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Journal articles on the topic 'Myocardial Infarctio'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Oleynikov, V. E., A. A. Chernova, E. V. Averyanova, and A. V. Kulyutsin. "Pathogenesis and clinical significance of reperfusion arrhythmias in acute myocardial infarctio." Russian Journal of Cardiology 29, no. 3S (2024): 5958. http://dx.doi.org/10.15829/1560-4071-2024-5958.

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The problem of ischemia-reperfusion injury, in particular, reperfusion arrhythmias, has remained controversial for many years. To date, there are no one frame of mind on the clinical and prognostic significance of tachyarrhythmias in the acute period of myocardial infarction. In addition, data on the incidence of reperfusion arrhythmias and related mortality are very contradictory. The review summarizes current concepts and results of studies devoted to the study of the clinical role of reperfusion arrhythmias. Their pathogenesis, structure, and impact on the long-term prognosis of patients ar

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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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5

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 (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 injectio

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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 w

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7

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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8

Song, Yi-Sun, Hyun-Woo Joo, In-Hwa Park, et al. "Transplanted Human Amniotic Epithelial Cells Secrete Paracrine Proangiogenic Cytokines in Rat Model of Myocardial Infarctio." Cell Transplantation 24, no. 10 (2015): 2055–64. http://dx.doi.org/10.3727/096368914x685609.

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9

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 (2013): A259.2—A259. http://dx.doi.org/10.1136/heartjnl-2013-304613.730.

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10

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 (1995): 3–10. http://dx.doi.org/10.1093/intqhc/7.1.3.

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11

Jin, Jiyang, Min Chen, Yongjun Li, et al. "Detecting Acute Myocardial Infarction by Diffusion-Weighted versus T2-Weighted Imaging and Myocardial Necrosis Markers." Texas Heart Institute Journal 43, no. 5 (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 myo

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12

Frangogiannis, Nikolaos G. "Pathophysiology of Myocardial Infarction." Comprehensive Physiology 5, no. 4 (2015): 1841–75. https://doi.org/10.1002/j.2040-4603.2015.tb00664.x.

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ABSTRACTMyocardial infarction is defined as sudden ischemic death of myocardial tissue. In the clinical context, myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function. Prolonged myocardial ischemia activates a “wavefront” of cardiomyocyte death that extends from the subendocardium to the subepicardium. Mitochondrial alterations are prominently involved in apoptosis and necrosis of cardiomyoc

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13

Nilsson, Stefan, Mats Wikström, Anders Ericsson, et al. "MR Imaging of Double-Contrast Enhanced Porcine Myocardial Infarction." Acta Radiologica 36, no. 4-6 (1995): 346–52. http://dx.doi.org/10.1177/028418519503600404.

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MR imaging was performed to investigate whether Gd-DTPA-BMA-induced contrast enhancement of myocardial infarction is counteracted by Dy-DTPA-BMA. Myocardial infarction was induced in 5 pigs. Microdialysate probes were inserted in ischemic and nonischemic myocardium. Gd-DTPA-BMA (0.3 mmol/kg b.w.) and Dy-DTPA-BMA (1.0 mmol/kg b.w.) were administered i.v. 4 hours post occlusion. The microdialysate was collected every 10 min and measured for Gd and Dy using inductively coupled plasma atomic emission spectrometry. The pigs were sacrificed 2 hours after administration of contrast media. The concent

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14

Hirsch, Alan T., John A. Opsahl, Mary M. Lunzer, and Stephen A. Katz. "Active renin and angiotensinogen in cardiac interstitial fluid after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 6 (1999): H1818—H1826. http://dx.doi.org/10.1152/ajpheart.1999.276.6.h1818.

