Relevant bibliographies by topics / Myocardial hypertrophy

Academic literature on the topic 'Myocardial hypertrophy'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Myocardial hypertrophy"

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Tang, Xin, Lihong Pan, Shuang Zhao, Feiyue Dai, Menglin Chao, Hong Jiang, Xuesong Li, et al. "SNO-MLP (S-Nitrosylation of Muscle LIM Protein) Facilitates Myocardial Hypertrophy Through TLR3 (Toll-Like Receptor 3)–Mediated RIP3 (Receptor-Interacting Protein Kinase 3) and NLRP3 (NOD-Like Receptor Pyrin Domain Containing 3) Inflammasome Activation." Circulation 141, no. 12 (March 24, 2020): 984–1000. http://dx.doi.org/10.1161/circulationaha.119.042336.

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Background: S-nitrosylation (SNO), a prototypic redox-based posttranslational modification, is involved in the pathogenesis of cardiovascular disease. The aim of this study was to determine the role of SNO of MLP (muscle LIM protein) in myocardial hypertrophy, as well as the mechanism by which SNO-MLP modulates hypertrophic growth in response to pressure overload. Methods: Myocardial samples from patients and animal models exhibiting myocardial hypertrophy were examined for SNO-MLP level using biotin-switch methods. SNO sites were further identified through liquid chromatography–tandem mass spectrometry. Denitrosylation of MLP by the mutation of nitrosylation sites or overexpression of S-nitrosoglutathione reductase was used to analyze the contribution of SNO-MLP in myocardial hypertrophy. Downstream effectors of SNO-MLP were screened through mass spectrometry and confirmed by coimmunoprecipitation. Recruitment of TLR3 (Toll-like receptor 3) by SNO-MLP in myocardial hypertrophy was examined in TLR3 small interfering RNA–transfected neonatal rat cardiomyocytes and in a TLR3 knockout mouse model. Results: SNO-MLP level was significantly higher in hypertrophic myocardium from patients and in spontaneously hypertensive rats and mice subjected to transverse aortic constriction. The level of SNO-MLP also increased in angiotensin II– or phenylephrine-treated neonatal rat cardiomyocytes. S-nitrosylated site of MLP at cysteine 79 was identified by liquid chromatography–tandem mass spectrometry and confirmed in neonatal rat cardiomyocytes. Mutation of cysteine 79 significantly reduced hypertrophic growth in angiotensin II– or phenylephrine-treated neonatal rat cardiomyocytes and transverse aortic constriction mice. Reducing SNO-MLP level by overexpression of S-nitrosoglutathione reductase greatly attenuated myocardial hypertrophy. Mechanistically, SNO-MLP stimulated TLR3 binding to MLP in response to hypertrophic stimuli, and disrupted this interaction by downregulating TLR3-attenuated myocardial hypertrophy. SNO-MLP also increased the complex formation between TLR3 and RIP3 (receptor-interacting protein kinase 3). This interaction in turn induced NLRP3 (nucleotide-binding oligomerization domain–like receptor pyrin domain containing 3) inflammasome activation, thereby promoting the development of myocardial hypertrophy. Conclusions: Our findings revealed a key role of SNO-MLP in myocardial hypertrophy and demonstrated TLR3-mediated RIP3 and NLRP3 inflammasome activation as the downstream signaling pathway, which may represent a therapeutic target for myocardial hypertrophy and heart failure.
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Xue, Honghong, Hongtao Shi, Fan Zhang, Hao Li, Chao Li, and Qinghua Han. "RIP3 Contributes to Cardiac Hypertrophy by Influencing MLKL-Mediated Calcium Influx." Oxidative Medicine and Cellular Longevity 2022 (April 14, 2022): 1–15. http://dx.doi.org/10.1155/2022/5490553.

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Receptor-interacting protein 3(RIP3), a RIP family member, has been reported as a critical regulator of necroptosis and involves in the pathogenesis of various heart diseases. However, its role in the development of myocardial hypertrophy after pressure overload is unclear. We aimed to investigate the roles of RIP3 in pathological cardiac hypertrophy. A rat model of myocardial hypertrophy induced by the aortic banding method was used in this study. Neonatal rat cardiomyocytes (NRCMs) were stimulated with angiotensin II (Ang-II) or phenylephrine (PE) to induce neurohumoral stress. Our results showed that RIP3 level was significantly elevated in the hypertrophic myocardium tissues from patients, rats subjected to AB surgery, and NRCMs treated with Ang-II or PE. After downregulation of RIP3 expression in NRCMs, the phenotypes of myocardial hypertrophy were obviously alleviated. In mechanism, we demonstrated that RIP3 interacts with mixed lineage kinase domain-like protein (MLKL) and promotes its cell membrane localization to increase the influx of calcium within cells, thereby mediating the development of myocardial hypertrophy. More interestingly, we found the blockage of calcium influx by 2-aminoethoxydiphenyl borate, and lanthanum chloride efficiently reverses RIP3-induced cardiac remodeling in NRCMs. Taken together, our findings indicate a key role of the RIP3-MLKL signaling pathway in myocardial hypertrophy, which may be a novel promising treatment strategy for myocardial hypertrophy.
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Parker, Thomas G., and James N. Tsoporis. "Induction of S100β in Myocardium: An Intrinsic Inhibitor of Cardiac Hypertrophy." Canadian Journal of Applied Physiology 23, no. 4 (August 1, 1998): 377–89. http://dx.doi.org/10.1139/h98-022.

