Imaging of Vascular Inflammation With [11C]-PK11195 and Positron Emission Tomography/Computed Tomography Angiography

Pugliese, Francesca; Gaemperli, Oliver; Kinderlerer, Anne; Lamare, F.; Shalhoub, Joseph; Davies, Alun H.; Rimoldi, Ornella; Mason, Justin C.; Camici, Paolo G.

doi:10.1016/j.jacc.2010.02.063

Cited by 139 publications

(101 citation statements)

References 30 publications

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“…However, it has become clear that for in vivo PET imaging of their distribution, there appears to be a wide spectrum of binding affinity of the receptors for these ligands in patients [98,99]. This may limit their clinical application, although there have been recent promising studies in vasculitis [100].…”

Section: Alternative Strategies For Imaging Vascular Inflammationmentioning

confidence: 99%

Vascular imaging with positron emission tomography

Joshi

Rosenbaum

Bordes

et al. 2011

Journal of Internal Medicine

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Atherosclerosis is an inflammatory disease that causes most myocardial infarctions, strokes and acute coronary syndromes. Despite the identification of multiple risk factors and widespread use of drug therapies, it still remains a global health concern with associated costs. Although angiography is established as the gold standard means of detecting coronary artery stenosis, it does not image the vessel wall itself, reporting only on its consequences such as luminal narrowing and obstruction. MRI and computed tomography provide more information about the plaque structure, but recently positron emission tomography (PET) imaging using [ 18 F]-fluorodeoxyglucose (FDG) has been advocated as a means of measuring arterial inflammation. This results from the ability of FDG-PET to highlight areas of high glucose metabolism, a feature of macrophages within atherosclerosis, particularly in high-risk plaques. It is suggested that the degree of FDG accumulation in the vessel wall reflects underlying inflammation levels and that tracking any changes in FDG uptake over time or with drug therapy might be a way of getting an early efficacy readout for novel anti-atherosclerotic drugs. Early reports also demonstrate that FDG uptake is correlated with the number of cardiovascular risk factors and possibly even the risk of future cardiovascular events. This review will outline the evidence base, shortcomings and emerging applications for FDG-PET in vascular imaging. Alternative PET tracers and other candidate imaging modalities for measuring vascular inflammation will also be discussed.

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Section: Alternative Strategies For Imaging Vascular Inflammationmentioning

confidence: 99%

Vascular imaging with positron emission tomography

Joshi

Rosenbaum

Bordes

et al. 2011

Journal of Internal Medicine

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“…11 Based on these reports, two subsequent pilot clinical imaging studies were performed in small groups of patients with arterial vasculitis and then in patients with carotid atherosclerosis using 11 C labeled PK11195 and imaging on a 16-slice PET/CT scanner. 13,14 In the first study, 6 patients with symptomatic large vessel vasculitis (giant cell arteritis, Takayasu's arteritis) were injected with 11 C-PK11195 and PET imaging acquired over 60 minutes in list mode and re-binned followed by CT angiography. 13 The CT scan matrix size was changed to match the PET scan and the images merged.…”

Section: See Related Article Pp 862-871mentioning

confidence: 99%

“…13,14 In the first study, 6 patients with symptomatic large vessel vasculitis (giant cell arteritis, Takayasu's arteritis) were injected with 11 C-PK11195 and PET imaging acquired over 60 minutes in list mode and re-binned followed by CT angiography. 13 The CT scan matrix size was changed to match the PET scan and the images merged. Focal uptake in the arterial wall segments of the aortic arch was identified corresponding to areas of aortic wall thickening on CT angiogram in all 6 of the vasculitis patients and minor uptake in the region of the carotid bifurcation in one subject with atheroma on CT in that area.…”

Section: See Related Article Pp 862-871mentioning

confidence: 99%

“…Focal uptake in the arterial wall segments of the aortic arch was identified corresponding to areas of aortic wall thickening on CT angiogram in all 6 of the vasculitis patients and minor uptake in the region of the carotid bifurcation in one subject with atheroma on CT in that area. 13 Using the same radioligand in a second study, this group of investigators imaged the carotid arteries in patients with both symptomatic and asymptomatic carotid atherosclerotic diseases.…”

Section: See Related Article Pp 862-871mentioning

confidence: 99%

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Targeting activated macrophages to identify the vulnerable atherosclerotic plaque

