scholarly journals Imaging Inflammation in Patients and Animals: Focus on PET Imaging the Vulnerable Plaque

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2573
Author(s):  
Benjamin Bartlett ◽  
Herbert P. Ludewick ◽  
Silvia Lee ◽  
Shipra Verma ◽  
Roslyn J. Francis ◽  
...  
Keyword(s):  
Risk Assessment ◽  
Pet Imaging ◽  
Vulnerable Plaque ◽  
Animal Studies ◽  
Plaque Progression ◽  
Vulnerable Atherosclerotic Plaque ◽  
Coronary Syndrome ◽  
18F Fdg ◽  
Different Characteristics ◽  
Disease Pathways

Acute coronary syndrome (ACS) describes a range of conditions associated with the rupture of high-risk or vulnerable plaque. Vulnerable atherosclerotic plaque is associated with many changes in its microenvironment which could potentially cause rapid plaque progression. Present-day PET imaging presents a plethora of radiopharmaceuticals designed to image different characteristics throughout plaque progression. Improved knowledge of atherosclerotic disease pathways has facilitated a growing number of pathophysiological targets for more innovative radiotracer design aimed at identifying at-risk vulnerable plaque and earlier intervention opportunity. This paper reviews the efficacy of PET imaging radiotracers 18F-FDG, 18F-NaF, 68Ga-DOTATATE, 64Cu-DOTATATE and 68Ga-pentixafor in plaque characterisation and risk assessment, as well as the translational potential of novel radiotracers in animal studies. Finally, we discuss our murine PET imaging experience and the challenges encountered.

scholarly journals Intravascular Ultrasound Studies and the Vulnerable Atherosclerotic Plaque (Literature Review)

2017 ◽  
pp. 82-87 ◽  
Author(s):  
N. A. Kochergin ◽  
A. M. Kochergina
Keyword(s):  
Atherosclerotic Plaque ◽  
Vulnerable Plaque ◽  
Preventive Treatment ◽  
Myocardial Infarctions ◽  
Main Question ◽  
Vulnerable Atherosclerotic Plaque ◽  
Coronary Syndrome ◽  
Vulnerable Plaques ◽  
Current Guidelines ◽  
Acute Event

The vulnerable plaque is an atherosclerotic plaque which can lead to  thrombosis of a coronary artery with development of an acute coronary  syndrome. Most myocardial infarctions occur in people with average  levels of risk factors and thrombosis mostly originate from lesions that  are less severely narrowed. Thus, in most cases, these plaques are clinically silent before the “unheralded” acute event and would not  be considered eligible for preventive treatment based on current  guidelines. The main question is to identify thrombosis-prone  “vulnerable” plaques before they rupture or become destabilized. IVUS  is a useful tool in identifying high risk plaque features and vulnerable lesions in patients.

Crossed Cerebellar Diaschisis in Alzheimer’s Disease

2018 ◽  
Vol 15 (13) ◽  
pp. 1267-1275 ◽  
Author(s):  
F.E. Reesink ◽  
D. Vállez García ◽  
C.A. Sánchez-Catasús ◽  
D.E. Peretti ◽  
A.T. Willemsen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Left Hemisphere ◽  
Pet Imaging ◽  
Fdg Pet ◽  
Pathophysiological Mechanism ◽  
Crossed Cerebellar Diaschisis ◽  
Amyloid Accumulation ◽  
Cerebellar Diaschisis ◽  
18F Fdg

Background: We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging - Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging. Methods: 18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum. 11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging techniques, although scarcely described in neurodegenerative dementias. Results: To our knowledge this is the first report describing CCD in AD subjects with documentation of both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment. Conclusion: This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological mechanism, clinical relevance and therapeutic implications of CCD and the role of the cerebellum in AD need further investigation.

scholarly journals Bone marrow-derived NGFR+ cells regulate arterial remodeling and those poor mobilizations in peripheral blood in acute coronary syndrome predicts plaque progression at the non-targeted lesion

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Takashima ◽  
S Usui ◽  
S Matsuura ◽  
C Goten ◽  
O Inoue ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Coronary Syndrome ◽  
Peripheral Blood ◽  
Funding Source ◽  
Arterial Remodeling ◽  
Plaque Progression ◽  
Wild Type ◽  
Plaque Volume ◽  
Coronary Syndrome

