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EJNMMI Research 2012
68Ga-DOTATATE PET/CT for the detection of inflammation of large arteries: correlation with18F-FDG, calcium burden and risk factorsKeywords: Atherosclerotic plaque, 68Ga-DOTATATE, Somatostatin receptor, Cardiovascular risk factors, Macrophage Abstract: Sixteen consecutive patients with neuroendocrine tumors or thyroid cancer underwent both 68Ga-DOTATATE and 18F-FDG PET/CT for staging or restaging purposes. Detailed clinical data, including common cardiovascular risk factors, were recorded. For a separate assessment, they were divided into a high-risk and a low-risk group. In each patient, we calculated the maximum target-to-background ratio (TBR) of eight arterial segments. The correlation of the TBRmean of both tracers with risk factors including plaque burden was assessed.The mean TBR of 68Ga-DOTATATE in all large arteries correlated significantly with the presence of CPs (r?=?0.52; p?<?0.05), hypertension (r?=?0.60; p?<?0.05), age (r?=?0.56; p?<?0.05), and uptake of 18F-FDG (r?=?0.64; p?<?0.01). There was one significant correlation between 18F-FDG uptake and hypertension (0.58; p?<?0.05). Out of the 37 sites with the highest focal 68Ga-DOTATATE uptake, 16 (43.2%) also had focal 18F-FDG uptake. Of 39 sites with the highest 18F-FDG uptake, only 11 (28.2%) had a colocalized 68Ga-DOTATATE accumulation.In this series of cancer patients, we found a stronger association of increased 68Ga-DOTATATE uptake with known risk factors of cardiovascular disease as compared to 18F-FDG, suggesting a potential role for plaque imaging in large arteries. Strikingly, we found that focal uptake of 68Ga-DOTATATE and 18F-FDG does not colocalize in a significant number of lesions.Cardiovascular disease (CVD) has become a global epidemic, being responsible for almost one third of all recorded deaths in men and women worldwide [1,2]. Atherosclerosis is the leading cause of cardiovascular disease morbidity, with the rupture of an atherosclerotic plaque as the critical event resulting in either occlusion of the vessel by a thrombus or thromboembolic event [3].Cardiovascular inflammatory processes with the accumulation of activated macrophages on the vascular wall play a crucial role in the initiation, progression, destabilization, and even
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