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The renin-angiotensin system promotes cardiac hypertrophy after myocardial infarction. The purpose of this study was to measure renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Infarction involving 45 ± 4% of left ventricular circumference with accompanying hypertrophy was induced in rats ( n = 14). Plasma and myocardial renin were increased after infarction compared with sham controls ( n = 8) (27.4 ± 3.2 vs. 7.5 ± 1.8 ng ANG I ⋅ ml plasma ⋅ h−1, P < 0.0002; and 8.8 ± 1.6 vs. 2.5 ± 0.1 ng ANG I ⋅ g myocardium−1 ⋅ h−1, P < 0.008, respectively). Afte

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Thukkani, Arun K., Bradley D. Martinson, Carolyn J. Albert, George A. Vogler, and David A. Ford. "Neutrophil-mediated accumulation of 2-ClHDA during myocardial infarction: 2-ClHDA-mediated myocardial injury." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (2005): H2955—H2964. http://dx.doi.org/10.1152/ajpheart.00834.2004.

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The pathophysiological sequelae of myocardial infarction include neutrophil infiltration into the infarct zone that contributes to additional damage to viable tissue and removal of cellular debris from necrosed tissue. Reactive chlorinating species produced by myeloperoxidase amplify the oxidant capacity of activated neutrophils. Plasmalogens are a major phospholipid subclass of both endothelial cells and cardiac myocytes. Recent studies have shown that plasmalogens are targeted by neutrophil-derived reactive chlorinating species that lead to the production of α-chloro fatty aldehydes. Results

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16

Gosselin, H., X. Qi, and J. L. Rouleau. "Correlation between cardiac remodelling, function, and myocardial contractility in rat hearts 5 weeks after myocardial infarction." Canadian Journal of Physiology and Pharmacology 76, no. 1 (1998): 53–62. http://dx.doi.org/10.1139/y97-175.

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Early after infarction, ventricular dysfunction occurs as a result of loss of myocardial tissue. Although papillary muscle studies suggest that reduced myocardial contractility contributes to this ventricular dysfunction, in vivo studies indicate that at rest, cardiac output is normal or near normal, suggesting that contractility of the remaining viable myocardium of the ventricular wall is preserved. However, this has never been verified. To explore this further, 100 rats with various-sized myocardial infarctions had ventricular function assessed by Langendorff preparation or by isolated papi

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17

Berg, J., R. Jablonowski, D. Nordlund, et al. "Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume." Journal of Applied Physiology 128, no. 2 (2020): 252–63. http://dx.doi.org/10.1152/japplphysiol.00480.2019.

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Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microem

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Soepriatna, Arvin H., A. Kevin Yeh, Abigail D. Clifford, Semih E. Bezci, Grace D. O'Connell, and Craig J. Goergen. "Three-dimensional myocardial strain correlates with murine left ventricular remodelling severity post-infarction." Journal of The Royal Society Interface 16, no. 160 (2019): 20190570. http://dx.doi.org/10.1098/rsif.2019.0570.

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Heart failure continues to be a common and deadly sequela of myocardial infarction (MI). Despite strong evidence suggesting the importance of myocardial mechanics in cardiac remodelling, many MI studies still rely on two-dimensional analyses to estimate global left ventricular (LV) function. Here, we integrated four-dimensional ultrasound with three-dimensional strain mapping to longitudinally characterize LV mechanics within and around infarcts in order to study the post-MI remodelling process. To induce infarcts with varying severities, we separated 15 mice into three equal-sized groups: (i)

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Sawall, Stefan, Danielle Franke, Anne Kirchherr, et al. "In Vivo Quantification of Myocardial Infarction in Mice Using Micro-CT and a Novel Blood Pool Agent." Contrast Media & Molecular Imaging 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/2617047.

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We herein developed a micro-CT method using the innovative contrast agent ExiTron™ MyoC 8000 to longitudinally monitor cardiac processes in vivo in small animals. Experiments were performed on healthy mice and mice with myocardial infarction inflicted by ligation of the left anterior descending artery. Time-dependent signal enhancement in different tissues of healthy mice was measured and various contrast agent doses were investigated so as to determine the minimum required dose for imaging of the myocardium. Due to its ability to be taken up by healthy myocardium but not by infarct tissue, Ex

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20

Niccoli, Giampaolo, Rocco A. Montone, Borja Ibanez, et al. "Optimized Treatment of ST-Elevation Myocardial Infarction." Circulation Research 125, no. 2 (2019): 245–58. http://dx.doi.org/10.1161/circresaha.119.315344.

