18F-FDG PET/CT in the diagnosis of prosthetic valve endocarditis.

Recent studies have shown promising results using (18)F-fluorodeoxyglucose positron emission tomography/computed tomography ((18)F-FDG PET/CT) in the diagnosis of prosthetic valve endocarditis (PVE). However, previous studies did not include negative controls. The aim of this study was to compare (18)F-FDG-uptake around prosthetic aortic valves in patients with and without PVE and to determine the diagnostic performance of (18)F-FDG PET/CT in the diagnosis of PVE. (18)F-FDG PET/CT examinations in patients with a prosthetic aortic valve performed 2008-2014 were retrieved. Eight patients with a final diagnosis of definite PVE were included in the analysis of the diagnostic performance of (18)F-FDG PET/CT. Examinations performed on suspicion of malignancy in patients without PVE (n = 19) were used as negative controls. Visual and semi-quantitative analysis was performed. Maximal standardized uptake value (SUVmax) in the valve area was measured and SUVratio was calculated by dividing valve SUVmax by SUVmax in the descending aorta. The sensitivity was 75 %, specificity 84 %, positive likelihood ratio [LR(+)] 4.8 and negative likelihood ratio [LR(-)] 0.3 on visual analysis. Both SUVmax and SUVratio were significantly higher in PVE patients [5.8 (IQR 3.5-6.5) and 2.4 (IQR 1.7-3.0)] compared to non-PVE patients [3.2 (IQR 2.8-3.8) and 1.5 (IQR 1.3-1.6)] (p < 0.001). ROC-curve analysis of SUVratio yielded an area under the curve of 0.90 (95 % CI 0.74-1.0). (18)F-FDG-uptake around non-infected aortic prosthetic valves was low. The level of (18)F-FDG-uptake in the prosthetic valve area showed a good diagnostic performance in the diagnosis of PVE.

Discrepancies in recommended criteria for grading of carotid stenosis with ultrasound.

The accuracy of duplex ultrasound for grading of internal carotid artery stenosis has been widely tested and shown to be high. However, different methods for measurement of the degree of carotid stenosis with the golden standard conventional angiography have been used in the different studies. This, together with other factors, has led to some confusion regarding the relation between the ultrasonographically measured flow velocity and the angiographically measured degree of stenosis. The ultrasound criteria that are used in Sweden (and in Germany) differ in an important way from the criteria recommended in North America and the United Kingdom for the same degree of angiographic stenoses. Possible reasons for the discrepancies are discussed in this article. The authors recommend absolute agreement locally whether ECST or NASCET criteria shall be used in the communication between radiologists, clinical physiologists, vascular surgeons, neurologists and other physicians involved in patient management decisions. Angle-dependent ultrasound criteria should be used and flow velocity measurements with ultrasound should be combined with assessment of plaque burden on 2D picture.

A study of plaque vascularization and inflammation using quantitative contrast-enhanced US and PET/CT.

BACKGROUND: Contrast-enhanced ultrasound (CEUS) is an in vivo methodology to quantify carotid plaque vascularization. Increased metabolism in plaques, measured as FDG uptake in PET/CT examination, has been associated with markers of inflammation in histological samples. In this study, we tested the association between FDG uptake and vascularization measured by CEUS to assess whether CEUS can be used as an in vivo marker of plaque vulnerability. METHODS: After informed consent, subjects aged >60 years with carotid plaque height exceeding 2.5mm were recruited. CEUS was performed and analyzed using earlier described protocol and software, Contrast Quantification Program, which calculates the fraction of the plaque being contrast positive (CQP value). PET/CT examination was performed within 3 months of CEUS (median time 7 days). PET/CT images were acquired 90 min after FDG injection (2.7 MBq/kg). FDG uptake was measured as tissue background index (TBI), calculated using Spearman's rho as mean standard uptake value (SUV) of the plaque divided by mean SUV in the jugular vein (mean of 7 measuring points). Local ethics committee approved the study. RESULTS: We recruited 13 subjects (5 women) with a mean age of 71 years, 6 had a history of stroke or TIA, 1 had a history of ipsilateral stroke. CQP values showed a significant, positive correlation with TBI of carotid plaques, r=0.67, p<0.02. CONCLUSIONS: Plaque vascularization measured by CEUS correlates positively with FDG uptake measured by PET/CT in humans. This indicates an association between vascularization and inflammation and/or hypoxia, supporting the use of CEUS as a non-invasive method to detect plaque vulnerability.

