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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerosis represents one of the main risk factors for the development of cardiovascular diseases. Their etiologies have been studied in recent years in order to better define therapeutic targets for intervention and to identify diagnostic methods. Two different subtypes of macrophages, M1 and M2, have been described in physiological conditions. They can also be found in the atherosclerotic process, where they both have opposite roles in disease progression. Perivascular brown adipose tissue is also involved in inflammation and endothelial damage. In this work, we provide insights into the protective role of melatonin in the atherosclerotic process by morphological and 18F-FDG-PET/CT analyses. In particular, we examined the effects of melatonin on pathways that are linked to atherosclerosis development. We showed that melatonin, by suppressing M1 activity, reduced inflammation and directed macrophage polarization toward the M2 macrophage subtype. Moreover, melatonin preserved the activity of perivascular brown adipose tissue. In addition, 18F-FDG uptake is very high in mice treated with melatonin, confirming that other factors may alter 18F-FDG distribution. In conclusion, we showed that melatonin affects inflammatory pathways that have been linked to atherosclerosis, assessed the relationships of the 18F-FDG PET/CT parameters with macrophage markers and the production of their cytokines, which that have been defined by morphological evaluations.
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PMID:Beneficial Effects of Melatonin on Apolipoprotein-E Knockout Mice by Morphological and 18F-FDG PET/CT Assessments. 3233 Dec 51

Cardiovascular diseases (CVDs) have been the leading cause of death in United States. While tremendous progress has been made for treating CVDs over the year, the high prevalence and substantial medical costs requires the necessity for novel methods for the early diagnosis and treatment monitoring of CVDs. Macrophages are a promising target due to its crucial role in the progress of CVDs (atherosclerosis, myocardial infarction and inflammatory cardiomyopathies). Positron emission tomography (PET) is a noninvasive imaging technique with high sensitivity and provides quantitive functional information of the macrophages in CVDs. Although 18F-FDG can be taken up by active macrophages, the PET imaging tracer is non-specific and susceptible to blood glucose levels. Thus, developing more specific PET tracers will help us understand the role of macrophages in CVDs. Moreover, macrophage-targeted PET imaging will further improve the diagnosis, treatment monitoring, and outcome prediction for patients with CVDs. In this review, we summarize various targets-based tracers for the PET imaging of macrophages in CVDs and highlight research gaps to advise future directions.
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PMID:PET imaging of macrophages in cardiovascular diseases. 3250 58

Atherosclerosis is a chronic and most often progressive disease with a long clinically apparently silent period, and can become unstable at any time, due to a plaque rupture or erosion, leading to an acute atherothrombotic event. Atherosclerosis has a progression rate that is highly variable among patients and in the same patient. The progression of atherosclerotic plaque from asymptomatic to symptomatic phase depends on its structure and composition in which inflammation plays an essential role. Prototype of the ruptured plaque contains a large, soft, lipid-rich necrotic core with intraplaque hemorrhage that accounts for more than half of the volume of the plaque covered by a thin and inflamed fibrous cap with few smooth muscle cells, and a heavy infiltrate of inflammatory cells. Noninvasive imaging modalities might provide an assessment of the atherosclerotic disease process through the exploration of these plaque features. Computed tomography angiography and magnetic resonance imaging can characterize plaque morphology, whereas molecular imaging, owing to the high sensitivity of nuclear medicine for the detection of radiopharmaceuticals in tissues, allows to explore plaque biology. During the last 2 decades, FDG-PET imaging has also emerged as a powerful tool to explore noninvasively inflammatory activities in atherosclerotic plaques providing new insights on the evolution of metabolic activities in the vascular wall over time. This review highlights the role of PET imaging for the exploration of metabolic activities in atherosclerotic plaques. It will resume the evidence that have been gathered from clinical studies using FDG-PET and will discuss the perspectives of new radiopharmaceuticals for vulnerable plaque imaging.
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PMID:A Clinical Role of PET in Atherosclerosis and Vulnerable Plaques? 3254 28