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Primary percutaneous coronary intervention is nowadays the preferred reperfusion strategy for patients with acute ST-segment–elevation myocardial infarction, aiming at restoring epicardial infarct-related artery patency and achieving microvascular reperfusion as early as possible, thus limiting the extent of irreversibly injured myocardium. Yet, in a sizeable proportion of patients, primary percutaneous coronary intervention does not achieve effective myocardial reperfusion due to the occurrence of coronary microvascular obstruction (MVO). The amount of infarcted myocardium, the so-called infa

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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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22

Li, Jianqiang, Danghui Sun, and Yue Li. "Novel Findings and Therapeutic Targets on Cardioprotection of Ischemia/ Reperfusion Injury in STEMI." Current Pharmaceutical Design 25, no. 35 (2019): 3726–39. http://dx.doi.org/10.2174/1381612825666191105103417.

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Acute ST-segment elevation myocardial infarction (STEMI) remains a leading cause of morbidity and mortality around the world. A large number of STEMI patients after the infarction gradually develop heart failure due to the infarcted myocardium. Timely reperfusion is essential to salvage ischemic myocardium from the infarction, but the restoration of coronary blood flow in the infarct-related artery itself induces myocardial injury and cardiomyocyte death, known as ischemia/reperfusion injury (IRI). The factors contributing to IRI in STEMI are complex, and microvascular obstruction, inflammatio

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Spath, N. B., D. M. L. Lilburn, G. A. Gray, et al. "Manganese-Enhanced T1 Mapping in the Myocardium of Normal and Infarcted Hearts." Contrast Media & Molecular Imaging 2018 (October 25, 2018): 1–13. http://dx.doi.org/10.1155/2018/9641527.

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Background. Manganese-enhanced MRI (MEMRI) has the potential to identify viable myocardium and quantify calcium influx and handling. Two distinct manganese contrast media have been developed for clinical application, mangafodipir and EVP1001-1, employing different strategies to mitigate against adverse effects resulting from calcium-channel agonism. Mangafodipir delivers manganese ions as a chelate, and EVP1001-1 coadministers calcium gluconate. Using myocardial T1 mapping, we aimed to explore chelated and nonchelated manganese contrast agents, their mechanism of myocardial uptake, and their a

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Nilsson, Stefan, Mats Wikström, Hans J. Martinussen, et al. "Dy-DTPA-BMA as an Indicator of Tissue Viability in MR Imaging." Acta Radiologica 36, no. 4-6 (1995): 338–45. http://dx.doi.org/10.1177/028418519503600403.

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The aim of this study was to investigate whether dysprosium (Dy) induced signal intensity (SI) loss in infarcted tissue in MR imaging. Myocardial infarction was induced in 12 pigs and Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. to 6 pigs 4 hours after occlusion and allowed to accumulate in the infarctions for 2 hours. Dy was analysed by inductively coupled plasma atomic emission spectrometry in infarcted and non-ischaemic tissue samples. The remaining 6 pigs, not administered contrast medium, served as controls. The infarctions demonstrated a high SI in the proton density- and T2-weig

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Stukalova, O. V., Yu O. Shalaginova, R. M. Shakhnovich, et al. "Features of myocardial characteristics of patients with acute ST-segment elevation myocardial infarction with diabetes mellitus as assessed by contrast-enhanced cardiac magnetic resonance imaging." Aterotromboz = Atherothrombosis 13, no. 1 (2023): 58–72. http://dx.doi.org/10.21518/at2023-001.

