Relevant bibliographies by topics / Infarcted Myocardium

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Infarcted Myocardium'

Author: Grafiati
Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "Infarcted Myocardium"

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Spath, Nick B., Trisha Singh, Giorgos Papanastasiou, et al. "Assessment of stunned and viable myocardium using manganese-enhanced MRI." Open Heart 8, no. 1 (2021): e001646. http://dx.doi.org/10.1136/openhrt-2021-001646.

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ObjectiveIn a proof-of-concept study, to quantify myocardial viability in patients with acute myocardial infarction using manganese-enhanced MRI (MEMRI), a measure of intracellular calcium handling.MethodsHealthy volunteers (n=20) and patients with ST-elevation myocardial infarction (n=20) underwent late gadolinium enhancement (LGE) using gadobutrol and MEMRI using manganese dipyridoxyl diphosphate. Patients were scanned ≤7 days after reperfusion and rescanned after 3 months. Differential manganese uptake was described using a two-compartment model.ResultsAfter manganese administration, health
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Shriki, J. E., K. Surti, A. Farvid, J. S. Shinbane, and P. M. Colletti. "Quantitative Evaluation of the Amount of Delayed Myocardial Enhancement as a Predictor of Systolic Dysfunction." Open Cardiovascular Medicine Journal 3, no. 1 (2009): 35–38. http://dx.doi.org/10.2174/1874192400903010035.

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30 patients with delayed contrast enhancement in patterns suggestive of myocardial infarctions were reviewed. Infarct mass was quantitatively measured using short axis images obtained in the delayed phase of gadopentetate administration. Left ventricular mass and ejection fraction were measured using short axis, steady state free precession images. A relationship is drawn between increased mass of infarction and decreased left ventricular ejection fraction. For each gram of infarct, there is a 0.5 % reduction in ejection fraction (EF = 50 - (0.48 x gm infarcted myocardium); r2= 0.49). For each
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O'Regan, Declan P., Rizwan Ahmed, Clare Neuwirth, et al. "Cardiac MRI of myocardial salvage at the peri-infarct border zones after primary coronary intervention." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (2009): H340—H346. http://dx.doi.org/10.1152/ajpheart.00011.2009.

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The purpose of this study was to use cardiac MRI to define the morphology of the reversibly injured peri-infarct border zone in patients treated with primary percutaneous coronary intervention (PPCI) for acute ST elevation myocardial infarction. In 15 patients, T2-weighted myocardial edema imaging was used to identify the ischemic bed or area at risk (AAR), and late gadolinium enhancement imaging was used to measure infarct size. Images were coregistered, and the boundaries of edema and necrosis were defined using an edge-detection methodology. We observed that infarction always involved the s
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Carlsson, M., P. C. Ursell, D. Saloner, and M. Saeed. "Multidetector computed tomography for characterization of calcium deposits in reperfused myocardial infarction." Acta Radiologica 50, no. 4 (2009): 396–405. http://dx.doi.org/10.1080/02841850902756540.

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Background: Calcium overload is a major cause of reperfusion myocardial injury. Multidetector computed tomography (MDCT) has been previously used in visualizing coronary artery calcium, but not calcium deposits in reperfused infarction. Purpose: To assess the ability of MDCT to 1) noninvasively visualize and characterize calcium deposits in reperfused infarcts, and 2) monitor regional wall swelling, regional systolic wall thickening, and infarct resorption. Material and Methods: Reperfused myocardial infarcts were created in seven pigs by 2-hour occlusion of the left anterior descending corona
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Song, Heesang, Hye Jin Hwang, Woochul Chang, et al. "Cardiomyocytes from phorbol myristate acetate-activated mesenchymal stem cells restore electromechanical function in infarcted rat hearts." Proceedings of the National Academy of Sciences 108, no. 1 (2010): 296–301. http://dx.doi.org/10.1073/pnas.1015873107.

