Conventional 2-dimensional planar imaging of 123 I-metaiodobenzylguanidine ( 123 I-mIBG) is not fully quantitative. To develop a more accurate quantitative imaging approach, we investigated dynamic SPECT imaging with kinetic modeling in healthy humans to obtain the myocardial volume of distribution (V T ) for 123 I-mIBG. Methods: Twelve healthy humans underwent 5 serial 15-min SPECT scans at 0, 15, 90, 120, and 180 min after bolus injection of 123 I-mIBG on a hybrid cadmium zinc telluride SPECT/CT system. Serial venous blood samples were obtained for radioactivity measurement and radiometabolite analysis. List-mode data of all the scans were binned into frames and reconstructed with attenuation and scatter corrections. Myocardial and blood-pool volumes of interest were drawn on the reconstructed images to derive the myocardial timeactivity curve and input function. A population-based blood-to-plasma ratio (BPR) curve was generated. Both the population-based metabolite correction (PBMC) and the individual metabolite correction (IMC) curves were generated for comparison. V T values were obtained from different compartment models, using different input functions with and without metabolite and BPR corrections. Results: The BPR curve reached the peak value of 2.1 at 13 min after injection. Parent fraction was approximately 58% ± 13% at 15 min and stabilized at approximately 40% ± 5% by 180 min after injection. Two radiometabolite species were observed. When the reversible 2-tissue-compartment fit was used, the mean V T value was 29.0 ± 12.4 mL/cm 3 with BPR correction and PBMC, a 188% ± 32% increase compared with that without corrections. There was significant difference in V T with BPR correction (P 5 2.3e-04) as well as with PBMC (P 5 1.6e-05). The mean difference in V T between PBMC and IMC was −3% ± 8%, which was insignificant (P 5 0.39). The intersubject coefficients of variation after PBMC (43%) and IMC (42%) were similar. Conclusion: The myocardial V T of 123 I-mIBG was established in healthy humans for the first time. Accurate kinetic modeling of 123 I-mIBG requires both BPR and metabolite corrections. Population-based BPR correction and metabolite correction curves were developed, allowing more convenient absolute quantification of dynamic 123 I-mIBG SPECT images. Met aiodobenzylguanidine labeled with 123 I ( 123 I-mIBG) is a norepinephrine analog that has a reuptake mechanism similar to that of norepinephrine without being catabolized in the myocardial sympathetic nerve endings and has been the most widely used sympathetic innervation imaging agent in research and clinical studies for risk stratification of patients with congestive heart failure (HF) (1-5). For conventional 123 I-mIBG imaging, early (15-30 min) and delayed (3-5 h) 2-dimensional (2D) planar images are typically acquired and used for calculating heart-to-mediastinum ratio (HMR) and washout rate (WOR). However, 2D planar imaging is not fully quantitative, because of the superposition of background structures with the 2D heart region of intere...
Assessment of cardiac I-meta iodobenzylguanidine (I-mIBG) uptake relies on the heart-to-mediastinum ratio (HMR) derived from planar images. We have developed novel semiautomated quantitative methodologies for assessing HMR from SPECT images using a dedicated cardiac multipinhole SPECT/CT system and determined the lower limit of normal (LLN) SPECT-derived HMR and the correlation to planar-derived HMR. Twenty-one healthy volunteers were injected withI-mIBG and imaged using 2 different cameras. Planar images were acquired using a conventional SPECT camera equipped with parallel hole collimators, and hybrid SPECT/CT images were acquired using a dedicated cardiac SPECT system with 19 pinhole collimators interfaced with 64-slice CT. Planar HMR was calculated as per standard guidelines (manual traditional method) and elliptic region-of-interest (Elip-ROI) and region-growing (RG-ROI) techniques. SPECT HMR was quantified using a new method that incorporates various cardiac and mediastinal segmentation schemes in which upper and lower limits of the heart were determined from CT and the left ventricular ROI, and mean counts were calculated using Elip-ROI and RG-ROI techniques. Mean counts in mediastinal ROI were computed from a fixed volume in 3 different regions: upper mediastinum (UM), lower mediastinum (LM), and contralateral lung (CL). HMRs were processed by 2 observers, and reproducibility was assessed by intraclass correlation coefficient and Bland-Altman analysis. Planar HMR calculated using the RG-ROI method showed highest intra- and interobserver levels of agreement compared with Elip-ROI and manual traditional methods. SPECT HMR calculated on the basis of UM, LM, and CL background regions showed excellent intra- and interobserver agreement. SPECT HMR with UM resulted in highest correlation ( = 0.91) with planar HMR compared with that with LM ( = 0.74) and CL ( = 0.73). The LLN of SPECT HMR with UM and that of planar HMR was calculated as 5.5 and 1.6, respectively. The normal values of SPECT-derived HMR and planar-derived HMR were correlated linearly. We reconfirmed the previous planar HMR threshold and determined SPECT LLN HMR for SPECT. Planar HMR can be estimated from SPECT HMR via a simple linear regression equation, allowing use of the new cardiac-dedicated SPECT camera forI-mIBG imaging.
The proposed segmentation-free PVC method has the potential of improving SPECT quantification accuracy and reducing noise without the need for premeasuring the image PSF.
The autopsy of a 65-year-old diabetic African American male revealed significant left myocardial involvement by adult T-cell leukemia/lymphoma (ATLL) despite normal pre-mortem fluorodeoxyglucose (FDG) uptake by positron emission tomography/computed tomography (PET/CT). Due to pre-existing diabetic cardiomyopathy with reduced ejection fraction (EF) and compatible imaging studies, cardiac lymphomatous involvement was not suspected. While peripheral blood was negative for leukemia, next-generation sequencing of a lymph node revealed at least eight novel mutations (AXIN1, R712Q, BARD1 R749K, CTNNB1 I315V, CUX1 P102T, DNMT3A S199R, FGFR2 S431L, LRP1B Y2560C and STAG2 I771M). These findings underscore a diagnostic pitfall in a rare lymphomatous variant of ATLL infiltrating myocardium and contribute to its molecular characterization.
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