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Introduction. The presence of diabetes mellitus in patients with acute infarction significantly worsens short- and long-term prognosis, but the features of the course of the infarction in this category of patients have not been fully studied.Objective. To compare clinical, functional and structural myocardial characteristics of patients with acute ST-segment elevation myocardial infarction with and without diabetes mellitus.Materials and methods. The study included 91 patients with revascularized ST-segment elevation myocardial infarction (41 patients with diabetes mellitus). All patients unde

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Jiang, Yi, Jianwen Bai, Lunxian Tang, Pei Zhang, and Jun Pu. "Anti-CCL21 Antibody Attenuates Infarct Size and Improves Cardiac Remodeling After Myocardial Infarction." Cellular Physiology and Biochemistry 37, no. 3 (2015): 979–90. http://dx.doi.org/10.1159/000430224.

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Background/Aims: Over-activation of cellular inflammatory effectors adversely affects myocardial function after acute myocardial infarction (AMI). The CC-chemokine CCL21 is, via its receptor CCR7, one of the key regulators of inflammation and immune cell recruitment, participates in various inflammatory disorders, including cardiovascular ones. This study explored the therapeutic effect of an anti-CCL21 antibody in cardiac remodeling after myocardial infarction. Methods and Results: An animal model of AMI generated by left anterior descending coronary artery ligation in C57BL/6 mice resulted i

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Li, Yingxu, Bing Li, Xuechun Wang, Yan Meng, Lu Bai, and Yuanyuan Zheng. "Safe and efficient magnetic resonance imaging of acute myocardial infarction with gadolinium-doped carbon dots." Nanomedicine 15, no. 24 (2020): 2385–98. http://dx.doi.org/10.2217/nnm-2020-0160.

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Aim: The magneto-fluorescent gadolinium-doped carbon dots (Gd-CDs) were developed as a cardiac MR imaging contrast agent to detect the infarcted myocardium on a myocardial ischemia/reperfusion (I/R) mice model. Materials & methods: The chemophysical features, cardiac MR imaging effect, biodistribution and biocompatibility of Gd-CDs were studied. Results: The ultrasmall size and good aqueous dispersibility endows Gd-CDs with high longitudinal relaxivity, intense fluorescence, excellent physiological stability and superior biocompatibility. More importantly, Gd-CDs preferentially target the

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Nilsson, S., G. Wikström, A. Ericsson, et al. "Myocardial Cell Death in Reperfused and Nonreperfused Myocardial Infarctions." Acta Radiologica 37, no. 1P1 (1996): 18–26. http://dx.doi.org/10.1177/02841851960371p105.

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Purpose: To investigate whether Dy-DTPA-BMA-enhanced MR imaging would permit identification of myocardial cell death, myocardial infarction was induced in 12 domestic pigs. Material and Methods: In 6 pigs with irreversible cell damage, Dy-DTPA-BMA (1.0 mmol/kg b.w.) was administered i.v. 70 min after coronary occlusion. In 6 other pigs, the infarctions were reperfused 80 min after the occlusion, followed by injection of Dy-DTPA-BMA after 30 min of reperfusion. In 4 additional pigs, the hearts were reperfused after 2 min of occlusion. All 16 pigs were sacrificed 10 min after the injection of Dy

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Kalinowski, Leszek, Lawrence W. Dobrucki, David F. Meoli, et al. "Targeted imaging of hypoxia-induced integrin activation in myocardium early after infarction." Journal of Applied Physiology 104, no. 5 (2008): 1504–12. http://dx.doi.org/10.1152/japplphysiol.00861.2007.

