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Relevant bibliographies by topics / Myocardial remodeling

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Academic literature on the topic 'Myocardial remodeling'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 May 2022

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Journal articles on the topic "Myocardial remodeling"

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Hellawell, Jennifer L., and Kenneth B. Margulies. "Myocardial Reverse Remodeling." Cardiovascular Therapeutics 30, no. 3 (November 25, 2010): 172–81. http://dx.doi.org/10.1111/j.1755-5922.2010.00247.x.

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Ushakov, Alexey, Vera Ivanchenko, and Alina Gagarina. "Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling." Current Cardiology Reviews 16, no. 1 (January 28, 2020): 11–24. http://dx.doi.org/10.2174/1573403x15666190509090832.

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The article represents literature review dedicated to molecular and cellular mechanisms underlying clinical manifestations and outcomes of acute myocardial infarction. Extracellular matrix adaptive changes are described in detail as one of the most important factors contributing to healing of damaged myocardium and post-infarction cardiac remodeling. Extracellular matrix is reviewed as dynamic constantly remodeling structure that plays a pivotal role in myocardial repair. The role of matrix metalloproteinases and their tissue inhibitors in fragmentation and degradation of extracellular matrix as well as in myocardium healing is discussed. This review provides current information about fibroblasts activity, the role of growth factors, particularly transforming growth factor β and cardiotrophin-1, colony-stimulating factors, adipokines and gastrointestinal hormones, various matricellular proteins. In conclusion considering the fact that dynamic transformation of extracellular matrix after myocardial ischemic damage plays a pivotal role in myocardial infarction outcomes and prognosis, we suggest a high importance of further investigation of mechanisms underlying extracellular matrix remodeling and cell-matrix interactions in cardiovascular diseases.

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Bhattacharya, Aniket, Nadia Al-Sammarraie, Mengistu G. Gebere, John Johnson, John F. Eberth, and Mohamad Azhar. "Myocardial TGFβ2 Is Required for Atrioventricular Cushion Remodeling and Myocardial Development." Journal of Cardiovascular Development and Disease 8, no. 3 (March 2, 2021): 26. http://dx.doi.org/10.3390/jcdd8030026.

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Among the three transforming growth factor beta (TGFβ) ligands, TGFβ2 is essential for heart development and is produced by multiple cell types, including myocardium. Heterozygous mutations in TGFB2 in patients of connective tissue disorders result in congenital heart defects and adult valve malformations, including mitral valve prolapse (MVP) with or without regurgitation. Tgfb2 germline knockout fetuses exhibit multiple cardiac defects but the role of myocardial-TGFβ2 in heart development is yet to be elucidated. Here, myocardial Tgfb2 conditional knockout (CKO) embryos were generated by crossing Tgfb2flox mice with Tgfb2+/−; cTntCre mice. Tgfb2flox/− embryos were normal, viable. Cell fate mapping was done using dual-fluorescent mT/mG+/− mice. Cre-mediated Tgfb2 deletion was assessed by genomic PCR. RNAscope in situ hybridization was used to detect the loss of myocardial Tgfb2 expression. Histological, morphometric, immunohistochemical, and in situ hybridization analyses of CKOs and littermate controls at different stages of heart development (E12.5–E18.5) were used to determine the role of myocardium-derived TGFβ2 in atrioventricular (AV) cushion remodeling and myocardial development. CKOs exhibit a thin ventricular myocardium, AV cushion remodeling defects and developed incomplete AV septation defects. The loss of myocardial Tgfb2 resulted in impaired cushion maturation and dysregulated cell death. Phosphorylated SMAD2, a surrogate for TGFβ signaling, was “paradoxically” increased in both AV cushion mesenchyme and ventricular myocardium in the CKOs. Our results indicate that TGFβ2 produced by cardiomyocytes acting as cells autonomously on myocardium and via paracrine signaling on AV cushions are required for heart development.

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Honjo, Haruo. "Myocardial Remodeling and Arrhythmogenesis." Japanese Journal of Electrocardiology 34, no. 1 (2014): 37–44. http://dx.doi.org/10.5105/jse.34.37.