Johnson

2017

Journal of Nuclear Cardiology

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“…18 F-FDG PET/CT is being clinically used as a noninvasive diagnostic tool in cardiovascular medicine to detect myocardial viability, myocardial ischemia, cardiac inflammation, and infections. [15][16][17][18] PET/CT is also being studied as a tool in demonstrating vascular inflammation in patients with vasculitis 19,20 and in identifying vulnerable plaques in atherosclerotic cardiovascular disease. 21 This study by Pervaiz et al adds another potential use of 18 F-FDG PET/CT for imaging the inflammation and injury to the muscle and possibly other organ systems from CCE.…”

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confidence: 99%

18F-FDG for imaging microvascular injury

Harikrishnan

Gerard

Jain

2018

Journal of Nuclear Cardiology

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Atherosclerosis is an inflammatory process where oxidation of low-density lipoproteins (LDL) in the arterial wall causes initiation and progression of the atherosclerotic plaque by attracting macrophages. 1 The necrotic core of the vulnerable atherosclerotic plaque is rich in free cholesterol crystals derived from apoptotic lipid-laden macrophages and from the membranes of red blood cells which enter the core during intraplaque hemorrhage. 2 Vulnerable plaque is more prone to rupture. The plaque rupture triggers macrophage activation, tissue factor release, platelet aggregation, thrombus formation, thromboembolization, cholesterol embolization, arterial obstruction, end organ ischemia and necrosis. Atherosclerosis is a dynamic process and many of its clinical manifestations such as myocardial infarction, ischemic stroke, transient ischemic attack, acute mesenteric ischemia, acute limb ischemia, and renal injury occur as a consequence of rupture of the vulnerable atherosclerotic plaque. So it is very important to understand the various mechanisms behind the distal organ injury caused by acute plaque rupture.Cholesterol crystal embolization (CCE) is one known mechanism of organ injury from atherosclerotic plaque rupture and it may happen spontaneously or by the endothelial trauma during instrumentation of an artery. 3 The prevalence of cholesterol crystal embolism in autopsy studies in unselected patients ranges from 0.7% to 4%. 4 This has also been shown to occur spontaneously in 1% of patients with transesophageal echocardiography-confirmed extensive thoracic aortic athersosclerotic disease when followed over 3 years. 5 CCE occurs in 3% of patients who underwent infrarenal aortic and infrainguinal vascular surgery or angiographic manipulation, 6 in 0.8% of patients undergoing cardiac catheterization, 7 and in 0.2% of patients undergoing cardiac surgery. 8 CCE causes organ injury by multiple mechanisms. In this issue of the Journal of Nuclear Cardiology, Pervaiz MH et al 9 examine the nonobstructive, non-ischemic, direct toxicity of cholesterol crystals as a cause of left thigh muscle inflammation and injury in a controlled animal study after injecting cholesterol crystals, polystyrene microsphere control, or saline control into the left femoral artery of rabbits. Thigh muscle inflammation and injury was assessed by 18 F-FDG PET/CT and angiography, which were then correlated with inflammatory markers such as tissue macrophage infiltration density and muscle injury markers such as creatine phosphokinase (CPK) levels. There was more muscle inflammation and injury in the cholesterol crystal group compared to the control groups as demonstrated by high maximum standardized uptake values of the left thigh muscles by PET/CT (0.40 ± 0.16 vs 0.21 ± 0.11 and 0.23 ± 0.06; P = .038 and P = .036, respectively), high CPK levels at 24 hours (7.46 ± 4.32 vs 1.57 ± 0.84 and 1.43 ± 0.57; P = .007 and P = .023, respectively), and high macrophage density in the muscle biopsy.CCE may cause organ injury by multiple mechanisms such as ...

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Imaging of Vascular Inflammation With [11C]-PK11195 and Positron Emission Tomography/Computed Tomography Angiography

Abstract: By binding to activated macrophages in the vessel wall, [11C]-PK11195 enables noninvasive imaging of vascular inflammation. Alternative longer-lived radioligands for probing peripheral benzodiazepine receptors are being tested for wider clinical applications.

Cited by 139 publications

References 30 publications

Vascular imaging with positron emission tomography

Vascular imaging with positron emission tomography

Targeting activated macrophages to identify the vulnerable atherosclerotic plaque

18F-FDG for imaging microvascular injury

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