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The αvβ3-integrin is expressed in angiogenic vessels in response to hypoxia and represents a potential novel target for imaging myocardial angiogenesis. This study evaluated the feasibility of noninvasively tracking hypoxia-induced αvβ3-integrin activation within the myocardium as a marker of angiogenesis early after myocardial infarction. Acute myocardial infarction was produced by coronary artery occlusion in rodent and canine studies. A novel 111In-labeled radiotracer targeted at the αvβ3-integrin (111In-RP748) was used to localize regions of hypoxia-induced angiogenesis early after infarct

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Chilukoti, Ravi K., Josefine Lendeckel, Katrin Darm, et al. "Integration of “omics” techniques: Dronedarone affects cardiac remodeling in the infarction border zone." Experimental Biology and Medicine 243, no. 11 (2018): 895–910. http://dx.doi.org/10.1177/1535370218788517.

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Dronedarone improves microvascular flow during atrial fibrillation and reduces the infarct size in acute models of myocardial infarction. However, dronedarone might be harmful in patients with recent decompensated heart failure and increases mortality in patients with permanent atrial fibrillation. A pathophysiological explanation for these discrepant data is lacking. This study investigated the effects of dronedarone on gene and protein expression in the infarcted area and border zone in pigs subjected to anterior ischemia/reperfusion myocardial infarction. The ischemia/reperfusion myocardial

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Coletti, G., L. Torracca, M. Zogno, et al. "Surgical Management of Left Ventricular Free Wall Rupture after Acute Myocardial Infarction." Cardiovascular Surgery 3, no. 2 (1995): 181–86. http://dx.doi.org/10.1177/096721099500300213.

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Left ventricular rupture after acute myocardial infarction occurs more often than suspected and diagnosis is rarely made before death. Left ventricular rupture has been reported to contribute to the overall in-hospital mortality after acute myocardial infarction in up to 24% of cases and to be present in 40% of patients dying within the first week after infarction. Only prompt diagnosis and aggressive surgical treatment can be lifesaving under these circumstances. Between February 1991 and August 1993 five patients underwent emergency operation for left ventricular rupture after acute myocardi

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Henning, Robert J., Jose D. Burgos, Mark Vasko, et al. "Human Cord Blood Cells and Myocardial Infarction: Effect of Dose and Route of Administration on Infarct Size." Cell Transplantation 16, no. 9 (2007): 907–17. http://dx.doi.org/10.3727/096368907783338299.

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There is no consensus regarding the optimal dose of stem cells or the optimal route of administration for the treatment of acute myocardial infarction. Bone marrow cells, containing hematopoietic and mesenchymal stem cells, in doses of 0.5 × 106 to >30 × 106 have been directly injected into the myocardium or into coronary arteries or infused intravenously in subjects with myocardial infarctions to reduce infarct size and improve heart function. Therefore, we determined the specific effects of different doses of human umbilical cord blood mononuclear cells (HUCBC), which contain hematopoieti

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Helle-Valle, Thomas, Espen W. Remme, Erik Lyseggen, et al. "Clinical assessment of left ventricular rotation and strain: a novel approach for quantification of function in infarcted myocardium and its border zones." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (2009): H257—H267. http://dx.doi.org/10.1152/ajpheart.01116.2008.

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Left ventricular (LV) circumferential strain and rotation have been introduced as clinical markers of myocardial function. This study investigates how regional LV apical rotation and strain can be used in combination to assess function in the infarcted ventricle. In healthy subjects ( n = 15) and patients with myocardial infarction ( n = 23), LV apical segmental rotation and strain were measured from apical short-axis recordings by speckle tracking echocardiography (STE) and MRI tagging. Infarct extent was determined by late gadolinium enhancement MRI. To investigate mechanisms of changes in s

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Grothusen, Christina, Angelika Hagemann, Tim Attmann, et al. "Impact of an Interleukin-1 Receptor Antagonist and Erythropoietin on Experimental Myocardial Ischemia/Reperfusion Injury." Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/737585.

