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Academic literature on the topic 'Myocardial Infarctio'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Myocardial Infarctio"

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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 (May 18, 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 % increase of infarcted myocardium, there is a 0.67 % reduction in ejection fraction (EF = 50 - (0.67 x percent of infarcted myocardium); r2= 0.39). Left ventricular ejection fraction correlates inversely with the mass of myocardium with delayed enhancement on cardiac MRI.
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O'Regan, Declan P., Rizwan Ahmed, Clare Neuwirth, Yvonne Tan, Giuliana Durighel, Joseph V. Hajnal, Imad Nadra, Simon J. Corbett, and Stuart A. Cook. "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 (July 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 subendocardium but showed variable transmural extension within the AAR. The mean infarct size was 22 ± 19% (range: 8–48%), and the mean AAR was 34 ± 12% (range: 20–57%). The infarcted myocardium was always smaller than the ischemic AAR and involved between 34% and 99% (mean 72 ± 21%) of the ischemic bed primarily due to variation in transmural infarct extension. Although a lateral border zone of potentially viable myocardium was often present, its extent was limited (range: 0–11 mm, mean: 5 ± 4 mm). As a result of this, infarcts occupied the majority (range: 70–100%, mean: 82 ± 13%) of the width of the AAR. The mean fractional wall thickening in the infarcted, peri-infarcted, and remote myocardium was 3.6 ± 16.0%, 40.5 ± 26.4%, and 88.2 ± 39.3%, respectively. These findings demonstrate that myocardial salvage is largely determined by epicardial limitation of the infarct within the ischemic AAR after PPCI. The lateral boundaries of necrosis approximate to the lateral extent of the ischemic bed and systolic wall motion abnormalities extend well beyond the infarct border zone.
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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 (May 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 coronary artery (LAD) after coronary catheterization. A 64-slice MDCT scanner was used for non-contrast images to depict calcium deposits. Furthermore, cine and delayed contrast-enhanced (DE) MDCT imaging were acquired to assess the chronological changes (2–4 hours, 1 week, and 8 weeks) in regional wall swelling, systolic wall thickening, and infarct size. Results: Non-contrast MDCT images depicted calcium deposits as “hot-spots.” Attenuation of calcium deposits was greater (89±6 Hounsfield units [HU]) than remote myocardium (36±3 HU; P<0.05). Calcium deposits were not evident at 2–4 hours and were substantially smaller at 8 weeks compared to 1 week. Correlations were found between the extent of calcium deposits, ejection fraction ( R=0.81), and infarction size ( R=0.70). Cine MCDT images demonstrated transient wall swelling (edema formation and resorption) at 2–4 hours and differences in regional systolic wall thickening among infarcted, peri-infarcted, and remote myocardium. Calcium-specific von Kossa stain confirmed the presence of calcium deposits in infarcted myocardium. Conclusion: 64-slice MDCT has the potential to demonstrate the progression and regression of calcium deposits, interstitial edema, and infarction. The presence of calcium deposits was transient and associated with reperfused recent infarction. The extent of calcium deposits was positively correlated with infarction size and negatively with global left-ventricular function.
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Nilsson, S., G. Wikström, A. Ericsson, M. Wikström, A. Waldenström, and A. Hemmingsson. "MR Imaging of Gadolinium-DTPA-BMA-Enhanced Reperfused and Nonreperfused Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (July 1995): 633–40. http://dx.doi.org/10.1177/028418519503600465.

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To investigate whether Gd-DTPA-BMA-enhanced MR imaging permits differentiation between reperfused and nonreperfused myocardial infarction, myocardial infarction was induced in 12 domestic pigs. In 6 pigs, Gd-DTPA-BMA, 0.3 mmol/kg b.w. was administered i.v. 60 min after the occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Gd-DTPA-BMA after 20 min of reperfusion. Radiolabeled microspheres were used to confirm zero-flow during the occlusion period and reperfusion in the infarcted myocardium. All pigs were killed 20 min after injection of contrast medium, and the hearts were excised and imaged with MR. The Gd concentration was measured in infarcted and nonischemic myocardium by ICPAES. In the reperfused hearts, the infarctions were strongly highlighted, corresponding to a 5-fold higher Gd concentration in infarcted vis-à-vis nonischemic myocardium. In the hearts subjected to occlusion without reperfusion, there was only a rim of enhancement in the peripheral part of the infarctions.
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Ristic-Andjelkov, Andjelka, Branislav Baskot, Milorad Damjanovic, and Sasa Rafajlovski. "Ischemic preconditioning." Vojnosanitetski pregled 62, no. 1 (2005): 73–77. http://dx.doi.org/10.2298/vsp0501073r.

