (77.48%). The area under the curve (AUC) for all patients was 0.88 (95%CI 0.87, 0.90) and there is no statistical significant in AUCs for all subgroups. CONCLUSIONS: Elevated RDW was significantly associated with a higher risk of myocardial injury in chest pain patients with potential acute myocardial infarction. The RDW may be helpful to identify myocardial injury in such patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 216867 MEDLINE  
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[PMID]: 29462681
[Au] Autor:Yang Z; Wan J; Pan W; Zou J
[Ad] Address:Department of Cardiovascular Medicine, People's Hospital of Nanhai District, Foshan City, Guangdong Province 528200, China. Electronic address: AnneClarkyn@yahoo.com.
[Ti] Title:Expression of vascular endothelial growth factor in cardiac repair: Signaling mechanisms mediating vascular protective effects.
[So] Source:Int J Biol Macromol;113:179-185, 2018 Feb 17.
[Is] ISSN:1879-0003
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The present study was aimed to investigate the vascular endothelial growth factor expression pattern in acute myocardial infarction induced rats. Serum level of vascular endothelial growth factor and its mRNA expression in myocardium were determined. Protein expression of vascular endothelial growth factor and endothelial nitric oxide synthase were measured. Serum level of vascular endothelial growth factor was increased 105.3, 260, 378.2 and 271.3% following the onset of acute myocardial infarction at 3, 6, 9 and 12days respectively. The mRNA and protein expression of vascular endothelial growth factor was substantially increased following the onset of acute myocardial infarction. Protein expression of endothelial nitric oxide synthase was increased up to 1.02 fold. Taking all these data together, it is concluded that the vascular endothelial growth factor was increased in serum and tissue and attained peak at 9th day following the onset of acute myocardial infarction. Increased vascular endothelial growth factor level in serum and tissue could increase endothelial cell proliferation and angiogenesis, and endothelial nitric oxide synthase could inhibit apoptosis and protect cardiomyocytes. In conclusion, the increased vascular endothelial growth factor expression could play an essential role in cardiac repair following the onset of acute myocardial infarction.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  8 / 216867 MEDLINE  
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[PMID]: 29432894
[Au] Autor:Boening A; Assling-Simon L; Heep M; Boengler K; Niemann B; Grieshaber P
[Ad] Address:Department of Cardiovascular Surgery, University Hospital Giessen, Germany.
[Ti] Title:Buckberg's blood cardioplegia for protection of adult and senile myocardium in a rat in vitro model of acute myocardial infarction.
[So] Source:Exp Gerontol;104:98-104, 2018 Feb 10.
[Is] ISSN:1873-6815
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: In patients undergoing surgical myocardial revascularization for acute myocardial infarction, excellent myocardial protection can be achieved by blood cardioplegia. We investigated the influence of age on cardiac function, metabolism, and infarct size using Buckberg's blood cardioplegia (BCP). METHODS: The hearts of male Wistar rats ("adult", age 3 months, n = 8; "senile", age 24 months, n = 8) were excised and mounted on a blood-perfused isolated heart apparatus. An acute myocardial infarction was induced by coronary artery ligation for 30 min before aortic clamping and infusion of Buckberg's BCP. Throughout the experiment, functional parameters were recorded: coronary blood flow (normalized by heart weight), left ventricular peak developed pressure (LVpdP), and positive and negative derived left ventricular pressure over time (dLVPdt and dLVPdt ). Oxygen consumption (MVO ) and lactate production of the hearts were calculated. The infarct size after 90 min of reperfusion (in % of the area at risk) was measured with triphenyl tetrazolium chloride staining of the myocardium. RESULTS: The baseline coronary flow normalized by heart weight was significantly lower in the senile hearts (1.6  0.4 ml/(min ∗ g)) compared with the adult hearts (2.0  0.3 ml/(min ∗ g); p = 0.04). After 90 min of aortic clamping, hemodynamic function of senile hearts recovered better than that of adult hearts: LVpdP (adult 57% of baseline [BL]; senile 88% BL; p = 0.044) and dLVPdt (adult 74% BL, senile 102% BL; p = 0.12). In contrast, myocardial infarct size was similar between the adult (26%) and senile (21%; p = 0.45) hearts, and coronary flow recovered to a similar extent (55% BL and 58% BL, respectively). During reperfusion, MVO (80% BL and 81% BL) and lactate production (1.2 and 1.3 mol/min) were similar in the two groups. CONCLUSION: After acute myocardial infarction in a rat model, hearts recovered function after reperfusion with Buckberg's BCP solution. Hearts from aged animals recovered better than those from younger animals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  9 / 216867 MEDLINE  
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[PMID]: 29343519
[Au] Autor:Kolachalama VB; Shashar M; Alousi F; Shivanna S; Rijal K; Belghasem ME; Walker J; Matsuura S; Chang GH; Gibson CM; Dember LM; Francis JM; Ravid K; Chitalia VC
[Ad] Address:Section of Computational Biomedicine and.