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Despite the safety and feasibility of mesenchymal stem cell (MSC) therapy, an optimal cell type has not yet emerged in terms of electromechanical integration in infarcted myocardium. We found that poor to moderate survival benefits of MSC-implanted rats were caused by incomplete electromechanical integration induced by tissue heterogeneity between myocytes and engrafted MSCs in the infarcted myocardium. Here, we report the development of cardiogenic cells from rat MSCs activated by phorbol myristate acetate, a PKC activator, that exhibited high expressions of cardiac-specific markers and Ca2+
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Širmenis, Raimondas, Antanas Kraniauskas, Rasa Jarašienė, Daiva Baltriukienė, Audronė Kalvelytė, and Virginija Bukelskienė. "Recovery of Infarcted Myocardium in an In Vivo Experiment." Medicina 47, no. 11 (2011): 88. http://dx.doi.org/10.3390/medicina47110088.

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Acute myocardial infarction leads to the loss of functional cardiomyocytes and structural integrity. The adult heart cannot repair the damaged tissue due to inability of mature cardiomyocytes to divide and lack of stem cells. The aim of this study was to evaluate the efficiency of introduced autologous skeletal musclederived stem cells to recover the function of acutely infarcted rabbit heart in the early postoperative period. Material and Methods. As a model for myocardium restoration in vivo, experimental rabbit heart infarct was used. Autologic adult myogenic stem cells were isolated from s
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Fang, Lu, Xiao-Ming Gao, Chrishan S. Samuel, et al. "Higher levels of collagen and facilitated healing protect against ventricular rupture following myocardial infarction." Clinical Science 115, no. 3 (2008): 99–106. http://dx.doi.org/10.1042/cs20070365.

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The mechanism of cardiac rupture after MI (myocardial infarction) is not fully understood. Rupture has not been reported in most laboratory species, including the rat, but does occur in mice. We have reported previously that β2-TG mice (transgenic mice with cardiac-restricted overexpression of β2-adrenergic receptors) had a lower incidence of rupture compared with NTG (non-transgenic) littermates. We hypothesized that the difference in the incidence of rupture between rodents and specific mouse strains is due to the difference in collagen content following MI. In the present study, we compared
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Carlsson, Marcus, Nael F. Osman, Philip C. Ursell, Alastair J. Martin, and Maythem Saeed. "Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (2008): H522—H532. http://dx.doi.org/10.1152/ajpheart.00280.2008.

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Previous studies have shown the beneficial effects of the hepatocyte growth factor (HGF) gene on myocardial perfusion and infarction size but not on the regional strain in relationship to global left ventricular function. A noninvasive magnetic resonance (MR) study was performed to determine the effect of a new HGF gene, VM202, expressing two isoforms of HGF, on regional and global left ventricular function. Pigs (8/group) were divided into three groups: 1) controls without infarction; 2) reperfused, infarcted controls; and 3) infarcted, treated (1 h after reperfusion) with VM202 injected at e
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Liu, Chunping, Zhijin Fan, Dongyue He, et al. "Designer Functional Nanomedicine for Myocardial Repair by Regulating the Inflammatory Microenvironment." Pharmaceutics 14, no. 4 (2022): 758. http://dx.doi.org/10.3390/pharmaceutics14040758.

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Acute myocardial infarction is a major global health problem, and the repair of damaged myocardium is still a major challenge. Myocardial injury triggers an inflammatory response: immune cells infiltrate into the myocardium while activating myofibroblasts and vascular endothelial cells, promoting tissue repair and scar formation. Fragments released by cardiomyocytes become endogenous “danger signals”, which are recognized by cardiac pattern recognition receptors, activate resident cardiac immune cells, release thrombin factors and inflammatory mediators, and trigger severe inflammatory respons
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Wu, Guifu, Jamal S. Rana, Joanna Wykrzykowska, et al. "Exercise-induced expression of VEGF and salvation of myocardium in the early stage of myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 2 (2009): H389—H395. http://dx.doi.org/10.1152/ajpheart.01393.2007.

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The mechanism of exercise-induced benefit and angiogenesis in ischemic heart disease remains poorly defined. This study was designed to investigate the effects of exercise training on the expression of angiogenic factors and angiogenesis in the infarcted myocardium [myocarial infaction (MI)]. Sixty-three male FVB mice were used for study and were divided into subgroups to test the response to exercise: the time-dependent expression of angiogenic factors to exercise training in normal ( group 1; n = 12) and infarcted myocardium ( group 2; n = 15) and the exercise-induced angiogenic response in
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Dissertations / Theses on the topic "Infarcted Myocardium"

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Kellar, Robert Shawn. "Tissue-engineered polymers stimulate angiogenesis in infarcted myocardium." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/279837.