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Background. Ischemic preconditioning is a phenomenon during which myocardium, subjected to brief episodes of ischemia followed by reperfusion, tolerates better the subsequent, more prolonged episode of this ischemia, thus reducing the infarction size substantially. Case report. Two patients with acute left anterior descendent artery occlusion received fibrinolytic therapy (alteplase) within 6 hours of the onset of chest pain, but developed myocardial infarctions of different sizes. The first patient, without the history of preinfarction angina, developed large anterior infarct, because there was no time either for ischemic preconditioning or for the coronary collateral vessels development. In the second patient, with 4-day history of preinfarction angina, the more favorable outcome was seen he developed smaller apical necrosis, with the great degree of myocardial viability in the infarct-related area. Conclusion. Ischemic preconditioning in patients with acute myocardal infarction results in the reduction of mortality, infarction size, as well as in the frequency of malignant arrhythmias.
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Spath, Nick B., Trisha Singh, Giorgos Papanastasiou, Andrew Baker, Rob J. Janiczek, Gerry P. McCann, Marc R. Dweck, Lucy Kershaw, David E. Newby, and Scott Semple. "Assessment of stunned and viable myocardium using manganese-enhanced MRI." Open Heart 8, no. 1 (June 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, healthy control and remote non-infarcted myocardium showed a sustained 25% reduction in T1 values (mean reductions, 288±34 and 281±12 ms). Infarcted myocardium demonstrated less T1 shortening than healthy control or remote myocardium (1157±74 vs 859±36 and 835±28 ms; both p<0.0001) with intermediate T1 values (1007±31 ms) in peri-infarct regions. Compared with LGE, MEMRI was more sensitive in detecting dysfunctional myocardium (dysfunctional fraction 40.5±11.9 vs 34.9%±13.9%; p=0.02) and tracked more closely with abnormal wall motion (r2=0.72 vs 0.55; p<0.0001). Kinetic modelling showed reduced myocardial manganese influx between remote, peri-infarct and infarct regions, enabling absolute discrimination of infarcted myocardium. After 3 months, manganese uptake increased in peri-infarct regions (16.5±3.5 vs 22.8±3.5 mL/100 g/min, p<0.0001), but not the remote (23.3±2.8 vs 23.0±3.2 mL/100 g/min, p=0.8) or infarcted (11.5±3.7 vs 14.0±1.2 mL/100 g/min, p>0.1) myocardium.ConclusionsThrough visualisation of intracellular calcium handling, MEMRI accurately differentiates infarcted, stunned and viable myocardium, and correlates with myocardial dysfunction better than LGE. MEMRI holds major promise in directly assessing myocardial viability, function and calcium handling across a range of cardiac diseases.Trial registration numbersNCT03607669; EudraCT number 2016-003782-25.
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Song, Yi-Sun, Hyun-Woo Joo, In-Hwa Park, Guang-Yin Shen, Yonggu Lee, Jeong Hun Shin, Hyuck Kim, Il-Seob Shin, and Kyung-Soo Kim. "Transplanted Human Amniotic Epithelial Cells Secrete Paracrine Proangiogenic Cytokines in Rat Model of Myocardial Infarctio." Cell Transplantation 24, no. 10 (October 2015): 2055–64. http://dx.doi.org/10.3727/096368914x685609.

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Jin, Jiyang, Min Chen, Yongjun Li, YaLing Wang, Shijun Zhang, Zhen Wang, Lin Wang, and Shenghong Ju. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (October 1, 2016): 383–91. http://dx.doi.org/10.14503/thij-15-5462.