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Background. Revascularization of infarcted myocardium results in release of inflammatory cytokines mediating myocardial reperfusion injury and heart failure. Blockage of inflammatory pathways dampens myocardial injury and reduces infarct size. We compared the impact of the interleukin-1 receptor antagonist Anakinra and erythropoietin on myocardial ischemia/reperfusion injury. In contrast to others, we hypothesized that drug administration prior to reperfusion reduces myocardial damage.Methods and Results. 12–15 week-old Lewis rats were subjected to myocardial ischemia by a 1 hr occlusion of th

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Buttrick, P., C. Perla, A. Malhotra, D. Geenen, M. Lahorra, and J. Scheuer. "Effects of chronic dobutamine on cardiac mechanics and biochemistry after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (1991): H473—H479. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h473.

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After myocardial infarction in rats, muscle performance in the remaining hypertrophied myocardium deteriorates and is associated with a decrease in myosin adenosinetriphosphatase (ATPase) activity and a shift to the V3 myosin heavy-chain isoform. We have previously shown in another model of hypertrophy, secondary to renovascular hypertension, that chronic intermittent adrenergic stimulation with dobutamine (Db) can prevent this biochemical adaptation. The present study was undertaken to assess the effects of chronic Db treatment on cardiac mass, function, metabolism, and myosin biochemistry in

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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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Berry, Mark F., Adam J. Engler, Y. Joseph Woo, et al. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.

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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 (MSCs) into the acutely ischemic myocardium. Two weeks postinfarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were twofold stiffer than myocardium from noninfarcted

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Vasudevan, Praveen, Ralf Gaebel, Piet Doering, et al. "18F-FDG PET-Based Imaging of Myocardial Inflammation Predicts a Functional Outcome Following Transplantation of mESC-Derived Cardiac Induced Cells in a Mouse Model of Myocardial Infarction." Cells 8, no. 12 (2019): 1613. http://dx.doi.org/10.3390/cells8121613.

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Cellular inflammation following acute myocardial infarction has gained increasing importance as a target mechanism for therapeutic approaches. We sought to investigate the effect of syngeneic cardiac induced cells (CiC) on myocardial inflammation using 18F-FDG PET (Positron emission tomography)-based imaging and the resulting effect on cardiac pump function using cardiac magnetic resonance (CMR) imaging in a mouse model of myocardial infarction. Mice underwent permanent left anterior descending coronary artery (LAD) ligation inducing an acute inflammatory response. The therapy group received a

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Mochizuki, Teruhito, Kenya Murase, Hiroshi Higashino, et al. "Ischemic “memory image” in acute myocardial infarctio of123I-BMIPP after reperfusion therapy: A comparison with99mTc-pyrophosphate and201Tl dual-isotope SPECT." Annals of Nuclear Medicine 16, no. 8 (2002): 563–68. http://dx.doi.org/10.1007/bf02988634.

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Hiesinger, William, Sergei A. Vinogradov, Pavan Atluri, et al. "Oxygen-dependent quenching of phosphorescence used to characterize improved myocardial oxygenation resulting from vasculogenic cytokine therapy." Journal of Applied Physiology 110, no. 5 (2011): 1460–65. http://dx.doi.org/10.1152/japplphysiol.01138.2010.

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This study evaluates a therapy for infarct modulation and acute myocardial rescue and utilizes a novel technique to measure local myocardial oxygenation in vivo. Bone marrow-derived endothelial progenitor cells (EPCs) were targeted to the heart with peri-infarct intramyocardial injection of the potent EPC chemokine stromal cell-derived factor 1α (SDF). Myocardial oxygen pressure was assessed using a noninvasive, real-time optical technique for measuring oxygen pressures within microvasculature based on the oxygen-dependent quenching of the phosphorescence of Oxyphor G3. Myocardial infarction w

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Janes, R. D., D. E. Johnstone, and J. A. Armour. "Functional integrity of intrinsic cardiac nerves located over an acute transmural myocardial infarction." Canadian Journal of Physiology and Pharmacology 65, no. 1 (1987): 64–69. http://dx.doi.org/10.1139/y87-012.

