Abstract
Abdominal aortic aneurysm (AAA) disease is characterized by an asymptomatic, permanent, focal dilatation of the abdominal aorta progressing towards rupture, which confers significant mortality. Patient management and surgical decisions rely on aortic diameter measurements via abdominal ultrasound surveillance. However, AAA rupture can occur at small diameters or may never occur at large diameters, implying that anatomical size is not necessarily a sufficient indicator. Molecular imaging may help identify high-risk patients through AAA evaluation independent of aneurysm size, and there is the question of the potential role of positron emission tomography (PET) and emerging role of novel radiotracers for AAA. Therefore, this review summarizes PET studies conducted in the last 10 years and discusses the usefulness of PET radiotracers for AAA risk stratification. The most frequently reported radiotracer was [18F]fluorodeoxyglucose, indicating inflammatory activity and reflecting the biomechanical properties of AAA. Emerging radiotracers include [18F]-labeled sodium fluoride, a calcification marker, [64Cu]DOTA-ECL1i, an indicator of chemokine receptor type 2 expression, and [18F]fluorothymidine, a marker of cell proliferation. For novel radiotracers, preliminary trials in patients are warranted before their widespread clinical implementation. AAA rupture risk is challenging to evaluate; therefore, clinicians may benefit from PET-based risk assessment to guide patient management and surgical decisions.
Highlights
Abdominal aortic aneurysm (AAA) disease is characterized by localized, irreversible dilatation of the abdominal aorta from a normal diameter of approximately 10–20 mm to an aneurysmal diameter of 30 mm or greater
Emerging evidence suggests that diabetes may play a protective role in patients who are susceptible to developing AAA; this correlation requires further investigation.[7,8]
Markers of cell proliferation and chemokine receptors such as [18F]FLT and [64Cu]DOTA-ECL1i are promising, and preliminary trials in patients are warranted to determine if these approaches may translate to the clinic.17,19,23 [18F]fluoromethylcholine, which is commonly implemented in prostate cancer staging, may be beneficial to incidentally detect AAA in patients with prostate cancer.[54]
Summary
Abdominal aortic aneurysm (AAA) disease is characterized by localized, irreversible dilatation of the abdominal aorta from a normal diameter of approximately 10–20 mm to an aneurysmal diameter of 30 mm or greater. The SoFIA3 trial demonstrated that [18F]NaF uptake is a positive predictor of aneurysm growth and clinical outcomes, which are independent but supplementary to classic clinical parameters such as aneurysm diameter.[50] The findings of this trial must be considered in light of the Gandhi et al PET for AAA risk stratification confounding issue of spill-in contamination from the nearby bone into the aneurysm; background correction techniques are likely necessary to provide more robust quantitative assessments of AAA using [18F]NaF.[51] Alternative radiotracers that may prove to be useful include markers of other characteristics of AAA development, such as angiogenesis, using integrinor endoglin-targeted agents.[18,52,53] Markers of cell proliferation and chemokine receptors such as [18F]FLT and [64Cu]DOTA-ECL1i are promising, and preliminary trials in patients are warranted to determine if these approaches may translate to the clinic.17,19,23 [18F]fluoromethylcholine, which is commonly implemented in prostate cancer staging, may be beneficial to incidentally detect AAA in patients with prostate cancer.[54] With these radiotracer applications, PET remains an attractive modality to advance our understanding of AAA pathophysiology, while novel molecular tracer agents are introduced, and hybrid multimodality systems are improved. More studies will confirm whether PET and MRI parameters are correlated or reveal different types of information.[46,64] technical developments in PET and hybrid PET systems will continually help our understanding of the pathophysiological factors contributing to AAA evolution
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