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We used a porcine model of acute myocardial infarction to study the signal evolution of ischemic myocardium on diffusion-weighted magnetic resonance images (DWI). Eight Chinese miniature pigs underwent percutaneous left anterior descending or left circumflex coronary artery occlusion for 90 minutes followed by reperfusion, which induced acute myocardial infarction. We used DWI preprocedurally and hourly for 4 hours postprocedurally. We acquired turbo inversion recovery magnitude T2-weighted images (TIRM T2WI) and late gadolinium enhancement images from the DWI slices. We measured the serum myocardial necrosis markers myoglobin, creatine kinase-MB isoenzyme, and cardiac troponin I at the same time points as the magnetic resonance scanning. We used histochemical staining to confirm injury. All images were analyzed qualitatively. Contrast-to-noise ratio (the contrast between infarcted and healthy myocardium) and relative signal index were used in quantitative image analysis. We found that DWI identified myocardial signal abnormity early (&lt;4 hr) after acute myocardial infarction and identified the infarct-related high signal more often than did TIRM T2WI: 7 of 8 pigs (87.5%) versus 3 of 8 (37.5%) (P=0.046). Quantitative image analysis yielded a significant difference in contrast-to-noise ratio and relative signal index between infarcted and normal myocardium on DWI. However, within 4 hours after infarction, the serologic myocardial injury markers were not significantly positive. We conclude that DWI can be used to detect myocardial signal abnormalities early after acute myocardial infarction—identifying the infarction earlier than TIRM T2WI and widely used clinical serologic biomarkers.
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Bo, Yang, and Li Min. "GW24-e0030 A multi-nationality study on gender differences in anxiety early after acute myocardial infarctio." Heart 99, Suppl 3 (August 2013): A259.2—A259. http://dx.doi.org/10.1136/heartjnl-2013-304613.730.

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PETTERSEN, K. I. "When Time is Precious--Time Lags as Indicators of Quality of Care in Acute Myocardial Infarctio." International Journal for Quality in Health Care 7, no. 1 (March 1, 1995): 3–10. http://dx.doi.org/10.1093/intqhc/7.1.3.

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Dissertations / Theses on the topic "Myocardial Infarctio"

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HANTIKAINEN, ESSI MARJATTA. "DIETARY NON ENZYMATIC ANTIOXIDANT CAPACITY AND THE RISK OF CARDIOVASCULAR DISEASES – AN EPIDEMIOLOGICAL APPROACH." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/263728.