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The development and maintenance of a vascular network is critical to the growth and survival of a tissue and ultimately an organism. An understanding of the mechanisms which regulate angiogenesis within and surrounding currently used polymeric devices would contribute to the success of these implants by establishing methods to enhance tissue in-growth and new vessel development. Furthermore, tissue-engineering currently used polymers such as expanded polytetrafluoroethylene (ePTFE) may create an angiogenic material that can be used to induce new microvessel formation in infarcted myocardium. M
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Arnal, Pastor María Pilar. "New scaffolding materials for the regeneration of infarcted myocardium." Doctoral thesis, Editorial Universitat Politècnica de València, 2015. http://hdl.handle.net/10251/46129.

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There is growing interest in the development of biomimetic matrices that are simultaneously cell-friendly, allow rapid vascularization, exhibit enough mechanical integrity to be comfortably handled and resist mechanical stresses when implanted in the site of interest. Meeting all these requirements with a single component material has proved to be very challenging. The hypothesis underlying this work was that hybrid materials obtained by combining scaffolds with bioactive hydrogels would result in a synergy of their best properties: a construct with good mechanical properties, easily han
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Moreno-Gonzalez, Alicia. "Mechanical properties of myocardium following cardiomyocyte transplantation into infarcted hearts and investigations of the role of troponin C Ca2+ binding kinetics in skeletal muscle contraction /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8053.

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Zhao, Xiaofeng. "Can promotion of neutrophil apoptosis enhance repair in the infarcted myocardium and resolution of sterile peritonitis?" Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25896.

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Efferocytosis, the clearance of apoptotic cells including apoptotic neutrophils by macrophage phagocytosis, is a key cellular mechanism for resolution of inflammation and tissue repair. Cyclin-dependent kinases (CDKs) 7 and 9 phosphorylate RNA polymerase II that is vital for neutrophil transcriptional capacity. CDK inhibitors such as R-roscovitine, and the more selective inhibitor AT7519, induce neutrophil apoptosis and promote resolution of several mouse models of inflammation including acute lung inflammation. The hypothesis investigated here was that AT7519 would promote neutrophil apoptosi
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Tambara, Keiichi. "Transplanted skeletal myoblasts can fully replace the infarcted myocardium when they survive in the host in large numbers." Kyoto University, 2005. http://hdl.handle.net/2433/144779.

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Anderl, Jeffrey Neil. "PLGA microsphere formulations for sustained local delivery of vascular endothelial growth factor : considerations for therapeutic angiogenesis of infarcted myocardium /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8110.

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Nussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.

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Chillou, de Churet Christian de. "Potentiels tardifs et infarctus myocardique." Nancy 1, 1989. http://www.theses.fr/1989NAN11287.

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Salame, Boulos. "Myocardite et infarctus du myocarde." Université Louis Pasteur (Strasbourg) (1971-2008), 1991. http://www.theses.fr/1991STR1M175.

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BOFFITO, MONICA. "Bioengineered Patches in the Regeneration of Infarcted Myocardial Tissue." Doctoral thesis, Politecnico di Torino, 2014. http://hdl.handle.net/11583/2572547.

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Ischemic heart diseases are the leading cause of death worldwide: approximately 3.8 million men and 3.4 million women die each year from coronary heart diseases (World Health Organization data). Among them, acute myocardial infarction (MI), usually known as a heart attack, accounts for about 23% of deaths each year. The term MI refers to the acute coronary syndrome due to the obstruction of one or more branches of the coronary arteries that blocks blood flow and determines necrosis of the myocardium. The process of cardiac myocyte death and regeneration is part of the normal heart homeostasis;
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Books on the topic "Infarcted Myocardium"

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G, Reves J., and Society of Cardiovascular Anesthesiologists, eds. Acute revascularization of the infarcted heart. Grune & Stratton, 1987.