[Ti] Title:Uremic Solute-Aryl Hydrocarbon Receptor-Tissue Factor Axis Associates with Thrombosis after Vascular Injury in Humans.
[So] Source:J Am Soc Nephrol;29(3):1063-1072, 2018 Mar.
[Is] ISSN:1533-3450
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Individuals with CKD are particularly predisposed to thrombosis after vascular injury. Using mouse models, we recently described indoxyl sulfate, a tryptophan metabolite retained in CKD and an activator of tissue factor (TF) through aryl hydrocarbon receptor (AHR) signaling, as an inducer of thrombosis across the CKD spectrum. However, the translation of findings from animal models to humans is often challenging. Here, we investigated the uremic solute-AHR-TF thrombosis axis in two human cohorts, using a targeted metabolomics approach to probe a set of tryptophan products and high-throughput assays to measure AHR and TF activity. Analysis of baseline serum samples was performed from 473 participants with advanced CKD from the Dialysis Access Consortium Clopidogrel Prevention of Early AV Fistula Thrombosis trial. Participants with subsequent arteriovenous thrombosis had significantly higher levels of indoxyl sulfate and kynurenine, another uremic solute, and greater activity of AHR and TF, than those without thrombosis. Pattern recognition analysis using the components of the thrombosis axis facilitated clustering of the thrombotic and nonthrombotic groups. We further validated these findings using 377 baseline samples from participants in the Thrombolysis in Myocardial Infarction II trial, many of whom had CKD stage 2-3. Mechanistic probing revealed that kynurenine enhances thrombosis after vascular injury in an animal model and regulates thrombosis in an AHR-dependent manner. This human validation of the solute-AHR-TF axis supports further studies probing its utility in risk stratification of patients with CKD and exploring its role in other diseases with heightened risk of thrombosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1681/ASN.2017080929

  10 / 216867 MEDLINE  
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[PMID]: 29305797
[Au] Autor:Lefcoski S; Kew K; Reece S; Torres MJ; Parks J; Reece S; de Castro Brs LE; Virag JAI
[Ad] Address:Department of Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, 27834, USA.
[Ti] Title:Anatomical-Molecular Distribution of EphrinA1 in Infarcted Mouse Heart Using MALDI Mass Spectrometry Imaging.
[So] Source:J Am Soc Mass Spectrom;29(3):527-534, 2018 Mar.
[Is] ISSN:1879-1123
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:EphrinA1 is a tyrosine kinase receptor localized in the cellular membrane of healthy cardiomyocytes, the expression of which is lost upon myocardial infarction (MI). Intra-cardiac injection of the recombinant form of ephrinA1 (ephrinA1-Fc) at the time of ligation in mice has shown beneficial effects by reducing infarct size and myocardial necrosis post-MI. To date, immunohistochemistry and Western blotting comprise the only experimental approaches utilized to localize and quantify relative changes of ephrinA1 in sections and homogenates of whole left ventricle, respectively. Herein, we used matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) coupled with a time-of-flight mass spectrometer (MALDI/TOF MS) to identify intact as well as tryptic fragments of ephrinA1 in healthy controls and acutely infarcted murine hearts. The purpose of the present study was 3-fold: (1) to spatially resolve the molecular distribution of endogenous ephrinA1, (2) to determine the anatomical expression profile of endogenous ephrinA1 after acute MI, and (3) to identify molecular targets of ephrinA1-Fc action post-MI. The tryptic fragments detected were identified as the ephrinA1-isoform with 38% and 34% sequence coverage and Mascot scores of 25 for the control and MI hearts, respectively. By using MALDI-MSI, we have been able to simultaneously measure the distribution and spatial localization of ephrinA1, as well as additional cardiac proteins, thus offering valuable information for the elucidation of molecular partners, mediators, and targets of ephrinA1 action in cardiac muscle. Graphical Abstract ᅟ.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1007/s13361-017-1869-7


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