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ABSTRACT Cardiovascular diseases are the leading cause of premature death and disability in the world. A diet containing high amounts of plant-based foods has been associated with a reduced risk of cardiovascular diseases and the beneficial effect has been attributed to the antioxidants found in the foods. However, findings from randomized controlled trials on the role of antioxidant supplementation have been disappointing, reporting null results or even harmful effects. It has been suggested that antioxidants interact with each other to promote cardiovascular health. Therefore, the Non Enzymatic Antioxidant Capacity (NEAC) assay has been proposed, which measures the antioxidant potential of different dietary sources considering interactions between them. This thesis aimed to further clarify the effect of dietary antioxidants on the risk of cardiovascular diseases, with particular interest in measuring NEAC from diet. The specific aims were to prospectively study whether dietary NEAC is associated with a lower risk of myocardial infarction, stroke and heart failure in subjects free from CVD or cancer. Four studies were conducted using data from two large Swedish cohorts. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). In the Swedish Women’s Lifestyle and Health Cohort (n = 45,882), a higher baseline dietary NEAC was inversely associated with the risk of myocardial infarction (quintile 5 vs. quintile 1: HR: 0.60, 95% CI: 0.45-0.81, p for trend < 0.05) and heart failure (tertile 3 vs. tertile 1: HR: 0.63; 95% CI: 0.43-0.93; p for trend < 0.05) in young to middle aged women, whereas no association was found between dietary NEAC and stroke. In the Swedish National March Cohort (n = 34,543), dietary NEAC was inversely associated with the risk of overall (quartile 4 vs. quartile 1: HR: 0.77, 95% CI: 0.61-0.96; p for trend < 0.05) and non-fatal myocardial infarction (quartile 4 vs. quartile 1: HR: 0.72; 95% CI: 0.56-0.92; p for trend < 0.05), but not with fatal myocardial infarction. The association seemed to further be stronger in women compared to men. To conclude, these findings support the hypothesis that a diet with high NEAC might protect from the development of myocardial infarction and heart failure and that the beneficial effect might be exerted through interactions between antioxidants. Whether this is true for stroke needs to be further investigated. Nevertheless, it is suggested to implement high amounts of antioxidant rich foods and beverages, such as fruits, vegetables, whole grains and tea, in the daily diet to lower the burden of cardiovascular diseases.
ABSTRACT Cardiovascular diseases are the leading cause of premature death and disability in the world. A diet containing high amounts of plant-based foods has been associated with a reduced risk of cardiovascular diseases and the beneficial effect has been attributed to the antioxidants found in the foods. However, findings from randomized controlled trials on the role of antioxidant supplementation have been disappointing, reporting null results or even harmful effects. It has been suggested that antioxidants interact with each other to promote cardiovascular health. Therefore, the Non Enzymatic Antioxidant Capacity (NEAC) assay has been proposed, which measures the antioxidant potential of different dietary sources considering interactions between them. This thesis aimed to further clarify the effect of dietary antioxidants on the risk of cardiovascular diseases, with particular interest in measuring NEAC from diet. The specific aims were to prospectively study whether dietary NEAC is associated with a lower risk of myocardial infarction, stroke and heart failure in subjects free from CVD or cancer. Four studies were conducted using data from two large Swedish cohorts. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). In the Swedish Women’s Lifestyle and Health Cohort (n = 45,882), a higher baseline dietary NEAC was inversely associated with the risk of myocardial infarction (quintile 5 vs. quintile 1: HR: 0.60, 95% CI: 0.45-0.81, p for trend < 0.05) and heart failure (tertile 3 vs. tertile 1: HR: 0.63; 95% CI: 0.43-0.93; p for trend < 0.05) in young to middle aged women, whereas no association was found between dietary NEAC and stroke. In the Swedish National March Cohort (n = 34,543), dietary NEAC was inversely associated with the risk of overall (quartile 4 vs. quartile 1: HR: 0.77, 95% CI: 0.61-0.96; p for trend < 0.05) and non-fatal myocardial infarction (quartile 4 vs. quartile 1: HR: 0.72; 95% CI: 0.56-0.92; p for trend < 0.05), but not with fatal myocardial infarction. The association seemed to further be stronger in women compared to men. To conclude, these findings support the hypothesis that a diet with high NEAC might protect from the development of myocardial infarction and heart failure and that the beneficial effect might be exerted through interactions between antioxidants. Whether this is true for stroke needs to be further investigated. Nevertheless, it is suggested to implement high amounts of antioxidant rich foods and beverages, such as fruits, vegetables, whole grains and tea, in the daily diet to lower the burden of cardiovascular diseases.
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Murphy, Megan K. "Fibrin microthreads promote stem cell growth for localized delivery in regenerative therapy." Worcester, Mass. : Worcester Polytechnic Institute, 2008. http://www.wpi.edu/Pubs/ETD/Available/etd-090208-143505/.

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Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.

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Surányi, Pál. "Relaxation rate-based magnetic resonance imaging quantification of myocardial infarction." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2007r/suranyi.pdf.

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Elhdere, Souada Ahmed. "Illness cognitions in myocardial infarction." Thesis, University of Surrey, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.548363.

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Williams, John. "Marker proteins in myocardial infarction." Thesis, University of Ulster, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359319.

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Ruparelia, Neil. "Monocytes in acute myocardial infarction." Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:02ad6ebd-a8c2-4cb6-a1f7-0cdf8cec59ed.