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Cardiac hypertrophy induced by pressure overload and following myocardial infarction entails regulation of myocardial gene expression, recapitulating an embryonic phenotype, including activation of fetal β-myosin heavy chain and skeletal α-actin. Progressive hypertrophy and alterations in gene expression may contribute to myocardial failure. Although signaling pathways that contribute to hypertrophy development have been identified, intrinsic cardiac regulators that limit hypertrophic response have not been determined. The β subunit of S100 protein is induced in the myocardium of human subjects and an experimental rat model following myocardial infarction. Forced S100β expression in neonatal rat cardiac myocyte cultures and high level expression of S100β in transgenic mice hearts inhibit cardiac hypertrophy and the associated phenotype by modulating protein kinase C-dependent pathways. S100β expression is probably a component of the myocyte response to trophic stimulation that serves as a negative feedback mechanism to limit cellular growth and the associated alterations in gene expression. Key words: gene expression, cardiac myocytes, growth factors, heart failure, calcium-binding proteins
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Tasnic, Mihail, Valeriu Revenco, and Ilia Catereniuc. "Correlations of myocardial bridges with left ventricle myocardial hypertrophy and prepontin coronary atherosclerosis." Moldovan Medical Journal 64, no. 5 (December 2021): 21–26. http://dx.doi.org/10.52418/moldovan-med-j.64-5.21.04.

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Background: Of particular interest are the studies researching the correlations of myocardial bridges with hypertrophic cardiomyopathy and correlations of thick myocardial bridges with the development of coronary atherosclerosis in the proximal to the bridge arterial part. Material and methods: Assessment of the correlation between myocardial bridges, coronary atherosclerosis, and the degree of hypertrophy of the left ventricle was performed by retrospective analysis of 6168 coronary angiography protocols (2012-2019) and echocardiographic data from patients’ clinical records. Results: Moderate systolic compression predominated, and the number of patients detected with severe under the bridge systolic coronary stenosis was double as in patients with nonsignificant coronary atherosclerosis. From the total number, patients with myocardial hypertrophy and myocardial bridges were twice less when compared with the patients with the normal myocardial thickness. The comparative research did not show any interdependence between the degree of vascular compression and the degree of left ventricular myocardial hypertrophy. Proximal to the bridges atherosclerosis was detected in 32% of cases without correlation with the force of the myocardial bridge. Conclusions: The study showed the absence of the correlation between the degree of arterial stenosis caused by the bridge and the degree of hypertrophy of the ventricular myocardium as well as the degree of proximal to the bridge atherosclerosis. Important finding was that the degree of coronary systolic compression is higher in patients with moderate and severe proximal to the bridge atherosclerosis.
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5

Ouattara, Alexandre, Olivier Langeron, Rachid Souktani, Stéphane Mouren, Pierre Coriat, and Bruno Riou. "Myocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy." Anesthesiology 95, no. 3 (September 1, 2001): 699–707. http://dx.doi.org/10.1097/00000542-200109000-00024.

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Background Myocardial effects of propofol have been previously investigated but most studies have been performed in healthy hearts. This study compared the cardiac effects of propofol on isolated normal and hypertrophic rabbits hearts. Methods The effects of propofol (10-1,000 microM) on myocardial contractility, relaxation, coronary flow and oxygen consumption were investigated in hearts from rabbits with pressure overload-induced left ventricular hypertrophy (LVH group, n = 20) after aortic abdominal banding and from sham-operated control rabbits (SHAM group, n = 10), using an isolated and erythrocyte-perfused heart model. In addition, to assess the myocardial and coronary effects of propofol in more severe LVH, hearts with a degree of hypertrophy greater than 140% were selected (severe LVH group, n = 7). Results The cardiac hypertrophy model induced significant left ventricular hypertrophy (136+/-21%, P < 0.05). The pressure-volume relation showed normal systolic function but an altered diastolic compliance in hypertrophic hearts. Propofol only decreased myocardial contractility and relaxation at supratherapeutic concentrations (> or = 300 microM) in SHAM and LVH groups. The decrease in myocardial performances was not significantly different in SHAM and LVH groups. Propofol induced a significant increase in coronary blood flow which was not significantly different between groups. In severe LVH group, the degree of hypertrophy reached to 157+/-23%. Similarly, the effects of concentrations of propofol were not significantly different from the SHAM group. Conclusions Propofol only decreased myocardial function at supratherapeutic concentrations. The myocardial and coronary effects of propofol were not significantly modified in cardiac hypertrophy.
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Lu, Dan, Jizheng Wang, Jing Li, Feifei Guan, Xu Zhang, Wei Dong, Ning Liu, Shan Gao, and Lianfeng Zhang. "Meox1 accelerates myocardial hypertrophic decompensation through Gata4." Cardiovascular Research 114, no. 2 (November 16, 2017): 300–311. http://dx.doi.org/10.1093/cvr/cvx222.

