Key result
123I-MIBG scintigraphy showed normal cardiac sympathetic innervation in congenital long QT syndrome, with relative regional uptake in 96% of regions within 2 standard deviations of normal controls.
Why the study?
Does 123I-MIBG scintigraphy reveal cardiac sympathetic neuronal dysinnervation in patients with congenital long QT syndrome compared to normal controls?
Case-Control (n=23)
Does 123I-MIBG scintigraphy reveal cardiac sympathetic neuronal dysinnervation in patients with congenital long QT syndrome compared to normal controls?
123I-MIBG scintigraphy demonstrates normal cardiac sympathetic innervation in congenital LQTS, challenging the hypothesis that sympathetic imbalance in this condition is due to abnormal distribution or kinetics of cardiac sympathetic nerves.
Answers are grounded in this paper and cite their sources.
Questions sympathetic imbalance mechanisms in congenital LQTS; challenges prior hypotheses but leaves open diagnostic utility pending prospective data.
The aim of this study was to determine whether sympathetic imbalance in congenital long QT syndrome (LQTS) can be identified by cardiac sympathetic neuronal dysinnervation. 123I-metaiodobenzylguanidine (MIBG) is a tracer of the norepinephrine analogue which reflects the regional innervation and norepinephrine kinetics in cardiac sympathetic nerves. Sixteen patients with LQTS, who were members of 12 families, and 7 normal controls underwent MIBG scintigraphy. Myocardial SPET and planar images were obtained 15 min and 4 h after the injection of MIBG in each patient. The relative regional uptake (RRU) and regional washout rate (rWR) of MIBG at 4 h in each of nine regions were compared with those in the control group. The heat-to-mediastinum ratio (H/M) and global washout rate (GWR) were also calculated. The RRU, rWR, H/M and GWR showed no significant difference between LQTS patients and normal controls. Furthermore, the RRU in 96% of all regions in LQTS was within the mean +/- 2 standard deviations of that in the control group. Patients with LQTS have normal cardiac sympathetic innervation, as assessed by MIBG. The sympathetic imbalance hypothesis is unlikely to be attributed to an abnormal distribution and different regional norepinephrine kinetics of cardiac sympathetic nerves.
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Momose et al. (1998) conducted a case-control in Congenital long QT syndrome (n=23). Congenital long QT syndrome vs. Normal controls was evaluated on Relative regional uptake, regional washout rate, heart-to-mediastinum ratio, and global washout rate of MIBG at 4 hours. 123I-MIBG scintigraphy showed normal cardiac sympathetic innervation in congenital long QT syndrome, with relative regional uptake in 96% of regions within 2 standard deviations of normal controls.
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