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Acute myocardial infarction (AMI) results in the activation of the innate immune system with monocytes playing critical roles in both the initial inflammation following myocardial ischaemia and subsequent recovery. Monocytes are a heterogeneous cell population and observations from experimental models demonstrate that immediately following myocardial injury, classical inflammatory monocytes, which are highly phagocytic, are recruited to ischaemic myocardium from the bone marrow and spleen and peak at 48 hours. This is followed by the recruitment of non-classical monocytes that are involved in repair and healing, peaking at day 5. The monocyte response in humans following AMI is currently poorly understood. Due to their central role in the pathogenesis of AMI, monocytes are attractive both as potential biomarkers to inform of extent of myocardial injury (and recovery) and also as therapeutic targets with the specific targeting of monocytes in experimental models resulting in reduced infarction size and improved LV remodelling. However, in spite of these promising results and our greater understanding of the pathogenesis of AMI, no immune-modulating therapeutic has been translated into routine clinical practice. We therefore hypothesized that characterisation of the monocyte response to AMI by flow cytometry and gene expression profiling in both experimental models and humans would give novel insights into underlying biological processes and function (both locally in the myocardium and systemically), identify novel therapeutic targets, enable their use as cellular biomarkers of disease, and test conservation between species validating the experimental model for future investigation. Classical inflammatory monocytes were found to significantly increase in the peripheral blood 48 hours following AMI in both mice and humans, with the magnitude of the monocyte response correlating with the extent of myocardial injury in both species. Gene expression profiling of peripheral circulating monocytes following AMI identified a number of candidate genes, biological pathways and upstream regulators that were conserved between species and that could represent novel therapeutic targets. Furthermore, in an experimental model of AMI, leukocytes appeared to have effects beyond the ischaemic myocardium, with leukocyte recruitment in remote myocardium and in kidneys associated with elevated inflammatory markers and endothelial activation.
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Buchanan, Lynne M. "Psychophysiological recovery after acute myocardial infarction /." Thesis, Connect to this title online; UW restricted, 1989. http://hdl.handle.net/1773/7244.

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Bouhidel, Jalaleddinne Omar. "Etude de la cardioprotection contre l'infarctus du myocarde au cours de l'obésité expérimentale." Thesis, Paris Est, 2010. http://www.theses.fr/2010PEST0034.

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L'infarctus du myocarde (IDM) est l'une des principales causes de morbi-mortalité dans les pays développés et ce malgré l'amélioration enregistrée ces dernières années dans sa prise en charge thérapeutique. L'obésité est classée comme étant un facteur de risque majeur pour les maladies coronaires par l'American Heart Association, et concerne 14,5 % de la population française (enquête ObEpi-Roche/INSERM, 2009). En utilisant un modèle expérimental d'obésité, la souris ob/ob génétiquement dépourvue en leptine, l'objectif du présent travail de thèse a été d'étudier l'efficacité de stratégies cardioprotectrices comme le postconditionnement (PCD) ischémique ou l'exercice physique chronique contre l'IDM. La première partie de ce travail de thèse a mis en évidence une perte de la cardioprotection par PCD ischémique au cours de l'obésité. L'étude des voies de signalisation aura permis de mettre en évidence l'implication des protéines phosphatases PTEN, MKP3 et PP2C dans l'inefficacité du PCD. La seconde partie de ce travail de thèse a montré un effet cardioprotecteur de l'exercice physique chronique contre l'IDM dans un contexte expérimental d'obésité. Cet effet est associé à une augmentation des défenses enzymatiques antioxydantes, à une amélioration des fonctions mitochondriales, à une activation des voies de signalisation cardioprotectrices RISK et SAFE et enfin à une diminution des protéines phosphatases impliquées dans la régulation négative des acteurs des voies de signalisation cardioprotectrices. La preuve scientifique des bienfaits de l'exercice est aujourd'hui un argument de poids pour poursuivre les efforts entrepris par les pouvoirs publics ces dernières années à travers le Programme National Nutrition Santé pour favoriser la pratique d'une activité physique et sportive et en particulier chez les obèses
Myocardial infarction (MI) remains the leading cause of morbidity and mortality in the developing countries despite significant therapeutic advances over these last years. Obesity is a major risk factor for coronary heart disease according to the American Heart Association and concern 14.5% of the French population (ObEpi-Roche/INSERM survey, 2009). Using the leptin-deficient ob/ob mice, an animal model of obesity, the aim of the present thesis was to investigate the efficacy of cardioprotective strategies such as ischemic postconditioning (PCD) or chronic physical exercise against MI. In the first part of this thesis, we have found that the cardioprotective effects of PCD vanish with obesity. The investigation of the cardioprotective pathways has revealed that protein phosphatases such as PTEN, MKP3 and PP2C are involved in the inability of PCD to protect the heart. The second part of this thesis has demonstrated for the first time a cardioprotective effect of chronic physical exercise against MI in an experimental model of obesity. This effect was associated with increased antioxidant enzymes, improved mitochondrial function, activation of the cardioprotective RISK and SAFE pathways and finally a decrease in the related protein phosphatases levels. The scientific proofs given by this work underlines the “Programme National Nutrition Santé” developed by the French government to encourage all people and especially obese people to observe physical and sport activities
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Dawson, Lynn Gail. "Coping behaviours in myocardial infarction rehabilitation." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/25722.