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AbstractAimsPathological hypertrophy is the result of gene network regulation, which ultimately leads to adverse cardiac remodelling and heart failure (HF) and is accompanied by the reactivation of a ‘foetal gene programme’. The Mesenchyme homeobox 1 (Meox1) gene is one of the foetal programme genes. Meox1 may play a role in embryonic development, but its regulation of pathological hypertrophy is not known. Therefore, this study investigated the effect of Meox1 on pathological hypertrophy, including familial and pressure overload-induced hypertrophy, and its potential mechanism of action.Methods and resultsMeox1 expression was markedly down-regulated in the wild-type adult mouse heart with age, and expression was up-regulated in heart tissues from familial dilated cardiomyopathy (FDCM) mice of the cTnTR141W strain, familial hypertrophic cardiomyopathy (FHCM) mice of the cTnTR92Q strain, pressure overload-induced HF mice, and hypertrophic cardiomyopathy (HCM) patients. Echocardiography, histopathology, and hypertrophic molecular markers consistently demonstrated that Meox1 overexpression exacerbated the phenotypes in FHCM and in mice with thoracic aorta constriction (TAC), and that Meox1 knockdown improved the pathological changes. Gata4 was identified as a potential downstream target of Meox1 using digital gene expression (DGE) profiling, real-time PCR, and bioinformatics analysis. Promoter activity data and chromatin immunoprecipitation (ChIP) and Gata4 knockdown analyses indicated that Meox1 acted via activation of Gata4 transcription.ConclusionMeox1 accelerated decompensation via the downstream target Gata4, at least in part directly. Meox1 and other foetal programme genes form a highly interconnected network, which offers multiple therapeutic entry points to dampen the aberrant expression of foetal genes and pathological hypertrophy.
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Chiu, Chiung-Zuan, Bao-Wei Wang, Tun-Hui Chung, and Kou-Gi Shyu. "Angiotensin II and the ERK pathway mediate the induction of myocardin by hypoxia in cultured rat neonatal cardiomyocytes." Clinical Science 119, no. 7 (June 22, 2010): 273–82. http://dx.doi.org/10.1042/cs20100084.

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Hypoxic injury to cardiomyocytes is a stress that causes cardiac pathology through cardiac-restricted gene expression. SRF (serum-response factor) and myocardin are important for cardiomyocyte growth and differentiation in response to myocardial injuries. Previous studies have indicated that AngII (angiotensin II) stimulates both myocardin expression and cardiomyocyte hypertrophy. In the present study, we evaluated the expression of myocardin and AngII after hypoxia in regulating gene transcription in neonatal cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to hypoxia, and the expression of myocardin and AngII were evaluated. Different signal transduction pathway inhibitors were used to identify the pathway(s) responsible for myocardin expression. An EMSA (electrophoretic mobility-shift assay) was used to identify myocardin/SRF binding, and a luciferase assay was used to identify transcriptional activity of myocardin/SRF in neonatal cardiomyocytes. Both myocardin and AngII expression increased after hypoxia, with AngII appearing at an earlier time point than myocardin. Myocardin expression was stimulated by AngII and ERK (extracellular-signal-regulated kinase) phosphorylation, but was suppressed by an ARB (AngII type 1 receptor blocker), an ERK pathway inhibitor and myocardin siRNA (small interfering RNA). AngII increased both myocardin expression and transcription in neonatal cardiomyocytes. Binding of myocardin/SRF was identified using an EMSA, and a luciferase assay indicated the transcription of myocardin/SRF in neonatal cardiomyocytes. Increased BNP (B-type natriuretic peptide), MHC (myosin heavy chain) and [3H]proline incorporation into cardiomyocytes was identified after hypoxia with the presence of myocardin in hypertrophic cardiomyocytes. In conclusion, hypoxia in cardiomyocytes increased myocardin expression, which is mediated by the induction of AngII and the ERK pathway, to cause cardiomyocyte hypertrophy. Myocardial hypertrophy was identified as an increase in transcriptional activities, elevated hypertrophic and cardiomyocyte phenotype markers, and morphological hypertrophic changes in cardiomyocytes.
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Liu, Xiuhua, Tianbo Li, Sheng Sun, Feifei Xu, and Yiguang Wang. "Role of myofibrillogenesis regulator-1 in myocardial hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 1 (January 2006): H279—H285. http://dx.doi.org/10.1152/ajpheart.00247.2005.