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Gropler, R. J., R. S. B. Beanlands, V. Dilsizian, E. D. Lewandowski, F. S. Villanueva, and M. C. Ziadi. "Imaging Myocardial Metabolic Remodeling." Journal of Nuclear Medicine 51, Supplement_1 (May 1, 2010): 88S—101S. http://dx.doi.org/10.2967/jnumed.109.068197.

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RAO, VIJAY U., and FRANCIS G. SPINALE. "Controlling Myocardial Matrix Remodeling." Cardiology in Review 7, no. 3 (May 1999): 136–43. http://dx.doi.org/10.1097/00045415-199905000-00010.

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Nadruz, W. "Myocardial remodeling in hypertension." Journal of Human Hypertension 29, no. 1 (May 8, 2014): 1–6. http://dx.doi.org/10.1038/jhh.2014.36.

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Vasques-Nóvoa, Francisco, António Angélico-Gonçalves, Nuno Bettencourt, Adelino F. Leite-Moreira, and Roberto Roncon-Albuquerque. "Myocardial Edema and Remodeling." Journal of the American College of Cardiology 75, no. 12 (March 2020): 1497–98. http://dx.doi.org/10.1016/j.jacc.2019.12.071.

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Cokkinos, Dennis V., and Costas Pantos. "Myocardial remodeling, an overview." Heart Failure Reviews 16, no. 1 (September 26, 2010): 1–4. http://dx.doi.org/10.1007/s10741-010-9192-4.

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Chaanine, Antoine H. "Autophagy and Myocardial Remodeling." Journal of the American College of Cardiology 71, no. 18 (May 2018): 2011–14. http://dx.doi.org/10.1016/j.jacc.2018.02.067.

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Dissertations / Theses on the topic "Myocardial remodeling"

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Agarwal, Udit. "Factors Affecting Ventricular Remodeling Post Myocardial Infarction." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1269627876.

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McDevitt, Todd C. "Spatially controlled engineering of myocardial tissue /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/8090.

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Krimpen, Cornelis van. "Cardiac remodeling and angiotensin II after an experimental myocardial infarction." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1991. http://arno.unimaas.nl/show.cgi?fid=5677.

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Daniels, Christopher Ray. "Extracellular Ubiquitin: Role in Cardiac Myocyte Apoptosis and Myocardial Remodeling." Digital Commons @ East Tennessee State University, 2014. https://dc.etsu.edu/etd/2341.

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Activation of sympathetic nervous system is a key component of myocardial remodeling that generally occurs following ischemia/reperfusion (I/R) injury and myocardial infarction. It induces cardiac myocyte apoptosis and myocardial fibrosis, leading to myocardial dysfunction. Intracellular ubiquitin (UB) regulates protein turnover by the UB-proteosome pathway. The biological functions of extracellular UB in the heart remain largely unexplored. Previously, our lab has shown that β-adrenergic receptor (β-AR) stimulation increases extracellular UB levels, and extracellular UB inhibits β-AR-stimulated apoptosis in adult rat ventricular myocytes (ARVMs). This study explores the role of extracellular UB in myocyte apoptosis, fibroblast phenotype and function, and myocardial remodeling following β-AR stimulation and I/R injury. First, left ventricular (LV) structural and functional remodeling was studied 7 days after chronic β-AR-stimulation in the presence or absence of UB infusion. Echocardiographic analyses showed UB infusion decreases β-AR-stimulated increases in percent fractional shortening and ejection fraction. It decreased cardiac myocyte apoptosis and myocardial fibrosis. UB activated Akt, and inhibition of Akt inhibited β-AR-stimulated increases in matrix metalloproteinase-2 expression. Second, using cardiac fibroblasts, we provide evidence that extracellular UB interacts with the cell surface and co-immunoprecipitates with CXCR4. UB treatment increased expression of α-smooth muscle actin (myofibroblast marker), and induced rearrangement of actin into stress fibers. It inhibited lamellopodia and filopodia formation, and cell migration into the wound. Third, using isolated mouse heart and I/R injury as a model, we provide evidence that UB treatment decreases I/R-mediated increases in infarct size. UB treatment improved functional recovery of the heart as measured by increased % LV developed pressure. Activation of proapoptotic proteins, p-STAT-1 and caspase-9, was significantly lower in UB I/R hearts versus I/R alone. In ARVMs, UB treatment decreased simulated I/R-induced apoptosis. It activated Akt (anti-apoptotic kinase) and inhibited activation of GSK-3β (pro-apoptotic kinase). It decreased I/R-induced oxidative stress and protected anoxia-induced mitochondrial polarization. In fibroblast and ARVMs, CXCR4 antagonism negated the effects of UB, while mutated UBs (unable to interact with CXCR4) had no effect. Thus, extracellular UB, most likely acting via CXCR4, modulates myocardial remodeling with effects on heart function, fibroblast phenotype and function and myocyte apoptosis.

