We have reported previously that 11 C-acetate ( 11 C-ACT) PET was complementary to 18 F-FDG PET in the evaluation of primary hepatocellular carcinoma (HCC) in relation to the degree of tumor cellular differentiation. In this retrospective study, our goals were to further explore the complementary role of 11 C-ACT and 18 F-FDG PET in the detection of metastatic HCC disease, to evaluate the tracer characteristics of individual organ metastasis, to identify the risk factors of metastasis, and to evaluate how these results could affect patient management. Methods: One hundred twenty-one patients were selected for this study. All patients had undergone a ''dual-tracer'' PET/CT same-day protocol with 11 C-ACT PET/CT followed by 18 F-FDG PET/CT. Sets of criteria were chosen to define ''metastasis'' and ''no metastasis'' on a patient basis. The patients considered as truepositive (n 5 97) were then divided into 4 groups on the basis of their primary HCC tracer avidity: 18 F-FDG-avid group, 11 C-ACT-avid group, 18 F-FDG-and 11 C-ACT-avid group, and a posttreatment group with metastasis but no baseline dual-tracer PET characterization of the primary tumor and no hepatic recurrence. Results: On a patient basis, dual-tracer PET/CT had a sensitivity of 98%, a specificity of 86%, a positive predictive value of 97%, a negative predictive value of 90%, and an accuracy of 96% in the detection of HCC metastasis. On a lesion basis, 273 metastatic HCC lesions considered as true-positive were detected and categorized according to the organ or site of metastasis: lymph node (abdominal and thoracic, 49%), lung (32%), bone (8%), and others (10%). The lesion-based and patientbased detection sensitivities were 60% and 64%, respectively, by 11 C-ACT and 77% and 79%, respectively, by 18 F-FDG, and they were complementary. In analyzing lesion tracer avidity, there was a positive statistical correlation between primary HCC avidity with the general tendency of metastasis. Clinically significant changes in management were found in patients with true-positive metastasis, of whom 19% were affected by 11 C-ACT PET alone. Dual-tracer PET/CT was more effective than single-tracer PET/CT in identifying candidates for curative therapy (negative predictive value of dual-tracer, 18 F-FDG, and 11 C-ACT PET/CT: 90%, 49%, and 37%, respectively). Conclusion: This study confirmed that 18 F-FDG PET/CT is useful in the evaluation of HCC metastasis, although its role in the diagnosis of primary HCC is more limited. Dual-tracer PET/CT had an incremental value and complementary advantage when compared with single-tracer imaging in the evaluation of HCC metastasis.

Chronic brain changes including WMCs, MTLA, and AD pathology are associated with incident dementia after stroke/TIA. Interventions targeting these chronic brain changes may reduce burden of vascular cognitive impairment.

C ognitive impairment in the context of stroke or transient ischemic attack (TIA) is a prototype of vascular cognitive impairment (VCI). Our recent in vivo study using carbon-11-labeled Pittsburgh compound B ( 11 C-PiB) positron emission tomography (PET) found that ≈30% of subjects with poststroke/TIA cognitive impairment harbored Alzheimer's pathology.1 Although some studies suggested that in patients with clinical Alzheimer's disease (AD), comorbid cerebrovascular disease was associated with a more rapid cognitive decline, 2,3 it is still unknown whether concurrent presence of Alzheimer's pathology is associated with a faster cognitive deterioration in patients with poststroke/TIA cognitive impairment.In this study, we compared the longitudinal cognitive changes between VCI patients with and without AD-like amyloid-beta (Aβ) deposition measured using 11 C-PiB PET. We hypothesized that over 3 years, PiB-positive VCI (mixed VCI [mVCI]) subjects would experience a more rapid and continuous course of cognitive deterioration, resulting in more severe cognitive impairment than those who were PiB-negative (pure VCI [pVCI]). Methods SubjectsSubjects of this study were participants of the ongoing Stroke Registry Investigating cognitive Decline (STRIDE) study. 1 In the Background and Purpose-We hypothesized that comorbid amyloid-beta (Aβ) deposition played a key role in long-term cognitive decline in subjects with stroke/transient ischemic attack. Methods-We recruited 72 subjects with cognitive impairment after stroke/transient ischemic attack to receive Carbon-11-labeled Pittsburgh compound B positron emission tomography. We excluded subjects with known clinical Alzheimer's disease. Those with and without Alzheimer's disease-like Aβ deposition were classified as mixed vascular cognitive impairment (mVCI, n=14) and pure VCI (pVCI, n=58), respectively. We performed Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment to evaluate global cognition and cognitive domains (memory, visuospatial function, language, attention, and executive function) at 3 to 6 months (baseline) and annually for 3 years after the index event. We compared cognitive changes between mVCI and pVCI using linear mixed models and analysis of covariance adjusted for age and education. Results-Over 3 years, there were significant differences between mVCI and pVCI on change of MMSE score over time (group×time interaction, P=0.007). We observed a significant decline on MMSE score (P=0.020) in the mVCI group but not in the pVCI group (P=0.208 6 were performed on subjects at 3 to 6 months (baseline) after the index event to index general cognition. Then subjects were further invited to return for annual follow-up. This study analyzed the data collected ≤3 years.This substudy included a sample of 72 subjects with cognitive impairment (CDR grade ≥0.5) from the STRIDE study. Clinical diagnoses were made by 2 neurologists specialized in dementia (V.C.T.M. and L.A.). Thirty-six subjects had CDR grade of ≥1 and met the criteria for dementia acco...