2008
DOI: 10.1253/circj.cj-08-0046
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Multifocal, Persistent Cardiac Uptake of [18-F]-Fluoro-Deoxy-Glucose Detected by Positron Emission Tomography in Patients With Acute Myocardial Infarction

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Cited by 7 publications
(7 citation statements)
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“…14 MicroPET has been used for monitoring metabolic events in the myocardium of small animals in stem cell transplantation after myocardial infarction, 41,42 progressive hypertrophy, 43 and left ventricular dilation. 44 Increased FDG uptake has been shown in vitro in leukocytes, 45 lymphocytes, and macrophages 46,47 and in vivo in acute myocardial infarction, 48 abdominal aortic aneurism, 49 and atherosclerosis. 50 The increased uptake of FDG in T. cruzi -infected mice correlates with the intense and diffuse myocarditis observed during the acute phase and chronic inflammation and myocardium reparative fibrosis that occurs during the chronic phase.…”
Section: Discussionmentioning
confidence: 99%
“…14 MicroPET has been used for monitoring metabolic events in the myocardium of small animals in stem cell transplantation after myocardial infarction, 41,42 progressive hypertrophy, 43 and left ventricular dilation. 44 Increased FDG uptake has been shown in vitro in leukocytes, 45 lymphocytes, and macrophages 46,47 and in vivo in acute myocardial infarction, 48 abdominal aortic aneurism, 49 and atherosclerosis. 50 The increased uptake of FDG in T. cruzi -infected mice correlates with the intense and diffuse myocarditis observed during the acute phase and chronic inflammation and myocardium reparative fibrosis that occurs during the chronic phase.…”
Section: Discussionmentioning
confidence: 99%
“…This widespread inflammation is in agreement with post-mortem observations [31,36]. (Modified from Godino et al [27], with permission) severity or plaque morphology does not allow to efficiently predict ACS [35,36]. Indeed, on the one hand, plaque fissure can be an asymptomatic event [37] and is frequently observed in stable CAD [38].…”
Section: Assessment Of Inflammatory Cell Activation In Atherosclerotimentioning
confidence: 55%
“…3). A possible explanation might reside into the hypothesis that inflammatory cells could be responsible for this 18 FDG enhancement not only in infarcted but also in remote myocardial regions [27]. In fact, in the acute phase of STEMI, several cytokines, released in infarcted regions and involved in migration of leucocytes, could increase glucose uptake in inflammatory [28] and endothelial cells, by translocation of the glucose transporter from the cytoplasm to the plasma membrane [29,30]; thus, uptake of 18 FDG at follow-up could be related to widespread coronary microvascular and myocardial inflammation [31,32].…”
Section: Assessment Of Myocardial Perfusion and Metabolismmentioning
confidence: 99%
“…31 Beyersdolf et al reported in an animal study that in cases of single-vessel disease, increased glucose metabolism associated with increases in blood flow and endogenous adenosine in normal areas adjacent to the infarct region causes mild increases in 18 F-FDG uptake and excessive contraction of the myocardium in areas not affected by culprit lesions because of abnormalities in vasodilators after MI. 32 Godino et al 33 reported that in the first AMI of single-vessel disease, abnormal accumulation of 18 F-FDG outside of isch- emic areas was observed, which was caused by the stimulation of GLUT-1 because of the inflammation associated with the MI. They also observed abnormal accumulation of 18 F-FDG at 1 year after the AMI.…”
Section: Serial Changes Inmentioning
confidence: 99%