Abstract Background In our previous 5-year cohort study, we demonstrated that low gene expression of nerve growth factor receptor (NGFR) in peripheral leucocytes in acute coronary syndrome (ACS) predicted repetitive coronary interventions at the de novo lesions. An NGFR-positive cell has been demonstrated to reside in bone marrow (BM) stromal fraction and to be increased in peripheral blood mononuclear cell (MNCs) fraction in patients with ischemic heart disease. Purpose To investigate whether the BM-NGFR+ cell is associated with arterial remodeling and the relationship between the levels of peripheral NGFR+ cells after ACS and coronary plaque progression in an experimental and prospective clinical study. Methods and results In an experimental study, 8-week-old C57B6/J wild type male mice were subjected to irradiation with 9.6 Gy and transplantation with BM (BMT) isolated from GFP-transgenic NGFR wild type (WT) or knock-out (KO) mice at day 1. Four weeks after BMT, the right carotid artery was ligated for 4 weeks. Induced neointimal area was increased (p<0.05), where cells under apoptosis were decreased (p<0.05) in NGFR-KO-BMT group compared to WT-BMT group (n=4). NGFR+ cells were not detected in wild type sham-operated artery, whereas in the ligated artery in WT-BMT group NGFR+ cells assembled in the developed neointima and exclusively presented double positive with GFP, but absent in NGFR-KO-BMT group (p<0.05, n=4). In a clinical study, thirty patients with ACS who underwent primary percutaneous coronary intervention (PCI) were enrolled. The peripheral blood sample was collected on days 0, 3 and 7, and 9 months follow-up and the number of NGFR+MNCs were measured by flowcytometric analysis. The plaque volume at non-targeted coronary lesion (non-TL:>5 mm proximal or distal to the implanted stents) were quantitatively analysed using gray-scale intravascular ultrasound (IVUS) and Q-IVUS™ software at the acute phase and 9 months follow-up. The number of NGFR+MNCs in peripheral blood was 1.5-fold increased at day 3 (0.064±0.056%) compared to day 0 (0.042±0.030%) (p<0.05). The change in normalized total plaque volume (TAVN) at non-TL at 9 months was negatively correlated with the number of NGFR+MNCs at day 0 (r=−0.51), day 3 (r=−0.51) and 9 months (r=−0.59) after ACS (p<0.05). Multiple regression analysis showed that NGFR+MNCs at day 0 (β=−0.48, p=0.01) and CRP (β=−0.53, P<0.01) are independent factors associating with TAVN change at non-TL at 9 months, regardless of LDL-cholesterol control level. ROC analysis revealed that NGFR+MNCs <0.049 at day 0 predicted the increase of TAVN with AUC 0.78; sensitivity 0.82 and specificity 0.67. Conclusions Bone marrow-derived peripheral NGFR+ cells negatively regulate arterial remodeling through appropriate apoptosis of neointimal cells and the peripheral level of NGFR+ cells in ACS predicts plaque progression at the non-targeted lesion. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): KAKENHI

Macrophage infiltrates in coronary plaque erosion portend a worse cardiovascular outcome in patients with acute coronary syndrome

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
R.A Montone ◽  
V Vetrugno ◽  
M Camilli ◽  
M Russo ◽  
M.G Del Buono ◽  
...  
Keyword(s):  
Acute Coronary Syndrome ◽  
Vulnerable Plaque ◽  
Cardiac Death ◽  
Cox Regression ◽  
Plaque Rupture ◽  
Culprit Lesion ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Plaque Erosion

Abstract Background Plaque erosion (PE) is responsible for at least one-third of acute coronary syndrome (ACS). Inflammatory activation is considered a key mechanism of plaque instability in patients with plaque rupture through the release of metalloproteinases and the inhibition of collagen synthesis that in turns lead to fibrous cap degradation. However, the clinical relevance of macrophage infiltration has never been investigated in patients with PE. Purpose In our study, we aimed at assessing the presence of optical coherence tomography (OCT)-defined macrophage infiltrates (MØI) at the culprit site in ACS patients with PE, evaluating their clinical and OCT correlates, along with their prognostic value. Methods ACS patients undergoing OCT imaging and presenting PE as culprit lesion were retrospectively selected. Presence of MØI at culprit site and in non-culprit segments along the culprit vessel was assessed. The incidence of major adverse cardiac events (MACEs), defined as the composite of cardiac death, recurrent myocardial infarction and target vessel revascularization (TVR), was assessed [follow-up median (interquartile range, IQR) time 2.5 (2.03–2.58) years]. Results We included 153 patients [median age (IQR) 64 (53–75) years, 99 (64.7%) males]. Fifty-one (33.3%) patients presented PE with MØI and 102 (66.7%) PE without MØI. Patients having PE with MØI compared with PE patients without MØI had more vulnerable plaque features both at culprit site and at non-culprit segments. In particular, culprit lesion analysis demonstrated that patients with PE with MØI had a significantly thinner fibrous cap [median (IQR) 100 (60–120) μm vs. 160 (95–190) μm, p<0.001], higher prevalence of thrombus [41 (80.4%) vs. 64 (62.7%), p=0.028], lipid plaque [39 (76.5%) vs. 50 (49.0%), p<0.001], TCFA [20 (39.2%) vs. 14 (13.7%), p=0.001], and a higher maximum lipid arc [median [IQR] 250.0° (177.5°-290.0°) vs. 190.0° (150.0°-260.0°), p=0.018) at the culprit lesion compared with PE without MØI. MACEs were significantly more frequent in PE with MØI patients compared with PE without MØI [11 (21.6%) vs. 6 (5.9%), p=0.008], mainly driven by a higher risk of cardiac death and TVR. At multivariable Cox regression model, PE with MØI [HR=2.95, 95% CI (1.09–8.02), p=0.034] was an independent predictor of MACEs. Conclusion Our study demonstrates that among ACS patients with PE the presence of MØI at culprit lesion is associated with a more aggressive phenotype of coronary atherosclerosis with more vulnerable plaque features, along with a worse prognosis at a long-term follow-up. These findings are of the utmost importance in the era of precision medicine because clearly show that macrophage infiltrates may identify patients with a higher cardiovascular risk requiring more aggressive secondary prevention therapies and a closer clinical follow-up. Prognosis Funding Acknowledgement Type of funding source: None