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Атаман, Юрій Олександрович, Юрий Александрович Атаман, Yurii Oleksandrovych Ataman, O. A. Vorozhko, and O. S. Voloshin. "Structural and functional features of myocardial remodeling in professional athletes." Thesis, Сумський державний університет, 2018. http://essuir.sumdu.edu.ua/handle/123456789/71676.

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Shao, Qiming. "Membrane remodeling in heart failure due to myocardial infarction in rats." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23662.pdf.

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Liao, Songyan, and 廖松岩. "Novel therapies for prevention of left ventricular remodeling following myocardial infarction." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197141.

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Heart failure (HF) following myocardial infarction (MI) is the leading cause of mortality and morbidity worldwide. Existing medical and interventional therapies can only reduce the cardiomyocytes (CMs) lost during MI. They are unable to replenish the permanent loss of CMs and this contributes to progressive pathological left ventricular (LV) remodeling and HF. Cell-based therapies using adult stem cells or embryonic stem cells (ESCs) and their cardiac derivatives have frequently been explored as a potential therapeutic approach to restore cardiac function in HF. The objectives of this thesis are to evaluate the efficacy and safety of different approaches of stem cell based therapy to improve cardiac function using small and large animal MI models. In Chapter 3, we studied the functional consequences of direct intramyocardial transplantation of ESCs and ESC-derived cardiomyocytes (ESC-CMs) in a murine model of acute MI. LV ejection fraction (LVEF) and maximal positive or negative pressure derivative (dP/dt) improved 4 weeks after transplantation of either ESCs or ESC-CMs. Nevertheless there was a higher incidence of inducible ventricular tachyarrhythmia (VT) and higher mortality in animals transplanted with ESC-CMs than those with ESCs. At a single cell level, ESC-CMs exhibited immature electrophysiological properties such as depolarized resting membrane potential (RMP), longer action potential duration (APD) and automaticity. In Chapter 4, we tested the hypothesis that genetic modification of these immature electrophysiological properties of ESC-CMs by overexpression of Kir2.1 gene encoding the ion channels for IK1, may alleviate the pro-arrhythmic risk. In this study, Kir2.1 channels expression could be controlled with the administration of doxycycline (DOX). The DOX-treated ESC-CMs were more mature with hyperpolarized RMP and shorter APD than their counterparts without DOX treatment. A similar improvement in LV systolic function was observed 4 weeks after both DOX treated and untreated ESCCMs transplantation, although those animals transplanted with DOX-treated ESC-CMs had a significantly lower incidence of spontaneous and inducible VT. Histological analysis in both studies suggested that the major mechanisms of improvement in cardiac function were related to angiogenesis and low apoptosis rate of native cardiomyocytes mediated via paracrine effects. Importantly, very limited retention of ESC-CMs was observed 4 weeks after transplantation. Cell-based patches that use different bioengineering techniques have been proposed to improve cell retention and survival following transplantation. In Chapter 5, the efficacy of a passive epicardial patch was tested in a chronic large animal MI model with HF created with catheter-based coronary embolization. The implantation of an epicardical patch over the infarcted LV region was performed 8 weeks after MI in pigs with impaired LVEF. At week 20, pigs implanted with epicardical patches had significantly thicker LV wall thickness at the infarction sites, smaller LV dilation and better LV systolic function compared with control animals. The expression of MMP-9 was significant lower in the epicardical patch group at the peri-infarct zones. These findings suggested that a passive epicardial patch can improve LV function in HF and provides important proof-of-principle data to support its use as a platform for delivery of cell-based therapies after MI.
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Medicine
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Chaggar, Parminder. "Plasma cytokines and markers of remodeling in myocardial injury and repair." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/plasma-cytokines-and-markers-of-remodeling-in-myocardial-injury-and-repair(ea82d837-8825-4f1e-ac75-890458294eff).html.

