Log in

Relevant bibliographies by topics / Infarcted Myocardium / Journal articles

To see the other types of publications on this topic, follow the link: Infarcted Myocardium.

Journal articles on the topic 'Infarcted Myocardium'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Infarcted Myocardium.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

Song, Heesang, Hye Jin Hwang, Woochul Chang, et al. "Cardiomyocytes from phorbol myristate acetate-activated mesenchymal stem cells restore electromechanical function in infarcted rat hearts." Proceedings of the National Academy of Sciences 108, no. 1 (2010): 296–301. http://dx.doi.org/10.1073/pnas.1015873107.

Full text

Abstract:

Despite the safety and feasibility of mesenchymal stem cell (MSC) therapy, an optimal cell type has not yet emerged in terms of electromechanical integration in infarcted myocardium. We found that poor to moderate survival benefits of MSC-implanted rats were caused by incomplete electromechanical integration induced by tissue heterogeneity between myocytes and engrafted MSCs in the infarcted myocardium. Here, we report the development of cardiogenic cells from rat MSCs activated by phorbol myristate acetate, a PKC activator, that exhibited high expressions of cardiac-specific markers and Ca2+

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

7

Fang, Lu, Xiao-Ming Gao, Chrishan S. Samuel, et al. "Higher levels of collagen and facilitated healing protect against ventricular rupture following myocardial infarction." Clinical Science 115, no. 3 (2008): 99–106. http://dx.doi.org/10.1042/cs20070365.

Full text

Abstract:

The mechanism of cardiac rupture after MI (myocardial infarction) is not fully understood. Rupture has not been reported in most laboratory species, including the rat, but does occur in mice. We have reported previously that β2-TG mice (transgenic mice with cardiac-restricted overexpression of β2-adrenergic receptors) had a lower incidence of rupture compared with NTG (non-transgenic) littermates. We hypothesized that the difference in the incidence of rupture between rodents and specific mouse strains is due to the difference in collagen content following MI. In the present study, we compared

APA, Harvard, Vancouver, ISO, and other styles

8

Carlsson, Marcus, Nael F. Osman, Philip C. Ursell, Alastair J. Martin, and Maythem Saeed. "Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (2008): H522—H532. http://dx.doi.org/10.1152/ajpheart.00280.2008.

Full text

Abstract:

Previous studies have shown the beneficial effects of the hepatocyte growth factor (HGF) gene on myocardial perfusion and infarction size but not on the regional strain in relationship to global left ventricular function. A noninvasive magnetic resonance (MR) study was performed to determine the effect of a new HGF gene, VM202, expressing two isoforms of HGF, on regional and global left ventricular function. Pigs (8/group) were divided into three groups: 1) controls without infarction; 2) reperfused, infarcted controls; and 3) infarcted, treated (1 h after reperfusion) with VM202 injected at e

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

10

Wu, Guifu, Jamal S. Rana, Joanna Wykrzykowska, et al. "Exercise-induced expression of VEGF and salvation of myocardium in the early stage of myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 2 (2009): H389—H395. http://dx.doi.org/10.1152/ajpheart.01393.2007.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

11

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

13

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

14

Correa, Alejandro, Gabriel Salles Ottoboni, Alexandra Cristina Senegaglia, et al. "Expanded CD133+ Cells from Human Umbilical Cord Blood Improved Heart Function in Rats after Severe Myocardial Infarction." Stem Cells International 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/5412478.

Full text

Abstract:

Pharmacological approaches are partially effective in limiting infarct size. Cell therapies using a cell population enriched with endothelial progenitor cells (EPCs) CD133+ have opened new perspectives for the treatment of ischemic areas after infarction. This preclinical study evaluated the effect of intramyocardial transplantation of purified or expanded human umbilical cord blood-derived CD133+ cells on the recovery of rats following acute myocardial infarction (AMI). Histology studies, electrocardiogram, and fluorescence in situ hybridization (FISH) were used to evaluate heart recovery. Pu

APA, Harvard, Vancouver, ISO, and other styles

15

Ajijola, Olujimi A., Robert L. Lux, Anadjeet Khahera, et al. "Sympathetic modulation of electrical activation in normal and infarcted myocardium: implications for arrhythmogenesis." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 3 (2017): H608—H621. http://dx.doi.org/10.1152/ajpheart.00575.2016.