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Acute transmural myocardial infarction has been reported to functionally denervate the normal myocardium distal to the infarcted zone by interrupting neurotransmission in axons coursing in the subepicardial region of the myocardial necrosis. To directly investigate the viability of such neurotransmission, the effects of acute transmural myocardial infarction on conduction in the intrinsic cardiac nerves overlying and distal to an experimentally induced acute transmural myocardial infarction were studied. In eight dogs, during control states electrical stimulation of the epicardium adjacent to

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Zheng, Wei, Robert M. Weiss, Xinguo Wang, et al. "DITPA stimulates arteriolar growth and modifies myocardial postinfarction remodeling." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (2004): H1994—H2000. http://dx.doi.org/10.1152/ajpheart.00991.2003.

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Myocardial infarction (MI) is characterized by ventricular remodeling, hypertrophy of the surviving myocardium, and an insufficient angiogenic response. Thyroxine is a powerful stimulus for myocardial angiogenesis. Male rats that underwent coronary artery ligation and subsequent MI were given 3,5-diiodothyropropionic acid (DITPA; MI+DITPA group) during a 3-wk period. We evaluated ventricular remodeling using echocardiography and histology and myocardial vessel growth using image analysis. Protein expression was assessed using Western blotting and immunohistochemistry. This study tested the hyp

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Boštjančič, E., N. Zidar, D. Štajer, and Damjan Glavač. "MicroRNA miR-1 is Up-regulated in Remote Myocardium in Patients with Myocardial Infarction." Folia Biologica 56, no. 1 (2010): 27–31. http://dx.doi.org/10.14712/fb2010056010027.

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MicroRNAs are small regulatory RNA molecules that mediate regulation of gene expression, thus affecting a variety of physiological, developmental and pathological conditions. They are believed to be new promising therapeutic targets. In recent studies two muscle-specific microRNAs were discovered to contribute to heart diseases and development: miR-1 and miR-133, but there is little data on their expression patterns in human myocardial infarction. We performed simultaneous expression analysis of miR-1, miR-133a, miR-133b in samples of infarcted tissue and remote myocardium from twenty-four pat

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Akhmedov, Alexander, Fabrizio Montecucco, Sarah Costantino, et al. "Cardiomyocyte-Specific JunD Overexpression Increases Infarct Size following Ischemia/Reperfusion Cardiac Injury by Downregulating Sirt3." Thrombosis and Haemostasis 120, no. 01 (2019): 168–80. http://dx.doi.org/10.1055/s-0039-3400299.

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AbstractIschemia/reperfusion (I/R) injury in acute myocardial infarction activates several deleterious molecular mechanisms. The transcription factor JunD regulates pathways involved in oxidative stress as well as in cellular proliferation, differentiation, and death. The present study investigated the potential role of JunD as a modulator of myocardial injury pathways in a mouse model of cardiac I/R injury. Infarct size, systemic and local inflammation, and production of reactive oxygen species, as well as cytosolic and mitochondrial apoptotic pathways were investigated in adult males after m

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Feldman, Dorothy, Gary Cavallo, and Lois Rosenberger. "Electron microscopic study of rat myocardial infarcts induced by a free radical generator system." Proceedings, annual meeting, Electron Microscopy Society of America 45 (August 1987): 876–77. http://dx.doi.org/10.1017/s0424820100128663.

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The role of oxygen free radicals in the development of tissue injury and necrosis, including myocardial ischemic damage, is well documented. In this investigation, application of a free radical generator system (FRG) to rat myocardium resulted in ECG alterations typical of myocardial infarction; 24 hours after treatment, plasma lactate dehydrogenase (LDH) levels were elevated and 20% of the left ventricle was infarcted. In order to characterize the type of cellular damage and the ultrastructural changes in the affected cells, myocardial infarcts and myocardium from control rats were examined i

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Saito, Takayuki, Ian W. Rodger, Hani Shennib, Fu Hu, Lara Tayara, and Adel Giaid. "Cyclooxygenase-2 (COX-2) in acute myocardial infarction: cellular expression and use of selective COX-2 inhibitor." Canadian Journal of Physiology and Pharmacology 81, no. 2 (2003): 114–19. http://dx.doi.org/10.1139/y03-023.