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Introduction: The heart failure (HF) phenotype is associated with multiple pathological changes at the cellular/biochemical level but this is not always a permanent state, despite sometimes extremely severe clinical and echocardiographic features. However, the underlying molecular and inflammatory processes are incompletely understood and often, contradictory effects are reported. This study examines a wide array of plasma pro-inflammatory markers and remodeling proteins in experimentally induced HF and recovery. Methods: Plasma IFNÎ3, CXCL-9, IP-10, IL-21, IL-17A, TNFÎ±, decorin, sFRP-3 and VEGF-A patterns were assessed in a series of ovine models; 8 sheep that underwent tachypaced-induced HF and recovery with cessation of pacing (Recovery group); 7 sheep that underwent tachypaced-induced asymptomatic LV dysfunction and subsequent treatment with tadalafil to prevent clinical deterioration in the context of continued tachypacing (Tadalafil sheep); and 5 sheep that underwent acute myocardial ischaemia-reperfusion injury (MI group). Baseline inflammatory profiles and remodeling proteins were validated in a separate cohort of 10 healthy sheep that underwent a comprehensive frailty assessment. Results: There was a borderline inverse association between IFNÎ3 with clinical HF in the Recovery group but no correlation with LV function. High baseline levels of pro-inflammatory cytokines did not impact on susceptibility to, severity of, or recovery from HF in sheep exposed to tachycardic pacing. Furthermore, plasma decorin increases significantly with tachypaced-HF and remains elevated despite improved LV function or tadalafil treatment. Conclusion: The present study has examined a broad inflammatory profile in HF and recovery, including those mediated via TH1 (IFNÎ3, CXCL-9 and IP-10), TH2 (IL-21), TH17 (IL-17A) and monocyte (TNFÎ±) cell lineages. The findings demonstrate that systemic inflammation has no impact on susceptibility to, severity of, or recovery from HF in sheep exposed to tachycardic pacing. The findings of this study may draw into question whether the immune system plays a pivotal role in HF disease progression and severity although further research is required before definitive conclusions can be secured. Furthermore, this study demonstrates plasma decorin increases significantly with the development of HF. This may represent a physiological response to attenuate the effects of adverse remodeling in HF. This is the first study to demonstrate temporal changes in plasma decorin during both myocardial injury and recovery in a large mammal. Decorin may serve as a biomarker of myocardial injury and could be a target for therapeutic manipulation. These findings require validation in a larger series.

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Singh, Mahipal, Cerrone R. Foster, Suman Dalal, and Krishna Singh. "Osteopontin: Role in Extracellular Matrix Deposition and Myocardial Remodeling Post-MI." Digital Commons @ East Tennessee State University, 2010. https://dc.etsu.edu/etsu-works/8576.

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Remodeling after myocardial infarction (MI) associates with left ventricular (LV) dilation, decreased cardiac function and increased mortality. The dynamic synthesis and breakdown of extracellular matrix (ECM) proteins play a significant role in myocardial remodeling post-MI. Expression of osteopontin (OPN) increases in the heart post-MI. Evidence has been provided that lack of OPN induces LV dilation which associates with decreased collagen synthesis and deposition. Inhibition of matrix metalloproteinases, key players in ECM remodeling process post-MI, increased ECM deposition (fibrosis) and improved LV function in mice lacking OPN after MI. This review summarizes — 1) signaling pathways leading to increased expression of OPN in the heart; 2) the alterations in the structure and function of the heart post-MI in mice lacking OPN; and 3) mechanisms involved in OPN-mediated ECM remodeling post-MI.

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McLaughlin, Sarah Joan Margaret. "Human Recombinant Collagen Hydrogel for Control of Ventricular Remodeling and Repair After Myocardial Infarction." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42543.