Full text

Abstract:

The influence of cardiac sympathetic innervation on electrical activation in normal and chronically infarcted ventricular myocardium is not understood. Yorkshire pigs with normal hearts (NL, n = 12) or anterior myocardial infarction (MI, n = 9) underwent high-resolution mapping of the anteroapical left ventricle at baseline and during left and right stellate ganglion stimulation (LSGS and RSGS, respectively). Conduction velocity (CV), activation times (ATs), and directionality of propagation were measured. Myocardial fiber orientation was determined using diffusion tensor imaging and histology

APA, Harvard, Vancouver, ISO, and other styles

16

Passier, R. C., J. F. Smits, M. J. Verluyten, and M. J. Daemen. "Expression and localization of renin and angiotensinogen in rat heart after myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 3 (1996): H1040—H1048. http://dx.doi.org/10.1152/ajpheart.1996.271.3.h1040.

Full text

Abstract:

Wistar-Kyoto rats underwent myocardial infarction (MI) or sham surgery. At different time points after surgery (1-90 days), hearts were removed and divided into infarcted left ventricle (LV), noninfarcted septum, and right ventricle. The tissues were used for total RNA isolation or Formalin fixation for in situ hybridization (ISH). Renin and angiotensinogen mRNA contents were quantified by the competitive reverse transcriptase polymerase chain reaction. We found a 4-, 14-, and 8-fold increase (P < 0.05, n = 6) in renin mRNA in the infarcted LV at 2, 4, and 7 days after MI, respectively. No

APA, Harvard, Vancouver, ISO, and other styles

17

Yu, Hui-Zhen, Xi Zheng, Li-Hong Lu, et al. "Inhibitory Factor and Matrix Metalloproteinases Expression in Rats With Myocardial Infarction." American Journal of Hypertension 35, no. 9 (2022): 834. http://dx.doi.org/10.1093/ajh/hpac037.

Full text

Abstract:

Abstract Background To investigate the effect of tissue kallikrein 1 (TK-1) overexpression on cardiac remodeling and myocardial expression of macrophage migration inhibitory factor (MIF) and matrix metalloproteinases (MMP) in myocardial infarction (MI) rats. Methods MI was induced by ligating left anterior descending arteries of Sprague-Dawley (SD) rats. Fifty-five SD rats were divided into sham operation, MI, MI + control adenovirus type 5 (Ad5), and MI + Ad5-TK-1 groups (n = 10–15 per group). Parameters of cardiac function were obtained by cardiac catheterization. Infarct area and infiltrati

APA, Harvard, Vancouver, ISO, and other styles

18

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

19

Schubert, Katja, Roland Hausmann, Barbara Dietel, et al. "Emergence of Dendritic Cells in the Myocardium after Acute Myocardial Infarction - Implications for Inflammatory Myocardial Damage." International Journal of Biomedical Science 6, no. 1 (2010): 27–36. http://dx.doi.org/10.59566/ijbs.2010.6027.

Full text

Abstract:

Dendritic cells (DC) are crucial for T cell mediated immune responses. Recently, we observed a significant decrease in circulating myeloid DC precursors in patients with acute myocardial infarction (AMI). The aim of the present study was to investigate whether myeloid DC are present in infarcted myocardium. Myocardial specimens of 10 patients with AMI and 7 accident victims (controls) were collected after autopsy. In immunostainings the presence of DC (CD209+, fascin+), T cells (CD3+), macrophages (CD68+), and HLA-DR expression was analyzed. Significantly higher numbers of CD209+-DC (97 vs. 44

APA, Harvard, Vancouver, ISO, and other styles

20

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

21

Loennechen, Jan P., Asbjørn Støylen, Vidar Beisvag, Ulrik Wisløff, and Øyvind Ellingsen. "Regional expression of endothelin-1, ANP, IGF-1, and LV wall stress in the infarcted rat heart." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 6 (2001): H2902—H2910. http://dx.doi.org/10.1152/ajpheart.2001.280.6.h2902.