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Myofibrillogenesis regulator-1 (MR-1) is a novel homologous gene, identified from a human skeletal muscle cDNA library, that interacts with contractile proteins and exists in human myocardial myofibrils. The present study investigated MR-1 protein expression in hypertrophied myocardium and MR-1 involvement in cardiac hypertrophy. Cardiac hypertrophy was induced by abdominal aortic stenosis (AAS) in Sprague-Dawley rats. Left ventricular (LV) hypertrophy was assessed by the ratio of LV wet weight to whole heart weight (LV/HW) or LV weight to body weight (LV/BW). Rat MR-1 (rMR-1) expression in the myocardium was detected by immunohistochemical and Western blotting analysis. Hypertrophy was induced by ANG II incubation in cultured neonatal rat cardiomyocytes. The effect of rMR-1 RNA interference on ANG II-induced hypertrophy was studied by transfection of cardiomyocytes with an RNA interference plasmid, pSi-1, which targets rMR-1. Hypertrophy in cardiomyocytes was assessed by [3H]Leu incorporation and myocyte size. rMR-1 protein expression in cardiomyocytes was detected by Western blotting. We found that AAS resulted in a significant increase in LV/HW and LV/BW: 89% and 86%, respectively ( P < 0.01). Immunohistochemistry and Western blot analysis demonstrated upregulated rMR-1 protein expression in hypertrophic myocardium. ANG II induced a 24% increase in [3H]Leu incorporation and a 65.8% increase in cell size compared with control cardiomyocytes ( P < 0.01), which was prevented by treatment with losartan, an angiotensin (AT1) receptor inhibitor, or transfection with pSi-1. rMR-1 expression increased in ANG II-induced hypertrophied cardiomyocytes, and pSi-1 transfection abolished the upregulation. These findings suggest that MR-1 is associated with cardiac hypertrophy in rats in vivo and in vitro.
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Lv, Shichao, Qiang Wang, Meifang Wu, Meng Li, Xiaojing Wang, Ling Xu, and Junping Zhang. "QiShenYiQi Pill Improves Myocardial Hypertrophy Caused by Pressure Overload in Rats." Evidence-Based Complementary and Alternative Medicine 2021 (June 16, 2021): 1–10. http://dx.doi.org/10.1155/2021/5536723.

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Pressure-overloaded myocardial hypertrophy is an independent risk factor for various cardiovascular diseases (CVDs), such as heart failure (HF), arrhythmia, and even sudden death. It is reported that QiShenYiQi pill (QSYQ) is widely used in the treatment of CVDs and can prevent pathological hypertrophy of myocardium, but its specific mechanism is still unclear. In this study, a rat model of myocardial hypertrophy was established through the pressure overload caused by abdominal aortic constriction in Wistar rats. The rats were randomly divided into model group, valsartan group, and QSYQ group, and sham-operated animals served as the control group. At the 4 and 8 weeks of intervention, the general morphology of the heart, myocardial collagen content, collagen volume factor (CVF), collagen type I, collagen type III, myocardial pathological changes, and the expression of ANP, β-MHC, TGF-β1, and CTGF were analyzed, respectively, in order to explore the possible effect of QSYQ on the mechanism of myocardial hypertrophy. We observed that QSYQ could effectively improve myocardial hypertrophy in pressure-overloaded rats, which was related to the regulatory mechanism of TGF-β1 and CTGF.
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Zheng, Xi, Fuxiang Su, Ze Kang, Jingyuan Li, Chenyang Zhang, Yujia Zhang, and Liying Hao. "Analysis of Therapeutic Targets of A Novel Peptide Athycaltide-1 in the Treatment of Isoproterenol-Induced Pathological Myocardial Hypertrophy." Cardiovascular Therapeutics 2022 (May 2, 2022): 1–13. http://dx.doi.org/10.1155/2022/2715084.