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This study was designed to discover the coping behaviours used by patients six to twelve months following a myocardial infarction (MI). The conceptualization of coping behaviours was based on the UBC Model for Nursing which directed the researcher to examine coping behaviours used to meet the patients' basic human needs. The specific research question was, "What new or already established coping behaviours have patients utilized after an MI in an attempt to satisfy their basic human needs?" Seven participants who had experienced an MI six to twelve months previously, were recruited from cardiologists. Data were collected from the participants during interviews using semi-structured open-ended questioning technique. Data were coded and analyzed using the constant comparative method developed by Glaser and Strauss. Three themes that emerged from the data were: 1) coping behaviours related to risk reduction, 2) coping behaviours related to returning to normal, 3) coping behaviours related to reaching a new normal. The findings supported the need for lifestyle changes involving the use of existing coping behaviours and/or the development of new coping behaviours to meet subjects' basic human needs. Certain unmet basic human needs were identified following an MI which required the development of new coping behaviours to meet them. Nurses are in a unique position to assist MI patients in developing coping behaviours to meet their basic human needs. The descriptions and explanations of coping behaviours identified in this study may serve as a useful guide for nurses to help patients deal with changes in their lives and develop necessary coping behaviours to meet their basic human needs.
Applied Science, Faculty of
Nursing, School of
Graduate
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Books on the topic "Myocardial Infarctio"

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J, Gersh Bernard, and Rahimtoola Shahbudin H, eds. Acute myocardial infarction. 2nd ed. NewYork: Chapman & Hall, 1996.

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David, McCall, ed. Acute myocardial infarction. New York: Churchill Livingstone, 1991.

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

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Blocker, William P. Rehabilitation after myocardial infarction. Basle: CIBA-Geigy, 1986.

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F, Oliver M., Vedin Anders, and Wilhelmsson Claes, eds. Myocardial infarction in women. Edinburgh: Churchill Livingstone, 1986.

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NHS Centre for Reviews & Dissemination., ed. Aspirin and myocardial infarction. York: NHS Centre for Reviews and Dissemination, University of York, 1995.

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E, Bush David, United States. Agency for Healthcare Research and Quality., and Johns Hopkins University. Evidence-based Practice Center., eds. Post-myocardial infarction depression. Rockville, MD: Agency for Healthcare Research and Quality, 2005.

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E, Manson JoAnn, ed. Prevention of myocardial infarction. New York: Oxford University Press, 1996.

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G, Nayler Winifred, Parratt James R, and International Society for Heart Research. European Section. Meeting., eds. Myocardial response to acute injury. Houndmills, Basingstoke: Macmillan Academic and Professional, 1991.

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R, Parratt James, and Nayler W. G. 1930-, eds. Myocardial response to acute injury. Basingstoke: Macmillan Press, 1992.

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Book chapters on the topic "Myocardial Infarctio"

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Becker, Christoph R. "Myocardial Infarction." In Integrated Cardiothoracic Imaging with MDCT, 251–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-72387-5_17.

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Selvester, Ronald H., David G. Strauss, and Galen S. Wagner. "Myocardial Infarction." In Electrocardiology, 169–264. London: Springer London, 2011. http://dx.doi.org/10.1007/978-0-85729-874-4_4.

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Seaver, Robert L. "Myocardial Infarction." In When Doctors Get Sick, 29–38. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2001-0_4.

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Roth, Elliot J. "Myocardial Infarction." In Encyclopedia of Clinical Neuropsychology, 2316–17. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_2192.