The aim of this study was to investigate the feasibility of FDG-PET/CT imaging to detect pulmonary artery atherosclerosis and to assess the correlation between pulmonary function testing (PFT) results and the overall pulmonary artery metabolic activity. Twenty-nine subjects between the ages of 57-75, with a history of clinical suspicion of lung cancer, underwent PET/CT imaging at 3 hours following the administration of FDG. Global FDG uptake in the central pulmonary artery branches was determined. Average SUVmax, SUVmean, and tissue-to-background (TBR) mean and maximum were calculated within each vessel. The degree of FDG uptake in non-COPD and COPD patients and its correlation with PFT were examined in this population. Furthermore, the results from patients were compared with those of 10 age-matched controls. Based on these data, the number of lesions with varying degrees of FDG uptake among patients was higher than that in the normal control group. However, there was no statistically significant difference in average SUVmax, average SUVmean, average TBRmax, or average TBRmean between non-COPD and COPD patients. This indicates that the atherosclerotic process is focal and is not diffuse in nature. Although the global quantitative data generated did not reveal evidence for diffuse artery inflammation in patients with COPD, qualitative examination showed clear-cut evidence for focally increased FDG uptake in the pulmonary arteries. This observation indicates the presence of atherosclerotic plaques which are prevalent in patients with COPD. Future prospective studies with larger numbers of subjects are needed to confirm this important observation.
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PMID:Detection of pulmonary artery atherosclerosis by FDG-PET/CT: a new observation. 3270 3

Positron emission tomography (PET) imaging can yield unique mechanistic insights into the pathophysiology of atherosclerosis. 18F-fluorodeoxyglucose (18F-FDG), a radiolabeled glucose analog, is retained by cells in proportion to their glycolytic activity. While 18F-FDG accumulates within several cell types in the arterial wall, its retention correlates with macrophage content, providing an index of arterial inflammation (ArtI) which predicts subsequent cardiovascular disease (CVD) events. Furthermore, 18F-FDG-PET imaging allows the simultaneous assessment of metabolic activity in several tissues (e.g., brain, bone marrow) and is performed in conjunction with cross-sectional imaging that enables multi-organ structural assessments. Accordingly, 18F-FDG-PET/computed tomography (CT) imaging facilitates evaluation of disease pathways that span multiple organ systems. Within this paradigm, 18F-FDG-PET/CT imaging has been implemented to study the mechanism linking chronic stress to CVD. To evaluate this, stress-associated neural activity can be quantified (as metabolic activity of the amygdala (AmygA)), while leukopoietic activity, ArtI, and coronary plaque burden are assessed concurrently. Such simultaneous quantification of tissue structures and activities enables the evaluation of multi-organ pathways with the aid of mediation analysis. Using this approach, multi-system 18F-FDG-PET/CT imaging studies have demonstrated that chronically heightened stress-associated neurobiological activity promotes leukopoietic activity and systemic inflammation. This in turn fuels more ArtI and greater non-calcified coronary plaque burden, which result in more CVD events. Subsequent studies have revealed that common stressors, such as chronic noise exposure and income disparities, drive the front end of this pathway to increase CVD risk. Hence, multi-tissue multimodality imaging serves as a powerful tool to uncover complex disease mechanisms.
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PMID:Multimodality molecular imaging: Gaining insights into the mechanisms linking chronic stress to cardiovascular disease. 3320 28

Over the past several decades, molecular imaging techniques to assess cellular processes in vivo have been integral in advancing our understanding of disease pathogenesis. 18F-fluorodeoxyglucose (18-FDG) positron emission tomography (PET) imaging in particular has shaped the field of atherosclerosis research by highlighting the importance of underlying inflammatory processes that are responsible for driving disease progression. The ability to assess physiology using molecular imaging, combining it with anatomic delineation using cardiac coronary angiography (CCTA) and magnetic resonance imaging (MRI) and lab-based techniques, provides a powerful combination to advance both research and ultimately clinical care. In this review, we demonstrate how molecular imaging studies, specifically using 18-FDG PET, have revealed that early vascular disease is a systemic process with multiple, concurrent biological mechanisms using inflammatory diseases as a basis to understand early atherosclerotic mechanisms in humans.
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PMID:The application of molecular imaging to advance translational research in chronic inflammation. 3324 75


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