Full text

Abstract:

We hypothesized that myocardial infarction induces regional and temporal differences in endothelin-1 (ET-1), atrial natriuretic peptide (ANP), and insulin-like growth factor-1 (IGF-1) gene expression that correlate with left ventricular (LV) wall stress. Echocardiography and LV pressure measurements were performed in coronary artery-ligated or sham-operated rats. Gene expression was measured by competitive RT-PCR in the infarct, border zone, and remote area and in regionally isolated cardiomyocytes. ET-1 and IGF-1 expression was highest in the infarcted myocardium, whereas ANP expression was h

APA, Harvard, Vancouver, ISO, and other styles

22

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

23

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

24

Patel, Amit N., Cristiano Spadaccio, Michael Kuzman, et al. "Improved Cell Survival in Infarcted Myocardium Using a Novel Combination Transmyocardial Laser and Cell Delivery System." Cell Transplantation 16, no. 9 (2007): 899–905. http://dx.doi.org/10.3727/096368907783338253.

Full text

Abstract:

Stem cell therapy has been used to treat ischemic cardiac disease with promising early results. However, there has been limited success using cell therapy in infarcted tissue. The cells have an inadequate microvascular environment in order to survive once implanted into scar tissue. The goal of this study was to create a microvascular environment into infarcted myocardial tissue using transmyocardial laser revascularization (TMR) as a pretreatment before cell implantation and evaluate cell survival afterwards. Balloon occlusion catheter-based myocardial infarct of the circumflex artery was cre

APA, Harvard, Vancouver, ISO, and other styles

25

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

26

Zeng, Zhipeng, Kunwu Yu, Long Chen, Weihua Li, Hong Xiao, and Zhengrong Huang. "Interleukin-2/Anti-Interleukin-2 Immune Complex Attenuates Cardiac Remodeling after Myocardial Infarction through Expansion of Regulatory T Cells." Journal of Immunology Research 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/8493767.

Full text

Abstract:

CD4+CD25+Foxp3+ regulatory T cells (Treg cells) have protective effects in wound healing and adverse ventricular remodeling after myocardial infarction (MI). We hypothesize that the interleukin- (IL-) 2 complex comprising the recombinant mouse IL-2/anti-IL-2 mAb (JES6-1) attenuates cardiac remodeling after MI through the expansion of Treg. Mice were subjected to surgical left anterior descending coronary artery ligation and treated with either PBS or IL-2 complex. The IL-2 complex significantly attenuates ventricular remodeling, as demonstrated by reduced infarct size, improved left ventricula

APA, Harvard, Vancouver, ISO, and other styles

27

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

28

Zhao, Le, Huaying Liu, Rui Gao, et al. "Brown Adipose Stem Cell-Loaded Resilin Elastic Hydrogel Rebuilds Cardiac Function after Myocardial Infarction via Collagen I/III Reorganisation." Gels 10, no. 9 (2024): 568. http://dx.doi.org/10.3390/gels10090568.