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Myocardial hypertrophy is a pathological feature of many heart diseases. This is a complex process involving all types of cells in the heart and interactions with circulating cells. This study is aimed at identifying the differentially expressed proteins (DEPs) in myocardial hypertrophy rats induced by isoprenaline (ISO) and treated with novel peptide Athycaltide-1 (ATH-1) and exploring the mechanism of its improvement. ITRAQ was performed to compare the three different heart states in control group, ISO group, and ATH-1 group. Pairwise comparison showed that there were 121 DEPs in ISO/control (96 upregulated and 25 downregulated), 47 DEPs in ATH-1/ISO (27 upregulated and 20 downregulated), and 116 DEPs in ATH-1/control (77 upregulated and 39 downregulated). Protein network analysis was then performed using the STRING software. Functional analysis revealed that Hspa1 protein, oxidative stress, and MAPK signaling pathway were significantly involved in the occurrence and development of myocardial hypertrophy, which was further validated by vivo model. It is proved that ATH-1 can reduce the expression of Hspa1 protein and the level of oxidative stress in hypertrophic myocardium and further inhibit the phosphorylation of p38 MAPK, JNK, and ERK1/2.
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Dissertations / Theses on the topic "Myocardial hypertrophy"

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Wallis, William Richard James. "The cellular pathophysiology of myocardial hypertrophy." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265997.

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Jager, Tertia de. "Estrogen action in the myocardium modulation of myocardial gene expression and the influence on cardiac hypertrophy /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964433621.

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Drawnel, Faye Marie. "Control of myocardial hypertrophic remodelling by integration of calcium signals, kinase cascades and microRNAs." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609969.

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Willems, Ingrid E. M. G. "The interstitium in myocardial infarction and hypertrophy experimental and clinical observations /." [Maastricht : Maastricht : Rijksuniversiteit Limburg] ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=5779.

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Senanayake, Eshan Lankapura. "Left ventricular hypertrophy and myocardial protection with perhexiline during cardiac surgery." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5942/.

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Myocardial protective strategies during cardiac surgery continue to improve yet they remain imperfect. Patients with left ventricular hypertrophy (LVH) are considered to be at greater risk of myocardial injury post cardiac surgery. Perhexiline is an anti-anginal agent known to modulate myocardial metabolism towards a more efficient glucose metabolic pathway. This metabolic modulation may improve myocardial protection. In this thesis I present a multi-centre double-blind randomised placebo controlled trial evaluating the role of perhexiline as an adjunct to standard myocardial protection in patients with LVH secondary to aortic stenosis undergoing an aortic valve replacement. Perhexiline does not augment myocardial protection. Magnetic Resonance Spectroscopy based energetic studies, echocardiographic and functional assessments in a homogenous patient cohort show no added benefit with perhexiline therapy in LVH. Therefore perhexiline should be limited to those patients refractory to maximum medical therapy. Metabolomic assessment of LVH has shown no change in the metabolomic profile within the myocardium. However any changes that do exist may be subtle. In LVH there is an increased activity of some innate cardioprotective mechanistic pathways in patients that do not sustain a low cardiac output episode post cardiac surgery. Further examination of these cardioprotective regulators is warranted.
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Crampton, Matthew S., and n/a. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070104.165826.

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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
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Crampton, Matthew S. "Differential Gene Expression in Pathological and Physiological Cardiac Hypertrophy." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/366605.