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Myocardial infarction (MI) leads to permanent loss of cardiac muscle due to the limited regenerative potential of the mammalian heart. The affected heart muscle is replaced by a fibrotic scar; however, the scar is not able to offset the increase in wall stress placed on the remaining myocardium. This distending pressure can lead to dilative remodeling of the ventricle, progressive loss of cardiac function, and heart failure. Despite current medical therapy, heart failure continues to have a high mortality rate. Therefore, there is a clinical need for treatments that can both improve cardiac function post-MI and reduce ventricular remodeling to prevent progression to heart failure. Injectable biomaterials aim to provide a scaffold to stimulate infarct repair by mimicking the healthy cardiac extracellular matrix (ECM). The ECM plays a critical role in tissue regeneration but after a MI it is pathologically modified. Injection of biomaterials post-MI can provide a scaffold that better stimulates infarct repair. In this study, hydrogels were developed from recombinant human type I and type III collagen (rHCI and rHCIII), the two most prevalent structural proteins in the cardiac ECM. Injection of rHCI and rHCIII hydrogels in a mouse model of MI improved cardiac function and reduced infarct size 28 days post-treatment. Infarcted hearts treated with rHCI exhibited improved myocardial salvage in the region bordering the scar with improved capillary density. rHCI hydrogel was also superior to rHCIII in reducing ventricular remodeling. The injection of rHCI hydrogel into the border zone post-MI resulted in an acute improvement of contractile function two days after treatment that was maintained long-term. At two days post-injection, rHCI treated animals had reduced apoptotic cardiomyocytes and lower levels of oxidative stress. Methylglyoxal modifies and crosslinks collagen in the ECM, leading to oxidative stress. Two days after injection, the rHCI hydrogel at the epicardial surface was modified by methylglyoxal, while methylglyoxal-derived advanced glycation end-product levels in the underlying myocardium were lower than in control animals. It appears that rHCI hydrogel injection is soaking up free methylglyoxal from the myocardium, reducing levels of oxidative stress in cardiac muscle and improving contractility of cardiomyocytes bordering the scar. These results suggest that rHC therapy is a promising approach to improve cardiac contractility, and limit ventricular remodeling post-MI.

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Books on the topic "Myocardial remodeling"

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Nguyen, Thao P., Mansoureh Eghbali, and Sally Ann Frautschy, eds. Oxidative Stress in Myocardial and Neural Remodeling. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-657-7.

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Sherman, Jerald. Cardiac Remodeling: Molecular Mechanisms, Treatment and Clinical Implications. Nova Science Publishers, Incorporated, 2016.

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K, Singal Pawan, ed. Cardiac remodeling and failure. Boston: Kluwer Academic Pub., 2003.

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Dhalla, Naranjan S., Pawan K. Singal, Ian M. C. Dixon, and Lorrie A. Kirshenbaum. Cardiac Remodeling and Failure. Springer, 2012.

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Cardiac Remodeling and Failure. Springer, 2012.

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1945-, Hori M., Janicki Joseph S, and Maruyama Yukio 1941-, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.

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1941-, Maruyama Yukio, Hori M. 1945-, and Janicki Joseph S, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.

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Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.

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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.

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(Editor), Pawan K. Singal, Ian M.C. Dixon (Editor), Lorrie A. Kirshenbaum (Editor), and Naranjan S. Dhalla (Editor), eds. Cardiac Remodeling and Failure (Progress in Experimental Cardiology). Springer, 2003.

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Hausenloy, Derek, and Derek Yellon, eds. Coronary No-Reflow and Microvascular Obstruction. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0005.

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• Following an AMI, the restoration of TIMI III coronary blood flow using thrombolytic therapy or primary percutaneous coronary intervention does not guarantee actual myocardial perfusion• In 40–60% of reperfused AMI cases, myocardial perfusion is impeded at the level of the capillaries due to microvascular obstruction (MVO)- a phenomenon termed coronary no-reflow• The presence of coronary no-reflow can be detected as impaired myocardial perfusion using non-invasive imaging modalities such as nuclear myocardial perfusion scanning, myocardial contrast echocardiography or contrast-enhanced cardiac magnetic resonance imaging• The presence of microvascular obstruction post-AMI is associated with a larger infarct size, impaired LV ejection fraction, adverse LV remodelling and poorer clinical outcomes• Current treatment strategies include; vasodilator therapy such as adenosine, calcium-channel blockers, and nitrates; distal protection to prevent microemboli; and glycoprotein IIb/IIIa inhibitors• Novel treatment strategies are required to prevent and treat coronary no-reflow, thereby improving myocardial perfusion, reducing myocardial infarct size, preserving LV ejection fraction, preventing LV remodeling and improving clinical outcomes.