Full text

Abstract:

Irreversible fibrosis following myocardial infarction (MI) stiffens the infarcted myocardium, which remains challenging to restore. This study aimed to investigate whether the injectable RLP12 hydrogel, derived from recombinant resilin protein, could serve as a vehicle for stem cells to enhance the function of the infarcted myocardium. The RLP12 hydrogel was prepared and injected into the myocardium of rats with MI, and brown adipose-derived mesenchymal stem cells (BADSCs) were loaded. The survival and differentiation of BADSCs in vivo were investigated using immunofluorescence one week and fo

APA, Harvard, Vancouver, ISO, and other styles

29

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

30

Uematsu, Manabu, Toru Yoshizaki, Takuya Shimizu та ін. "Sustained myocardial production of stromal cell-derived factor-1α was associated with left ventricular adverse remodeling in patients with myocardial infarction". American Journal of Physiology-Heart and Circulatory Physiology 309, № 10 (2015): H1764—H1771. http://dx.doi.org/10.1152/ajpheart.00493.2015.

Full text

Abstract:

The role of stromal cell-derived factor-1α (SDF-1α) expressed in infarcted myocardium is unknown in humans. We examined whether SDF-1α produced in an infarcted myocardial lesion may play a role in left ventricle (LV) remodeling and dysfunction in patients with acute myocardial infarction (AMI). We measured SDF-1α levels in plasma obtained from aortic root (AO) and anterior interventricular vein (AIV) in the early phase (2 wk after MI) and the chronic phase (6 mo after MI) in 80 patients with anterior MI. An increment in SDF-1α level from AO to AIV, reflecting SDF-1α release from infarcted myoc

APA, Harvard, Vancouver, ISO, and other styles

31

Dang, Alan B. C., Julius M. Guccione, Jacob M. Mishell, et al. "Akinetic myocardial infarcts must contain contracting myocytes: finite-element model study." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 4 (2005): H1844—H1850. http://dx.doi.org/10.1152/ajpheart.00961.2003.

Full text

Abstract:

Infarcted segments of myocardium demonstrate functional impairment ranging in severity from hypokinesis to dyskinesis. We sought to better define the contributions of passive material properties (stiffness) and active properties (contracting myocytes) to infarct thickening. Using a finite-element (FE) model, we tested the hypothesis that infarcted myocardium must contain contracting myocytes to be akinetic and not dyskinetic. A three-dimensional FE mesh of the left ventricle was developed with echocardiographs from a reperfused ovine anteroapical infarct. The nonlinear stress-strain relationsh

APA, Harvard, Vancouver, ISO, and other styles

32

Tsujita, Kenichi, Koichi Kaikita, Takanori Hayasaki, et al. "Targeted Deletion of Class A Macrophage Scavenger Receptor Increases the Risk of Cardiac Rupture After Experimental Myocardial Infarction." Circulation 115, no. 14 (2007): 1904–11. http://dx.doi.org/10.1161/circulationaha.106.671198.

Full text

Abstract:

Background— Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A–deficient (SR-A −/− ) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Methods and Results— Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A −/− and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in

APA, Harvard, Vancouver, ISO, and other styles

33

Mester-Tonczar, Julia, Patrick Einzinger, Johannes Winkler, et al. "Novel Identified Circular Transcript of RCAN2, circ-RCAN2, Shows Deviated Expression Pattern in Pig Reperfused Infarcted Myocardium and Hypoxic Porcine Cardiac Progenitor Cells In Vitro." International Journal of Molecular Sciences 22, no. 3 (2021): 1390. http://dx.doi.org/10.3390/ijms22031390.

Full text

Abstract:

Circular RNAs (circRNAs) are crucial in gene regulatory networks and disease development, yet circRNA expression in myocardial infarction (MI) is poorly understood. Here, we harvested myocardium samples from domestic pigs 3 days after closed-chest reperfused MI or sham surgery. Cardiac circRNAs were identified by RNA-sequencing of rRNA-depleted RNA from infarcted and healthy myocardium tissue samples. Bioinformatics analysis was performed using the CIRIfull and KNIFE algorithms, and circRNAs identified with both algorithms were subjected to differential expression (DE) analysis and validation