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Saclarides, Theodore J. "Myocardial Infarction." In Common Surgical Diseases, 103–6. New York, NY: Springer New York, 1998. http://dx.doi.org/10.1007/978-1-4757-2945-0_24.

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Liu, Peijun, Yining Wang, and Zheng-yu Jin. "Myocardial Infarction." In Cardiac CT, 9–14. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5305-9_2.

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Roth, Elliot J. "Myocardial Infarction." In Encyclopedia of Clinical Neuropsychology, 1–2. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-56782-2_2192-2.

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Ko, Hanjo. "Myocardial Infarction." In Anesthesiology, 13–18. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50141-3_2.

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Blake, Thomas M. "Myocardial Infarction." In The Practice of Electrocardiography, 173–85. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4612-0291-2_11.

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Miura, Tetsuji, Derek M. Yellon, and James M. Downey. "Myocardial Infarction." In Physiology and Pathophysiology of the Heart, 955–74. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0873-7_47.

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Conference papers on the topic "Myocardial Infarctio"

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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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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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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of Scar Mechanical Properties During Myocardial Infarct Healing in Rat." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176422.

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The mechanics of healing myocardial infarcts are an important determinant of post-infarction left ventricular (LV) function and remodeling. Large animal infarct models are well studied; healing infarct scars have been shown to be mechanically and structurally anisotropic [1], and this anisotropy may help preserve LV function during some stages of healing [2]. At the same time, it has been suggested that the rat model of myocardial infarction is more similar to humans in the range of infarct sizes and observed LV dysfunction [3]. However, in the rat model, infarct mechanics and their effect on the overall LV function have not been described so far.
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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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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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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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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 rat heart during diastolic filling. Biventricular geometries of healthy and infarcted rat hearts reconstructed from magnetic resonance images were imported in Abaqus©. The passive myocardium was modelled as a nearly incompressible, hyperelastic, transversely isotropic material represented by the strain energy function W = ½C(eQ − 1) with Q = bfE112 + bt(E222 + E332 + E322) + bfs(E122 + E212 + E132 + E312). Material parameters were obtained from literature [1]. As boundary conditions, the circumferential and longitudinal displacements at the base were set to zero. The radial displacements at the base were left free. A linearly increasing pressure from 0 to 3.80 kPa and 0.86 kPa, respectively, was applied to the endocardial surfaces of left and right ventricle. Average radial, circumferential and longitudinal strains during passive filling were −0.331, 0.135, 0.042 and −0.250, −0.078 and 0.046 for the healthy heart and the infarcted heart, respectively. The average radial, circumferential and longitudinal stresses were −1.196 kPa, 3.87 kPa in the healthy heart and 0.424 kPa and −1.90 kPa, 8.74 kPa and 1.69 kPa in the infarcted heart. The strains were considerable lower in the infarcted heart compared to the health heart whereas stresses were higher in the presence of an infarct compared to the healthy case. The results of this study indicate the feasibility of the models developed for a more comprehensive assessment of mechanics of the infarcted ventricle including extension to account for cardiac contraction.
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Teddy Weiss, A., David G. Fine, David Applebaum, Sima Welber, Dan Sapoznikov, Chaim Lotan, Morris Mosseri, Yonathan Hasin, and Meryyn S. Gotsman. "PREHOSPITAL CORONARY THROMBOLYSIS: A NEW STRATEGY IN ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642979.

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Thirty-four patients with acute myocardial infarction were treated prospectively using a new strategy of pre-hospital intravenous streptokinase given by a physician-operated mobile intensive care unit. Prehospital treated patients who had experienced no previous myocardial infarction were compared to a similar group treated with streptokinase in-hospital. All patients underwent cardiac catheterization on day 6.Patients receiving streptokinase in the pre-hospital phase of acute myocardial infarction had smaller infarcts and better residual myocardial function than the group given streptokinase in-hospital in terms of peak creatine phosphokinase (900 v.1298 IU, p=0.023), ejection fraction (62 v. 55%, p=0,004), computer-derived dysfunction index (427 v. 727, p=0.003), and electrocardiographic QRS score (4.1 v. 6.4, p=0.001). The only difference between these groups at baseline was the duration of pain prior to initiation of streptokinase therapy (1.0 ± 0.4 hours vs. 1.9 ± 0.9 hours). There were no major complications related to pre-hospital administration of streptokinase.Pre-hospital stretokinase infusion is feasible, safe and practical. It reduces ischemia time because treatment is not delayed until hospital arrival and therapy limits infarct size. Thrombolytic therapy for acute myocardial infarction can be initiated at home and should not be limited to hospitalized patients.
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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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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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Reports on the topic "Myocardial Infarctio"