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Book chapters on the topic "Myocardial remodeling"

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DeLeon, Kristine Y., Lisandra E. de Castro Brás, Yonggang Ma, Ganesh V. Halade, Jianhua Zhang, and Merry L. Lindsey. "Extracellular Matrix Biomarkers of Adverse Remodeling After Myocardial Infarction." In Cardiac Remodeling, 383–412. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_22.

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Jugdutt, Bodh I., and Anwar Jelani. "Aging and Markers of Adverse Remodeling After Myocardial Infarction." In Cardiac Remodeling, 487–512. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_27.

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Jugdutt, Bodh I. "Regulation of Fibrosis After Myocardial Infarction: Implications for Ventricular Remodeling." In Cardiac Remodeling, 525–45. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_29.

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De Keulenaer, Gilles W., Luc J. Andries, Paul F. Fransen, Puneet Mohan, Gregory Kaluza, Jean L. Rouleau, Dirk L. Brutsaert, and Stanislas U. Sys. "Endocardial—Myocardial Interaction." In Cardiac-Vascular Remodeling and Functional Interaction, 163–78. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67041-4_13.

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Vanhoutte, Davy, and Stephane Heymans. "Role of SPARC in Cardiac Extracellular Matrix Remodeling After Myocardial Infarction." In Cardiac Remodeling, 427–44. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_24.

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Singh, Kaustabh, Keith R. Brunt, Richard D. Weisel, and Ren-Ke Li. "Optimizing Stem Cell Therapy for Cardiac Repair Following a Myocardial Infarction." In Cardiac Remodeling, 513–24. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_28.

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Cokkinos, Dennis V. "Cardiac Remodeling: The Course Toward Heart Failure – I. General Concepts." In Myocardial Preservation, 215–45. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-98186-4_12.

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Shikatani, Eric A., and Mansoor Husain. "The Role of Growth Differentiation Factor 5 in Cardiac Repair Post-Myocardial Infarction." In Cardiac Remodeling, 365–82. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_21.

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Adeboye, Adedayo A., Kevin P. Newman, Dwight A. Dishmon, Shadwan Alsafwah, Syamal K. Bhattacharya, and Karl T. Weber. "A Mitochondriocentric Pathway to Cardiomyocyte Necrosis: An Upstream Molecular Mechanism in Myocardial Fibrosis." In Cardiac Remodeling, 113–25. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5930-9_7.

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Mitchell, Gary F., Gervasio A. Lamas, and Marc A. Pfeffer. "Ventricular Remodeling after Myocardial Infarction." In Advances in Experimental Medicine and Biology, 265–76. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2946-0_25.

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Conference papers on the topic "Myocardial remodeling"

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Singh, Krishna. "OSTEOPONTIN: ROLE IN MYOCARDIAL REMODELING." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.274.

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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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"Myocardial dynamics analysis for cardiac remodeling." In 2021 International Symposium on Intelligent Signal Processing and Communication Systems (ISPACS). IEEE, 2021. http://dx.doi.org/10.1109/ispacs51563.2021.9651117.

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Tous, Elena, Jamie L. Ifkovits, Shauna M. Dorsey, Spencer E. Szczesny, Kevin J. Koomalsingh, Takashi Shuto, Toru Soeda, et al. "Tunable Hyaluronic Acid Hydrogels to Alter and Understand Left Ventricular Remodeling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80284.

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Heart disease causes about 15% of deaths in the United States; about two thirds of these cases are due to coronary artery disease [1]. Post myocardial infarction (MI), left ventricular (LV) remodeling ensues and leads to geometric changes that result in dilation and thinning of the myocardial wall. This increases stress in the infarct and healthy tissue and ultimately results in heart failure. Injectable bulking agents have recently emerged as a promising therapy to address these maladaptive changes. As suggested by the Law of Laplace, thickening of the myocardium should decrease stress on the heart and potentially attenuate the negative effects of LV remodeling [2].