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Cardiac hypertrophy defines an adaptive process brought about in response to sustained increases in haemodynamic work. Cardiomyocytes undergo an initial compensatory phase in which enlargement and contractility alterations normalise wall stress and maintain adequate perfusion of organs. In pathological hypertrophy, this deteriorates to a decompensated state characterised by ventricular dysfunction and predisposition to heart failure. In contrast, physiological hypertrophy and associated enhanced cardiac functioning arising from chronic exercise training does not progress to heart failure. Determination of the molecular pathways underlying myocardial hypertrophy remains a challenge for cardiovascular research. The objective of the work presented in this thesis was to identify genes differentially expressed during pathological and physiological hypertrophy in order to enhance our knowledge of the mechanistic processes involved. A reverse Northern hybridisation method was applied to profile the expression of specifically selected genes in the hypertrophic models examined. Functional categories represented in the gene panel assembled included cardiac contractile and cytoskeletal markers, matrix metalloproteinases, vasoactive pathway factors, calcium handling genes, ion channels, cardiac regulatory factors, signalling pathway intermediates, apoptotic factors and histone deacetylases. In order to investigate pathological hypertrophy, a deoxycorticosterone acetate-salt (DOCA-salt) rat model was utilised. DOCA-salt treated rats used in this study demonstrated a 1.4-fold increase in heart weight to body weight ratio compared to controls. Impaired cardiac function indicative of a decompensated pathological phenotype in the DOCA-salt treated group was demonstrated by way of decreased chamber size, impaired myocardial compliance and significantly reduced cardiac output. Reverse Northern hybridisation analysis of 95 selected genes identified a number of candidates with differential expression in hearts of DOCA-salt treated rats. Increased gene expression was demonstrated for the collagenase MMP1 and stress-activated signal transduction factor Sin1. In contrast, the sarcoplasmic reticulum calcium ATPase SERCA-2 and anti-apoptotic factor BCL2l-10 genes exhibited decreased expression. To investigate changes in gene expression associated with physiological hypertrophy, use was made of an endurance run-trained rat model. The run-trained rats used in this study demonstrated a 24.1% increase in heart weight to body weight ratio and improvements in performance consistent with physiological cardiac adaptation. These performance indicators included improvements in systolic volume, cardiac output, myocardial compliance and bio-energetic function. Reverse Northern hybridisation expression analysis of 56 genes identified a number of differentially expressed mRNA transcripts in run-trained hypertrophied hearts. Four genes shown to demonstrate reduced expression in the run-trained rat model were interleukin-1 receptor associated kinase (IRAK1) and the developmentally expressed transcription factors Nkx-2.3, dHAND, and IRX-2. Based upon the reverse Northern hybridisation results, four genes were selected for Western blotting analysis of rat cardiac tissue. Of these, MMP1 and a putative isoform of Sin1 exhibited increased levels in DOCA-salt treated hypertrophic left ventricular tissue, results that correlate with the findings of increased mRNA expression for these two genes. Therefore, this study identified MMP1 and Sin1 as candidates involved in pathological but not physiological hypertrophy. This finding is in accord with other recent investigations demonstrating that pathological hypertrophy and physiological hypertrophy are associated with distinct molecular phenotypes. An aside to the major objective of identifying genes differentially regulated in left ventricular hypertrophy involved the application of the P19CL6 cell in vitro model of cardiomyogenesis to compare protein expression during hypertrophy and development. The Sin1 isoform, found to be up-regulated during DOCA-salt induced hypertrophy, was also shown to be more abundant in differentiating, than non-differentiating, P19CL6 cells. This result is consistent with the developing paradigm that implicates 'fetal' genes in the hypertrophic remodelling process.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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TAKEMURA, Haruki, Noriko NIWA, Mayumi HOJO, Jong-Kook LEE, Kenji YASUI, Yuichi UEDA, and Itsuo KODAMA. "Altered I_f Channel Gene Expression in Mouse Hearts after Myocardial Infarction." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2794.

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Takemura, Haruki, Kenji Yasui, Noriko Niwa, Mayumi Hojo, Mitsuru Horiba, Jong-Kook Lee, Ueda Yuichi, and Itsuo Kodama. "Down-regulation of Connexin 43 mRNA in Mouse Hearts after Myocardial Infarction." Research Institute of Environmental Medicine, Nagoya University, 2003. http://hdl.handle.net/2237/7571.

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Sneddon, Kenneth Paxton. "Dispersion of repolarisation and refractoriness induced by amiodarone, d-sotalol, myocardial ischaemia and hypertrophy." Thesis, University of Glasgow, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300739.

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Books on the topic "Myocardial hypertrophy"

1

Yang, Phillip Chung-Ming. Hypertrophic response in primary single-cell culture of adult rat myocardial cells. [New Haven: s.n.], 1989.

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Green, Nicola Kim. Regulation of rat myocardial gene expression by thyroid status and in experimental models of cardiac hypertrophy. Birmingham: University of Birmingham, 1991.

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A, Raineri, Leachman Robert D, and International School of Medical Sciences (1990 : Ettore Majorana Centre for Scientific Culture), eds. The big heart: Proceedings of a course held at the International School of Medical Sciences, Ettore Majorana Centre for Scientific Culture, Italy, 2-8 April 1990. Chur, Switzerland: Harwood Academic Publishers, 1994.

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Swynghedauw, B. Hypertrophie et insuffisance cardiaques. Paris: Editions INSERM, 1990.

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Cooklin, Michael J. The effects of hypertrophy on action potential conduction in myocardium. Manchester: University of Manchester, 1995.

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M, Carlson Bruce, ed. Growth and hyperplasia of cardiac muscle cells. London, U.K: Harwood Academic Publishers, 1991.

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C, Claycomb William, Di Nardo Paolo, and New York Academy of Sciences., eds. Cardiac growth and regeneration. New York, N.Y: New York Academy of Sciences, 1995.

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Ball, Warren Todd. Expression of IGF-I and TGF[beta]-1 in cultured human myocardium insights into the role of growth factors in hypertrophic obstructive cariomyopathy. Ottawa: National Library of Canada, 1998.

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1929-, Ison-Franklin Eleanor L., Sandler Harold 1929-, and Hawthorne Edward William 1922-1986, eds. Myocardial hypertrophy: A symposium. Washington, D.C: Howard University Press, 1991.

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Ison-Franklin, Eleanor L. Myocardial Hypertrophy: A Symposium. Howard Univ Pr, 1991.

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Book chapters on the topic "Myocardial hypertrophy"

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Cokkinos, Dennis V. "Cardiac Hypertrophy." In Myocardial Preservation, 63–86. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_5.