Cerebrospinal fluid markers of brain injury, inflammation, and blood-brain barrier dysfunction in cardiac surgery.

BACKGROUND: Neurocognitive dysfunction occurs frequently after open-heart surgery. Cerebral microembolization, inflammation, blood-brain barrier (BBB) dysfunction, and impaired cerebral oxygenation are considered among possible etiologies. The relationships between intraoperative microembolic signals and the release of cerebrospinal fluid (CSF) markers of inflammation, neuronal and glial cell injuries, and BBB function were evaluated after cardiac surgery with cardiopulmonary bypass. METHODS: Ten patients undergoing aortic valve replacement were included. The CSF was obtained the day before and 24 hours after surgery for assessment of neuronal damage (neuron-specific enolase, total tau, and neurofilament light chain protein), glial cell injury (S-100B, glial fibrillary acidic protein), BBB integrity (CSF to serum albumin ratio) and cytokines (interleukin-6, interleukin-8). Intraoperative extent of microemboli and their occurrence were described using the transcranial Doppler technique. RESULTS: Intraoperatively, 354±79 microemboli were detected; 81% after release of the aortic cross clamp. The S-100B and glial fibrillary acidic protein increased by 35% (p<0.01) and 25% (p=0.055), respectively. Neuron-specific enolase, total tau, and neurofilament light chain protein, were not significantly affected by the surgery. The CSF albumin increased by 13% (p<0.05) while serum albumin decreased by 27% (p<0.0001). Thus, CSF to serum albumin ratio increased by 61% (p=0.011). There was a 3.5- and 12-fold increase in interleukin-6 (p<0.001) and interleukin-8 (p<0.05), respectively. Microembolic signals did not correlate to changes in CSF glial injury markers, the CSF to serum albumin ratio, or CSF cytokines. CONCLUSIONS: Cardiac surgery with cardiopulmonary bypass causes cerebral inflammation, glial cell injury, and BBB dysfunction without biochemical signs of neuronal damage. These changes are not associated with intraoperative microembolization.

Asymmetric cerebral blood flow in patients with mild cognitive impairment: possible relationship to further cognitive deterioration.

AIM: To explore patterns of cerebral blood flow in patients with mild cognitive impairment (MCI), who (1) eventually deteriorate into overt dementia, with no particular focus on the type of dementia, or (2) do not appear to further deteriorate in their cognitive functions. METHODS: Thirty-seven MCI patients, with or without vascular pathology, were studied prospectively. The patients underwent (99m)Tc-HMPAO SPECT analysis at baseline. Possible clinical conversion into dementia within a 2-year period was assessed. RESULTS: Nineteen patients had progressive MCI (PMCI), while 18 patients were considered clinically stable (SMCI). PMCI patients had more often abnormally low cerebral blood flow in at least one of the frontal, temporal, parietal or occipital lobes compared to SMCI patients (12/19 vs. 5/18; p = 0.049). At least one of the temporal regions was found to be abnormal in 9 PMCI patients in contrast to only 1 SMCI patient (p = 0.008). More specifically, blood flow in the medial portion of the left temporal region was abnormal in 8 PMCI patients, a pattern seen in 1 SMCI patient only (p = 0.019). CONCLUSION: The results suggest that blood flow reductions particularly in the left medial temporal region indicate an elevated risk of further cognitive decline in MCI patients.