APA, Harvard, Vancouver, ISO, and other styles

34

&NA;. "Accurately targeting the infarcted myocardium." Inpharma Weekly &NA;, no. 848 (1992): 11. http://dx.doi.org/10.2165/00128413-199208480-00017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Cochain, Clement, Keith M. Channon, and Jean-Sébastien Silvestre. "Angiogenesis in the Infarcted Myocardium." Antioxidants & Redox Signaling 18, no. 9 (2013): 1100–1113. http://dx.doi.org/10.1089/ars.2012.4849.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

del Rio, Carlos L., Patrick I. McConnell, Monica Kukielka, et al. "Electrotonic remodeling following myocardial infarction in dogs susceptible and resistant to sudden cardiac death." Journal of Applied Physiology 104, no. 2 (2008): 386–93. http://dx.doi.org/10.1152/japplphysiol.01106.2007.

Full text

Abstract:

Passive electrical remodeling following myocardial infarction (MI) is well established. These changes can alter electrotonic loading and trigger the remodeling of repolarization currents, a potential mechanism for ventricular fibrillation (VF). However, little is known about the role of passive electrical markers as tools to identify VF susceptibility post-MI. This study investigated electrotonic remodeling in the post-MI ventricle, as measured by myocardial electrical impedance (MEI), in animals prone to and resistant to VF. MI was induced in dogs by a two-stage left anterior descending (LAD)

APA, Harvard, Vancouver, ISO, and other styles

37

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

38

Greco, C., M. Ciavolella, G. Tanzilli, et al. "Preoperative Identification of Viable Myocardium: Effectiveness of Nitroglycerine-Induced Changes in Myocardial Sestamibi Uptake." Cardiovascular Surgery 6, no. 2 (1998): 149–55. http://dx.doi.org/10.1177/096721099800600208.

Full text

Abstract:

In order to predict tissue viability in infarcted myocardial areas, changes induced by nitroglycerine infusion on Sestamibi myocardial uptake were evaluated in 37 patients with previously confirmed myocardial infarction undergoing coronary artery bypass grafting, and compared with echocardiographic and perfusional changes occurring after the operation. The improvement of Sestamibi uptake after nitroglycerine correctly classified 24/26 (92%) patients showing postoperative improvement of wall motion in the infarcted area, whereas 24/31 (77%) patients with nitroglycerine-induced increase in Sesta

APA, Harvard, Vancouver, ISO, and other styles

39

Fellenius, E., C. A. Hansen, O. Mjos, and J. R. Neely. "Chronic infarction decreases maximum cardiac work and sensitivity of heart to extracellular calcium." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (1985): H80—H87. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h80.

Full text

Abstract:

Rat hearts were infarcted in vivo by ligation of the left ventricular coronary artery to cause an initial 40% loss of viable tissue by weight. Due to compensatory hypertrophy of the surviving myocardium and progression of the infarct to scar tissue, the infarct represented approximately 25% by weight of the whole heart after 1 wk. After 1 or 3 wk, these infarcted hearts were removed and perfused in vitro by the working hearts technique. Ventricular pressure development and positive dP/dt were lower in infarcted hearts compared with sham-operated ones. O2 consumption and glucose utilization by

APA, Harvard, Vancouver, ISO, and other styles

40

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.

Full text

Abstract:

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)

APA, Harvard, Vancouver, ISO, and other styles

41

Chan, Shing Fai, Xingmin Guan, Keyur P. Vora, Rohan Dharmakumar, and Behzad Sharif. "HEMORRHAGIC MYOCARDIAL INFARCTION DRIVES LIPOMATOUS METAPLASIA OF INFARCTED MYOCARDIUM." Journal of the American College of Cardiology 81, no. 8 (2023): 1289. http://dx.doi.org/10.1016/s0735-1097(23)01733-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Klyachkin, Yuri M., Anush V. Karapetyan, Mariusz Z. Ratajczak, and Ahmed Abdel-Latif. "The Role of Bioactive Lipids in Stem Cell Mobilization and Homing: Novel Therapeutics for Myocardial Ischemia." BioMed Research International 2014 (2014): 1–12. http://dx.doi.org/10.1155/2014/653543.

