Non-invasive assessment of endarteritis in Marfan syndrome with aortic dissection after surgical treatment

Carvajal-Juárez, Isabel; Alexánderson-Rosas, Erick; Meave-González, Aloha; Ortega-Silva, Susana; Espínola‐Zavaleta, Nilda

doi:10.1007/s12350-018-1370-0

Cited by 1 publication

(3 citation statements)

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“…29,35,38,39 In contrast, there is evidence that 2-[ 18 F]-FDG could be a useful tool in detecting complications after endovascular aneurysm repair and aortic arch graft in Marfan syndrome. [62][63][64] The results could be confounded for a variety of reasons such as the stage of AAA evaluated (eg, asymptomatic, symptomatic, and end stage), small number of subjects recruited and only a small percentage of subjects with detectable AAA. In addition, only end-stage AAA subjects have been studied, and the data may suggest that 2-[ 18 F]-FDG cannot predict growth during this period of disease progression.…”

Section: Macrophages and Metabolismmentioning

confidence: 99%

“…Activation of the CCR2 pathway by MCP (monocyte chemoattractant protein)-1 has shown recruitment of monocytes, migration of endothelial cells, angiogenesis, and proliferation of VSMC. Synthesis of the novel CCR2-specific radiotracer [ 64 Cu]Cu-DOTA-ECL1i showed detection of AAA in rats with PPE-induced aneurysms at day 7, with uptake reported to be double that of sham models. 46 In addition, high uptake correlated with risk of rupture.…”

Section: Chemokine Receptorsmentioning

confidence: 99%

“…Radiotracer binding occurs between ECL1i and extracellular loop 1 on CCR2. 93 Clinical translation of [ 64 Cu] could be problematic due to the 12.1-hour halflife and radiation dose given to a subject. An alternative positron-emitting Cu radionuclide with a shorter half-life, such as [ 62 Cu] (9 minutes) or [ 60 Cu] (23 minutes), could overcome this hurdle, although these come with their own limitations.…”

Section: Chemokine Receptorsmentioning

confidence: 99%

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Imaging Biological Pathways in Abdominal Aortic Aneurysms Using Positron Emission Tomography

Bell

Gandhi

Shawer

et al. 2021

ATVB

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Abdominal aortic aneurysm (AAA) is a focal dilation of the aorta associated with high mortality through rupture. Most of our understanding of the biology that drives AAA progression originates from surgical samples acquired in cases of elective open repair. These markers, which include macrophage infiltration and angiogenesis, have led to the exploration of novel radiopharmaceuticals to study AAA in preclinical models and human patients. Current clinical practice to detect AAA involves ultrasound-based screening and surveillance. Although ultrasound is cheap and without radiation risk, aortic diameter does not predict the heterogenous growth of AAA between patients. Positron emission tomography takes advantage of novel radiolabeled markers of disease to track biological changes. In human trials, the role of 2-[ 18 F]-fluorodeoxyglucose in detecting aneurysm growth and outcome is still debated, whereas sodium [ 18 F]-fluoride (microcalcification) has been shown to predict AAA growth and clinical outcome. Murine studies have been used to assess the suitability of radiotracers detecting inflammation, angiogenesis, and proliferation. However, in the absence of human data, the clinical suitability and applicability of these tracers remain speculative. This review examines how markers of AAA change over time and the ability of positron emission tomography to track these changes and discusses the radiopharmaceuticals that could have an application in stratifying AAA subjects.

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