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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.

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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.

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Wu, Changfu, Won-Bae Chang, Marc Gibber, P. Griffith Bartley, and Zhongjun J. Wu. "Bioengineering Quantification of Left Ventricular Remodeling Following Myocardial Infarction." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206779.

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Myocardial infarction (MI)-induced heart failure is the prevailing cause of morbidity and mortality in the western world. It is the sequela of the deleterious left ventricular (LV) remodeling process. So far, the mechanisms of the cardiac remodeling process are not completely understood. A clinically relevant large animal model is an essential vehicle for studying the mechanisms of cardiac remodeling. In our laboratory, we have developed a reproducible ovine model of post-infarct chronic cardiac remodeling. Throughout the study period of an animal, the functional and geometric changes of the LV were monitored by echocardiographic and bioengineering means.

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Ifkovits, Jamie L., Elena Tous, Masato Morita, Joseph H. Gorman, Robert C. Gorman, and Jason A. Burdick. "Injectable Hyaluronic Acid Hydrogels to Attenuate Post-Infarction Left Ventricular Remodeling." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206461.

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Several investigators have been successful in reducing the adverse left ventricular (LV) remodeling and expansion that exists in response to myocardial infarction (MI) via the use of various restraints, such as knitted polypropylene meshes [1] and injectable materials [2]. A recent finite element model simulation of the theoretical impact of injection of a material into the myocardium after MI confirmed the suspected stress reduction potential of intramyocardial infarct stiffening with an acellular, non-contractile material. As peak LV wall stress has been implicated in the pathogenesis of post-infarct LV remodeling, this approach to LV wall stress reduction has significant therapeutic potential [3].

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Zhang, Song, John A. Crow, Robert C. Cooper, Ronald M. McLaughlin, Shane Burgess, Ali Borazjani, and Jun Liao. "Detection of Myocardial Fiber Disruption in Artificial Lesions With 3D DT-MRI Tract Models." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193121.

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In the United States, it is estimated that in 2008 approximately 1.2 million people will suffer a new or recurrent myocardial infarction. In 2005, the latest full year for which statistics are available, 16 million Americans (7.3% of the population) had some form of coronary heart disease. Loss of myocardium as a result of myocardial infarction increases wall stress locally and globally and triggers adaptive responses at the molecular, cellular, and tissue levels. These adaptive responses can lead to left ventricular dilation and congestive heart failure. Accurate non-invasive evaluation of myocardial structural degeneration (damage) and left ventricular remodeling following an infarct would have both prognostic and therapeutic value clinically.

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Richardson, William J., and Jeffrey W. Holmes. "Do Infarcts Really Expand or Compact? Relationship Between Changing Material Properties and Apparent Infarct Remodeling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14411.

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Myocardial infarction (MI) is a leading cause of mortality and morbidity with over 600,000 new Americans suffering an MI each year [1]. Following infarction, damaged muscle is gradually replaced by collagenous scar tissue, while undamaged (remote) myocytes remodel due to altered load. Remodeling of both the infarcted and remote myocardium are important determinants of cardiac function and the risk of progression to heart failure.

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Prabhakar, Shashi, Laxmansa Katwa, Fatiha Moukdar, Wayne Cascio, and Robert Lust. "Episodic Diesel Particulate Exposure After Myocardial Infarction Alters Cardiac Remodeling." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1724.

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Reports on the topic "Myocardial remodeling"

1

Voynalovich-Khanova, Y. A. SYNDROME OF MYOCARDIAL REMODELING (CLINICAL OBSERVATION). "PLANET", 2019. http://dx.doi.org/10.18411/978-5-907192-54-6-2019-xxxvi-46-49.

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2

Liu, Xiaofang, and Dichuan Liu. Effects of the sacubitril/valsartan on cardiac remodeling in patients with Acute Myocardial Infarction: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2021. http://dx.doi.org/10.37766/inplasy2021.7.0044.

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