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Hamrell, Burt B., and Norman R. Alpert. "Experimental Myocardial Hypertrophy." In The Ventricle, 185–207. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2599-4_9.

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Kontaridis, Maria Irene, Eleni V. Geladari, and Charalampia V. Geladari. "Pathways to Myocardial Hypertrophy." In Introduction to Translational Cardiovascular Research, 167–86. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08798-6_10.

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van Dantzig, J. M., R. Bronsaer, and P. A. F. M. Doevendans. "Myocardial Hypertrophy and Failure: A Molecular Approach." In Left Ventricular Hypertrophy, 151–61. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_12.

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Salerno, Michael, and Christopher M. Kramer. "T1 Mapping in Cardiac Hypertrophy." In T1-Mapping in Myocardial Disease, 15–25. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-91110-6_2.

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Weiss, H. R., and G. J. Grover. "Coronary reserves in myocardial hypertrophy." In Developments in Cardiovascular Medicine, 567–82. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3313-2_36.

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Bache, Robert J. "Coronary Circulation in Myocardial Hypertrophy." In Coronary Circulation, 235–43. Tokyo: Springer Japan, 1990. http://dx.doi.org/10.1007/978-4-431-68087-1_18.

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Camilión de Hurtado, María C., Néstor G. Pérez, Irene L. Ennis, Bernardo V. Alvarez, and Horacio E. Cingolani. "Na+/H+ Exchanger and Myocardial Hypertrophy." In Signal Transduction and Cardiac Hypertrophy, 125–35. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_10.

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Chilian, William M., Robert J. Tomanek, and Melvin L. Marcus. "The Coronary Vasculature During Myocardial Hypertrophy." In Developments in Cardiovascular Medicine, 87–105. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2041-8_5.

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Isoyama, Shogen. "Interplay of Hypertrophy and Myocardial Ischemia." In Diastolic Relaxation of the Heart, 203–11. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2594-3_21.

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Conference papers on the topic "Myocardial hypertrophy"

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Zhang, Pei, Tieluo Li, Katrina Williams, Shuyin Li, Xufeng Wei, Hosung Son, Pablo Sanchez, Bartley P. Griffith, and Zhongjun J. Wu. "Analysis of Infarct Size on Myocardial Infarction Remodeling." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53117.

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In the United States, over one million patients sustain left ventricular (LV) injury after myocardial infarction (MI). LV remodeling is an adaptive process of hypertrophy that includes infarct expansion, reduced contractility and LV dilation. Progressive enlargement of non-ischemic, hypocontractile myocardium in the adjacent zone (AZ) following the transmural MI has been identified clinically, which contributes to the development post-MI cardiomyopathy in patients. Till now, how the early regional biomechanical and cellular changes, particularly in the AZ, relate to LV remodeling process remains incompletely understood. This study aims to investigate the temporal and/or spatial variations of strain/stress and myocyte size in an ovine model with various MI sizes.
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Goktepe, Serdar, Joseph P. Ulerich, and Ellen Kuhl. "How to Treat the Loss of Beat: Modeling and Simulation of Ventricular Growth and Remodeling and Novel Post-Infarction Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193159.

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Heart disease is the primary cause of death in industrialized nations. In 2007 alone, an estimated 79 million adults in the U.S., one in three, had one or more types of cardiovascular disease, generating health care costs in excess of $430 billion. A leading cause of congestive heart failure is myocardial infarction. Within the first few hours after the infarct, a complex cascade of events is initiated in the myocardium manifesting itself clinically in disproportionate thinning and dilation of the infarct region accompanied by distortion in form and function of the entire heart, figure 1. As remodeling progresses, volume-overloaded hypertrophy and further deterioration of cardiac function are common natural consequences. Historically, therapies for myocardial infarction have been developed by trial and error methods, as opposed to therapy design and development through scientific understanding of the functional and structural changes in the infarcted tissue. Continuum theories, in combination with modern computer simulation technologies, offer the potential to provide greater insight into the complex pathways of myocardial infarction, and thereby guide the design of successful post-infarction therapies such as direct cell injection into the damaged myocardium1 and implantation of tissue engineered vascular grafts2 as sketched in figure 1.
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Das, Ashish, William Gottliebson, and Rupak K. Banerjee. "Comparison of Right Ventricular Stroke Work for Tetralogy Patient and Normal Subject." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193145.