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Li, Xiao, Fayang Ling, Wenchuan Qi, Sanmei Xu, Bingzun Yin, Zihan Yin, Qianhua Zheng, Xiang Li, and Fanrong Liang. Preclinical Evidence of Acupuncture on infarction size of Myocardial ischemia: A Systematic Review and Meta-Analysis of Animal Studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0044.

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Review question / Objective: Whether acupuncture is effective for infarction size on myocardial ischemia rat models. Condition being studied: Myocardial ischemia is a typical pathological condition of coronary heart disease (CHD), which has been a global issue with high incidence and mortality. Myocardial infarction caused by myocardial ischemia leads to cardiac dysfunction, and the size of myocardial infarction also determines the recovery and prognosis of cardiac function. Acupuncture, a long history of traditional Chinese medicine, is widely used to treat symptoms like thoracalgia and palpitation. Many researches based on rat experiments have shown that acupuncture affects infarction size, cardiac function, myocardial enzyme or arrhythmias severity on myocardial ischemia models; nevertheless, few literatures have systematically reviewed these studies, assessing the risk of bias, quality of evidence, validity of results, and summarizing potential mechanisms. A systematic review of animal studies can benefit future experimental designs, promote the conduct and report of basic researches and provide some guidance to translate the achievements of basic researches to clinical application in acupuncture for myocardial ischemia. Therefore, we will conduct this systematic review and meta analysis to evaluate effects of acupuncture on infarction size on myocardial ischemia rat models.
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Dejong, Marla J., Kyungeh An, Candace C. Cherrington, and Debra K. Moser. Predictors of Symptom Appraisal for Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada427523.

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Crowley, James P., C. R. Valeri, and Joseph Chazan. Myocardial Infarction and Transfusion Requirements in Transfusion Dependent Anemic Patients. Fort Belvoir, VA: Defense Technical Information Center, May 1990. http://dx.doi.org/10.21236/ada360239.

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Naydenov, Stefan, Nikolay Runev, Emil Manov, Nadya Naydenova, Mikhail Matveev, and Plamen Krastev. Diagnostic Potential of Signal-Averaged Orthogonal Electrocardiography in Acute Myocardial Infarction. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, February 2021. http://dx.doi.org/10.7546/crabs.2021.02.16.

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Liu, Sihan, Shuo Han, Yingzi Lin, and Yingzhe Jin. The obesity paradox in patients with ST-segment elevation myocardial infarction. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0015.

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Zhang, John Q. Post-Myocardial Infarction and Exercise Training on Myosin Heavy Chain and Cardiac Function. Science Repository, April 2019. http://dx.doi.org/10.31487/j.jicoa.2019.01.08.

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Yin, Ruoyun, Fan Zhang, Zhaoya Fan, Lei Tang, and Yuan Yang. Association between Abacavir Use With Myocardial Infarction: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0054.

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De Jong, Marla J. A Cross-Sectional Examination of Changes in Anxiety Early After Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada416443.

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Ratib, Karim, and Jim Nolan. ST-segment Elevation Myocardial Infarction Intervention in a Patient with Variant Radial Artery Anatomy. Radcliffe Cardiology, June 2017. http://dx.doi.org/10.15420/rc.2017.m007.

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De Jong, Marla J., Kyungeh An, Sharon McKinley, Bonnie J. Garvin, and Lynne A. Hall. Using a 0-10 Scale for Assessment of Anxiety in Patients with Acute Myocardial Infarction. Fort Belvoir, VA: Defense Technical Information Center, January 2003. http://dx.doi.org/10.21236/ada424770.

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