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2

H, Schmutzler, Rutsch W. 1941-, and Dougherty F. C. 1946-, eds. Limitation of infarct size. Springer-Verlag, 1989.

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1931-, Frohlich Edward D., ed. Preventive aspects of coronary heart disease. Davis, 1990.

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Sproule, Laurie Kathleen. Carboxypeptidase N and U in myocardial infarct and angina patients. s.n.], 1992.

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H, Mattingly Patrick, Lohr Kathleen N. 1941-, and Institute of Medicine (U.S.). Division of Health Care Services., eds. Acute myocardial infarction: Setting priorities for effectiveness research : report of a study by a committee of the Institute of Medicine, Division of Health Care Services. National Academy Press, 1990.

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Reeves, François. Prévenir l'infarctus ou y survivre: Les voies du coeur. Éditions du CHU Sainte-Justine, 2007.

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1954-, Topol Eric J., ed. Acute coronary syndromes. 3rd ed. Marcel Dekker, 2005.

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Veldkamp, Rolf Frederik. Continuous digital 12-lead ST-segment monitoring in Acute Myocardial Infarction =: Continue digitale 12-afleidingen ST-segment bewaking tijdens het acute myocard infarct : proefschrift. The Author, 1995.

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Inc, NetLibrary, ed. Acute coronary syndromes. Marcel Dekker, 1998.

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Levin, Rhoda F. Vivre avec un cardiaque: Les voies de la serenite et de l'espoir. Editions de l'Homme, 1992.

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Book chapters on the topic "Infarcted Myocardium"

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Wang, Junhong, and Nikolaos G. Frangogiannis. "Repair of the Infarcted Myocardium." In Introduction to Translational Cardiovascular Research. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08798-6_16.

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Saxena, Amit, and Nikolaos G. Frangogiannis. "Fibroblast Activation in the Infarcted Myocardium." In Cardiac Fibrosis and Heart Failure: Cause or Effect? Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17437-2_2.

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Hartogh, S. C. Den, J. P. Sluijter, P. A. Doevendans, and L. W. Van Laake. "Cellular Therapy for the Infarcted Myocardium." In Translational Cardiology. Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-891-7_11.

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Chang, Woochul, Byeong-Wook Song, and Ki-Chul Hwang. "Mesenchymal Stem Cell Survival in Infarcted Myocardium: Adhesion and Anti-death Signals." In Stem Cells and Cancer Stem Cells, Volume 10. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6262-6_4.

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Alnasser, Sulaiman, Mabrouk AL-Rasheedi, Mateq A. Alreshidi, Saleh F. Alqifari, and Khawaja Husnain Haider. "Augmenting Mesenchymal Stem Cell-Based Therapy of the Infarcted Myocardium with Statins." In Handbook of Stem Cell Therapy. Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2655-6_20.

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Li, Junjun, Li Liu, Itsunari Minami, Shigeru Miyagawa, and Yoshiki Sawa. "Fabrication of Thick and Anisotropic on Nanofibrous Substrate for Repairing Infarcted Myocardium." In Methods in Molecular Biology. Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1484-6_7.

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Alnasser, Sulaiman, Mabrouk AL-Rasheedi, Mateq A. Alreshidi, Saleh F. Alqifari, and Khawaja Husnain Haider. "Augmenting Mesenchymal Stem Cell-Based Therapy of the Infarcted Myocardium with Statins." In Handbook of Stem Cell Therapy. Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-6016-0_20-1.

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Soares, Joao S., David S. Li, Eric Lai, Joseph H. Gorman III, Robert C. Gorman, and Michael S. Sacks. "Modeling of Myocardium Compressibility and its Impact in Computational Simulations of the Healthy and Infarcted Heart." In Functional Imaging and Modelling of the Heart. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-59448-4_47.

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Wang, Shan, and Yaojiong Wu. "The role of chemokines in mesenchymal stromal cell homing to sites of inflammation, including infarcted myocardium." In The Biology and Therapeutic Application of Mesenchymal Cells. John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118907474.ch23.

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Weber, K. T., Y. Sun, and J. P. M. Cleutjens. "Structural remodeling of the infarcted rat heart." In Myocardial Ischemia: Mechanisms, Reperfusion, Protection. Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-8988-9_30.