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Tetralogy of Fallot (TOF), also called blue-baby syndrome is one of the most common congenital heart defects in children after infancy and is estimated to account for 10% of all congenital heart defects [3]. TOF consists of four interrelated lesions: i) ventricular septal defect ii) Pulmonary stenosis iii) Right ventricular (RV) hypertrophy and (iv) Overriding Aorta [3]. TOF has been successfully repaired for several decades (Fig. 1). There are now an estimated 100,000 adult “repaired TOF” patients in the United States alone. As a result, long-term sequelae of the disease and repair have become important clinical issue. Specifically, residual pulmonary valve insufficiency (PI) is one such accepted and often unavoidable sequela. PI, when severe, abnormally alters the RV loading conditions, thereby triggering RV hypertrophy and dilatation. In turn, RV dilatation can evolve into irreversible RV myocardial contractile dysfunction, and has been related to sudden death in many “repaired TOF” patients. To normalize RV loading conditions, pulmonary valve replacement is often necessary and should be performed prior to the onset of irreversible RV myocardial damage.
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Navitsky, Michael A., Steven Deutsch, and Keefe B. Manning. "A Comparison of Thrombus Susceptibility for Two Pulsatile 50 CC Left Ventricular Assist Pumps." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80570.

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Approximately 5.7 million Americans are afflicted with heart disease, with a reported 670,000 new cases and 300,000 deaths each year [1]. While the success rate of transplantation procedures continues to improve, organ availability remains limited. Left ventricular assist devices (LVADs) function as a bridge to transplant for advanced staged heart failure patients awaiting a donor heart. The devices have also been used, more recently, as a bridge to recovery by helping to unload the native ventricle. Along with pharmacological intervention, LVADs can act to help reverse pathological hypertrophy and recover normal myocardial function [2].
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Ulerich, Joseph P., Serdar Goktepe, and Ellen Kuhl. "First Attempts Towards the Computational Simulation of Novel Stem-Cell Based Post Infarct Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192715.

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Cardiac disease is the most common cause of death in developed nations and affects more than 80 million American adults every year. Among cardiac diseases, myocardial infarction is one of the leading causes of congestive heart failure. Due to an infarct, the loads within the heart alter and within hours a remodeling process begins as the heart attempts to optimize function given its diminished capacity. This remodeling process itself can cause inconsistent thinning and dilation leading to potential problems such as volume overloaded hypertrophy and often causes further functional deterioration.
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Engel, Emily, Zhongjun J. Wu, and Bartley P. Griffith. "Early Remodeling Strain Levels Can Predict the Progression of Remodeling of the Left Ventricle Post Myocardial Infarction." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19442.

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Over one million patients are affected with left ventricular (LV) injury annually after sustaining a myocardial infarction (MI). In order to compensate for the loss in pumping function, the heart undergoes changes meant to maintain homeostasis. This process actually leads to a remodeling process that is initially compensatory and later becomes maladaptive. Remodeling after MI often involves loss of contractility and hypertrophy of the LV in response to increased loading conditions. Some patients are able to recover with the use of medicine and surgical intervention. However, others experience a progression of the remodeling process which leads to LV dysfunction and heart failure as the heart becomes more spherical and loses its ability to effectively contract. [1]
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Huwez, F. U., and P. W. Macfarlane. "The influence of Q-wave acute anteroseptal myocardial infarction on the voltage criteria for left ventricular hypertrophy." In Computers in Cardiology, 2003. IEEE, 2003. http://dx.doi.org/10.1109/cic.2003.1291282.

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Zhmurov, V. A., D. V. Zhmurov, and V. G. Yarkova. "CHRONIC KIDNEY DISEASE AND THE STATE OF THE CARDIOVASCULAR SYSTEM IN LOCOMOTIVE CREW WORKERS." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-208-211.

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Abstract: 967 employees of locomotive crews (drivers and their assistants of the Sverdlovsk railway of JSC «Russian Railways») were examined. It was revealed that CKD occurs in 12, 09% of employees of locomotive crews. As the CKD stage increases, the progression of changes in the cardiovascular system was found in locomotive crew workers. A high percentage of the prognostically unfavorable variant of left ventricular remodeling - eccentric myocardial hypertrophy (25% - 39.1%, depending on the stage of CKD) was found. These changes may be a factor of adverse cardiovascular events in employees of locomotive crews, which must be taken into account when admitting to professional activities.
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Cabrera Solé, Ricardo. "Non invasive Measurements of Myocardial Hypertrophy in Patients with Essential Hypertension Treated with Eprosartan: Contribution of the Physics." In FRONTIERS OF FUNDAMENTAL PHYSICS: Eighth International Symposium FFP8. AIP, 2007. http://dx.doi.org/10.1063/1.2737000.

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Li, Le, Hao Shang, Cailing Zhang, Houquan Tao, and Jirkun Cheng. "Fasudil Protects Against the Myocardial Hypertrophy of Transverse Aortic Constriction Via Modulating the Expression of Caspase-3 and Bcl-2 Protein." In International Conference on Biomedical and Biological Engineering. Paris, France: Atlantis Press, 2016. http://dx.doi.org/10.2991/bbe-16.2016.47.

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