Dynamic planar scintigraphy for the rapid kinetic measurement of myocardial (123)I-MIBG turnover can identify Lewy body disease

BACKGROUND: Using two static scans for (123)I-meta-iodobenzyl-guanidine ((123)I-MIBG) myocardial scintigraphy ignores the dynamic response from vesicular trapping in nerve terminals. Moreover, the long pause between scans is impractical for patients with Lewy body diseases (LBDs). Here, we optimized indices that capture norepinephrine kinetics, tested their diagnostic performance, and determined the differences in (123)I-MIBG performance among disease groups. METHODS: We developed a new 30-min protocol for (123)I-MIBG dynamic planar imaging for suspected LBD patients. Pharmacokinetic modelling of time-activity curves (TACs) was used to calculate three new indices: unidirectional uptake of (123)I-MIBG to vesicular trapping (iUp), rate of myocardial (123)I-MIBG loss (iLoss), and non-specific fractional distribution of (123)I-MIBG in the interstitial space. We compared the performance of the new and existing indices with regard to discrimination of patients with or without LBDs. Subgroup analysis was performed to examine differences in (123)I-MIBG turnover between patients in a dementia with Lewy bodies (DLB) group and two Parkinson’s disease (PD) groups, one with and the other without REM sleep behaviour disorder (RBD). RESULTS: iLoss was highly discriminative, particularly for patients with low myocardial (123)I-MIBG trapping, and the new indices outperformed existing ones. ROC analysis revealed that the AUC of iLoss (0.903) was significantly higher than that of early HMR (0.863), while comparable to that of delayed HMR (0.892). The RBD-positive PD group and the DLB group had higher turnover rates than the RBD-negative PD group, indicating a potential association between prognosis and iLoss. CONCLUSION: (123)I-MIBG turnover can be quantified in 30 min using a three-parameter model based on (123)I-MIBG TACs. The discriminatory performance of the new model-based indices might help explain the neurotoxicity or neurodegeneration that occurs in LBD patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13550-021-00864-w.