scholarly journals Biological evaluation of [18F]FDG-Tz as a tracer candidate for pretargeted PET imaging

2021 ◽  
Vol 96-97 ◽  
pp. S71-S72
Author(s):  
Tatsiana Auchynnikava ◽  
Xiang-Guo Li ◽  
Heidi Liljenbäck ◽  
Anne Roivainen ◽  
Anu Airaksinen
Keyword(s):  
Pet Imaging ◽  
Biological Evaluation ◽  
18F Fdg

Optical coherence tomography and coronary angioscopy assessment of healed vulnerable plaque components in patients with coronary artery lesions undergoing elective percutaneous coronary intervention

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S Kimura ◽  
K Hara ◽  
M Ohmori ◽  
R Tateishi ◽  
T Kaneda ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Coronary Artery ◽  
Vulnerable Plaque ◽  
Multivariate Logistic Regression Analysis ◽  
Low Grade ◽  
Optical Coherence ◽  
Coronary Artery Lesions ◽  
Coronary Syndrome ◽  
Yellow Plaque ◽  
Coronary Angioscopy

Abstract Background Many vulnerable plaques would progress without clinical events and might result in healed plaques (HPs). Histopathological or intracoronary image assessment of HPs has been reported. However, the morphological characteristics of HPs remain unclear yet. Purpose We sought to assess the healed vulnerable plaque components in patients with coronary artery lesions using optical coherence tomography (OCT) and coronary angioscopy (CAS). Methods We enrolled 47 patients with 50 native coronary artery lesions with angiographical severe stenosis (>90% diameter-stenosis) and without severe calcification (36 lesions with stable angina pectoris (SAP) and 14 acute coronary syndrome (ACS)) undergoing pre-intervention OCT and CAS. HPs was defined as layered phenotype on OCT. Lesion morphologies and plaque characteristics in lesions with HPs were assessed using OCT and CAS images. Results HPs were observed in 27 lesions (54.0%) and their prevalence were similar among each clinical status (SAP 52.8%, ACS 57.1%, p=1.00). Lesions with HPs had higher prevalence of OCT-macrophage (88.0% vs. 52.0%, p=0.01), CAS-red thrombus (88.8% vs. 52.2%, p=0.004) and CAS-low grade-yellow plaque (grade 1) (55.6% vs. 21.7%, p=0.02) than those without. SAP lesions with HPs had higher prevalence of CAS-yellow plaque (35.3% vs. 5.9%, p=0.09) and OCT-thin-cap fibroatheroma (42.1% vs. 5.9%, p=0.04) than SAP without HPs. ACS lesions with HPs had less CAS-red thrombus (0.0% vs. 50.0%, p=0.03) and OCT-plaque rupture (12.5% vs. 66.7%, p=0.04) than ACS without HPs. Multivariate logistic regression analysis revealed that OCT-macrophages (odds ratio (OR): 6.65, 95%-confidence intervals: 1.07–41.5, p=0.043), CAS-red thrombus (OR 8.77, 95% CI 1.33–57.8, p=0.02), and low grade-yellow plaque (OR 13.05, 95% CI 1.97–86.5, p=0.008) were independently related with the existence of HPs lesions. Combination of these 3 factors showed a high predictive value of OCT-HPs lesions (90.9%). Conclusions HPs lesions showed the lower lesion vulnerability than common ACS lesions but had more intraplaque inflammatory condition compared with common SAP lesions. Combined CAS and OCT examination might be useful to clarify the plaque components of HPs lesions in vivo, leading to help us understand the clinical significance of HPs. Funding Acknowledgement Type of funding source: None

The effect of PPAR-γ agonist on 18F-FDG PET imaging for differentiating tumors and inflammation lesions

2015 ◽  
Vol 42 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Su-Jin Cheong ◽  
Chang-Moon Lee ◽  
Eun-Mi Kim ◽  
Seok Tae Lim ◽  
Myung-Hee Sohn ◽  
...  
Keyword(s):  
Pet Imaging ◽  
Fdg Pet ◽  
Ppar Γ ◽  
18F Fdg
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