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Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery. Animals were either treated with a selective COX-2 inhibitor (5 mg·kg1·day1) or vehicle. Three days after ligation, cardiac function was assessed and infarct size was determi

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Watanabe, Eiichi, Duane M. Smith, Joseph B. Delcarpio, et al. "Cardiomyocyte Transplantation in a Porcine Myocardial Infarction Model." Cell Transplantation 7, no. 3 (1998): 239–46. http://dx.doi.org/10.1177/096368979800700302.

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Transplantation of cardiomyocytes into the heart is a potential treatment for replacing damaged cardiac muscle. To investigate the feasibility and efficiency of this technique, either a cardiac-derived cell line (HL-1 cells), or normal fetal or neonatal pig cardiomyocytes were grafted into a porcine model of myocardial infarction. The myocardial infarction was created by the placement of an embolization coil in the distal portion of the left anterior descending artery in Yorkshire pigs (n = 9). Four to 5 wk after creation of an infarct, the three preparations of cardiomyocytes were grafted, at

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Kuhn, Donald E., Sashwati Roy, Jared Radtke, Savita Khanna, and Chandan K. Sen. "Laser microdissection and capture of pure cardiomyocytes and fibroblasts from infarcted heart regions: perceived hyperoxia induces p21 in peri-infarct myocytes." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 3 (2007): H1245—H1253. http://dx.doi.org/10.1152/ajpheart.01069.2006.

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Myocardial infarction caused by ischemia-reperfusion in the coronary vasculature is a focal event characterized by an infarct-core, bordering peri-infarct zone and remote noninfarct zone. Recently, we have reported the first technique, based on laser microdissection pressure catapulting (LMPC), enabling the dissection of infarction-induced biological responses in multicellular regions of the heart. Molecular mechanisms in play at the peri-infarct zone are central to myocardial healing. At the infarct site, myocytes are more sensitive to insult than robust fibroblasts. Understanding of cell-spe

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Bohl, Steffen, Craig A. Lygate, Hannah Barnes, et al. "Advanced methods for quantification of infarct size in mice using three-dimensional high-field late gadolinium enhancement MRI." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 4 (2009): H1200—H1208. http://dx.doi.org/10.1152/ajpheart.01294.2008.

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Conventional methods to quantify infarct size after myocardial infarction in mice are not ideal, requiring either tissue destruction for histology or relying on nondirect measurements such as wall motion. We therefore implemented a fast, high-resolution method to directly measure infarct size in vivo using three-dimensional (3D) late gadolinium enhancement MRI (3D-LGE). Myocardial T1 relaxation was quantified at 9.4 Tesla in five mice, and reproducibility was tested by repeat imaging after 5 days. In a separate set of healthy and infarcted mice ( n = 8 of each), continuous T1 measurements were

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Teng, Xiaomei, Lei Chen, Weiqian Chen, Junjie Yang, Ziying Yang, and Zhenya Shen. "Mesenchymal Stem Cell-Derived Exosomes Improve the Microenvironment of Infarcted Myocardium Contributing to Angiogenesis and Anti-Inflammation." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2415–24. http://dx.doi.org/10.1159/000438594.

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Background/Aims: Bone marrow mesenchymal stem cells (MSCs) widely applied for treating myocardial infarction face survival challenges in the inflammatory and ischemia microenvironment of acute myocardial infarction. The study hypothesized that MSC-derived exosomes play a significant role in improving microenvironment after acute myocardial infarction and aimed to investigate the paracrine effects of exosomes on angiogenesis and anti-inflammatory activity. Methods: MSCs were cultured in DMEM/F12 supplemented with 10% exosome-depleted fetal bovine serum and 1% penicillin-streptomycin for 48 h. M

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