Full text

Abstract:

Despite significant advances in medical therapy and interventional strategies, the prognosis of millions of patients with acute myocardial infarction (AMI) and ischemic heart disease (IHD) remains poor. Currently, short of heart transplantation with all of its inherit limitations, there are no available treatment strategies that replace the infarcted myocardium. It is now well established that cardiomyocytes undergo continuous renewal, with contribution from bone marrow (BM)-derived stem/progenitor cells (SPCs). This phenomenon is upregulated during AMI by initiating multiple innate reparatory

APA, Harvard, Vancouver, ISO, and other styles

43

Usov, V. Yu, E. V. Vyshlov, O. V. Mochula, et al. "CONTRAST-EHANCED MRI IN TIME-STRUCTURE ANALYSIS OF MYOCARDIAL DAMAGE IN ACUTE INFARCTION AND EARLY PREHOSPITAL THROMBOLYTIC THERAPY." Medical Visualization, no. 2 (April 28, 2018): 56–69. http://dx.doi.org/10.24835/1607-0763-2018-2-56-69.

Full text

Abstract:

Purpose:to evaluate the dependence of absolute and relative thickness of damaged myocardium in the acute myocardial infarction (AMI) area from the time interval between oncet of pain and start of intravenous thrombolysis (so-called “pain–needle time”), in AMI patients treated with prehospital intravenous thrombolysis and also later on with subsequent percutaneous coronary angiplasty (PCA) and stenting, using contrast-enhanced MRI of the heart Materials and methods. The study comprised data of CE-MRI studies in 25 patients with theyr first acute myocardial infarction, in whom the pre-hospital t

APA, Harvard, Vancouver, ISO, and other styles

44

Ribuot, Christophe, Claude Mossiat, Michelle Devissaguet, and Luc Rochette. "Beneficial effect of perindopril, an angiotensin-converting enzyme inhibitor, on left ventricular performance and noradrenaline myocardial content during cardiac failure development in the rat." Canadian Journal of Physiology and Pharmacology 68, no. 12 (1990): 1548–51. http://dx.doi.org/10.1139/y90-235.

Full text

Abstract:

The left coronary artery in rats was ligated for a period of 15 days to induce hypertrophy of the non-infarcted myocardium. Left ventricular performances were evaluated in the working heart model. In addition, cardiac hypertrophic indices and noradrenaline content were measured. Variables were determined in the absence or presence of the angiotensin-converting enzyme inhibitor, perindopril. A 35 and 60% decrease in the coronary and cardiac output, respectively, and a 57% decrease in the noradrenaline content of the non-infarcted left ventricular free wall were seen. Furthermore, a 15% increase

APA, Harvard, Vancouver, ISO, and other styles

45

Hertenstein, Bernd, Kai C. Wollert, Michael Hofmann, et al. "Monitoring of Bone Marrow Cell Homing in the Infarcted Human Myocardium by PET." Blood 104, no. 11 (2004): 2696. http://dx.doi.org/10.1182/blood.v104.11.2696.2696.

Full text

Abstract:

Abstract Intracoronary transfer of autologous bone marrow cells (BMCs) has been shown to promote recovery of left ventricular (LV) systolic function in patients with acute myocardial infarction. (BOOST Trial; Wollert et al. Lancet, 2004, 364 141-8). Although the mechanisms of this effect remain to be established, homing of BMCs to the infarcted LV is probably a crucial early event. We determined BMC tissue distribution after therapeutic application in nine patients with a first ST-elevation myocardial infarction, who had undergone stenting of the infarct-related artery (all male; median age 43

APA, Harvard, Vancouver, ISO, and other styles

46

Saba, Shahryar G., John N. Makaryus, Navid Rahmani, and Ram Jadonath. "Histologic Sequelae of Apical Hypertrophic Cardiomyopathy: Dystrophic Calcification." Clinical Medicine Insights: Cardiology 11 (January 1, 2017): 117954681771093. http://dx.doi.org/10.1177/1179546817710934.