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Conference papers on the topic "Infarcted Myocardium"

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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-infarcte
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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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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 r
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Masithulela, Fulufhelo. "Analysis of Passive Filling With Fibrotic Myocardial Infarction." In ASME 2015 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/imece2015-50003.

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Cardiovascular diseases account for one third of all deaths worldwide, more than 33% of which are related to ischemic heart disease, involving a myocardial infarction (MI). Following myocardial infarction, the injured region and ventricle undergo structural changes which are thought to be caused by elevated stresses and reduction of strains in the infarcted wall. The fibrotic phase is defined as the period when the amount of new collagen and number of fibroblasts rapidly increase in the infarcted tissue. We studied through finite element analysis the mechanics of the infarcted and remodeling r
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Ghanbari, Elmira, Atefeh Solouk, Rouhollah Mehdinavaz Aghdam, Masoumeh Haghbin Nazarpak, Seyed Hossein, and Ahmadi Tafti. "Erythropoietin-Loaded Nanofibrous Patch for Regeneration of Infarcted Myocardium." In 2017 24th National and 2nd International Iranian Conference on Biomedical Engineering (ICBME). IEEE, 2017. http://dx.doi.org/10.1109/icbme.2017.8430247.

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Larroza, Andres, Maria P. Lopez-Lereu, Jose V. Monmeneu, Vicente Bodi, and David Moratal. "Texture analysis for infarcted myocardium detection on delayed enhancement MRI." In 2017 IEEE 14th International Symposium on Biomedical Imaging (ISBI 2017). IEEE, 2017. http://dx.doi.org/10.1109/isbi.2017.7950700.

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Goergen, Craig J., Howard H. Chen, Alexei Bogdanov, David E. Sosnovik, and Anand T. N. Kumar. "In Vivo Fluorescence Lifetime Detection of a Cathepsin-Activatable Probe in Infarcted Myocardium." In Biomedical Optics. OSA, 2012. http://dx.doi.org/10.1364/biomed.2012.bm2a.4.

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Trubelja, Alen, John W. MacArthur, Joseph J. Sarver, et al. "Bioengineered SDF-1a Analogue Delivered as an Angiogenic Therapy Significantly Normalizes Elastic and Viscoelastic Material Properties of Infarcted Cardiac Muscle." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14602.

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Heart disease is a leading cause of death worldwide, and coronary heart disease causes 1 of every 6 deaths in the United States [1]. Following a myocardial infarction, scar tissue gradually replaces myocardium that is lost through a process of collagen deposition and an increase in tensile strength of the tissue [2]. This leads to infarct expansion, adverse ventricular remodeling and dysfunction, and ultimately heart failure. Dilation of the left ventricle (LV) leads to increased LV wall stress and is ultimately responsible for adverse ventricular remodeling. LV dilation causes stretching and
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Shanmuganathan, Mayooran, Ambra Masi, Matthew K. Burrage, et al. "1 Long-term prognosis after acute ST-segment elevation myocardial infarction is determined by characteristics in both non-infarcted and infarcted myocardium on cardiovascular magnetic resonance imaging." In British Society of Cardiovascular Magnetic Resonance 2021 Annual Meeting. BMJ Publishing Group Ltd and British Cardiovascular Society, 2021. http://dx.doi.org/10.1136/heartjnl-2021-bscmr.1.

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Wu, Changfu, Tieluo Li, Kinjal Savai, Bartley P. Griffith, and Zhongjun J. Wu. "Strain Mapping of LV Myocardium and its Correlation With Activation of Apoptotic Molecular Pathways Post Infarction." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193133.

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The American Heart Association reported that in 2004 alone, myocardial infarction (MI) related mortality rate was as high as 38% among the 1.2 million reported MI cases [1]. After an MI, the self-repair capability of the infarcted heart is limited. As a result, the heart undergoes a remodeling process, characterized by progressive weakening of contractile function. It is believed that increased left ventricular (LV) loading to survival myocytes post-MI activates the apoptotic pathways in the cells, leading to progressive loss of cardiomyocytes.
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