Full text

Abstract:

We present cardiac computed tomography (CT) findings demonstrating apical hypertrophic cardiomyopathy with dystrophic calcification of the left ventricular apex. The absence of significant epicardial coronary artery disease demonstrated by coronary CT angiography suggests that increased wall tension and decreased microvascular perfusion over time account for the dyskinetic apical myocardium, rather than myocardial infarction secondary to atherosclerotic plaque rupture. These observations support CT as the imaging modality of choice to visualize the deposition of calcium in injured myocardial t

APA, Harvard, Vancouver, ISO, and other styles

47

Frangogiannis, Nikolaos G., Leonardo H. Mendoza, Guofeng Ren, et al. "MCSF expression is induced in healing myocardial infarcts and may regulate monocyte and endothelial cell phenotype." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (2003): H483—H492. http://dx.doi.org/10.1152/ajpheart.01016.2002.

Full text

Abstract:

Myocardial infarction is associated with the rapid induction of mononuclear cell chemoattractants that promote monocyte infiltration into the injured area. Monocyte-to-macrophage differentiation and macrophage proliferation allow a long survival of monocytic cells, critical for effective healing of the infarct. In a canine infarction-reperfusion model, newly recruited myeloid leukocytes were markedly augmented during early reperfusion (5–72 h). By 7 days, the number of newly recruited myeloid cells was reduced, and the majority of the inflammatory cells remaining in the infarct were mature mac

APA, Harvard, Vancouver, ISO, and other styles

48

Saxena, Amit, Marcin Dobaczewski, Vikrant Rai, et al. "Regulatory T cells are recruited in the infarcted mouse myocardium and may modulate fibroblast phenotype and function." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 8 (2014): H1233—H1242. http://dx.doi.org/10.1152/ajpheart.00328.2014.

Full text

Abstract:

Regulatory T cells (Tregs) play a pivotal role in suppressing immune responses regulating behavior and gene expression in effector T cells, macrophages, and dendritic cells. Tregs infiltrate the infarcted myocardium; however, their role the inflammatory and reparative response after myocardial infarction remains poorly understood. We used FoxP3EGFP reporter mice to study Treg trafficking in the infarcted heart and examined the effects of Treg depletion on postinfarction remodeling using an anti-CD25 antibody. Moreover, we investigated the in vitro effects of Tregs on cardiac fibroblast phenoty

APA, Harvard, Vancouver, ISO, and other styles

49

Gatzke, Nora, Nadija Güc, Philipp Hillmeister, et al. "Cardiovascular drugs attenuated myocardial resistance against ischaemia-induced and reperfusion-induced injury in a rat model of repetitive occlusion." Open Heart 5, no. 2 (2018): e000889. http://dx.doi.org/10.1136/openhrt-2018-000889.

Full text

Abstract:

ObjectiveWe investigated the impact of cardioprotective drugs on ST-elevation, arrhythmias and infarct size in a rat model of repetitive coronary artery occlusion.MethodsSeventy Sprague-Dawley rats were randomised to two control and five treatment groups. Placebo was either implantation of a pneumatic occluder onto the left anterior descending coronary artery (LAD) without starting repetitive occlusion (SHAM) or subsequent RO of the LAD over 10 days without medication (ROP). Treatment groups underwent RO and additionally received nitroglycerin (NTG), metoprolol, verapamil (VER), ranolazine (RA

APA, Harvard, Vancouver, ISO, and other styles

50

Orlic, Donald, Jan Kajstura, Stefano Chimenti, et al. "Bone marrow cells regenerate infarcted myocardium." Nature 410, no. 6829 (2001): 701–5. http://dx.doi.org/10.1038/35070587.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!