In patients with PD without autonomic failure, only cardiac MIBG uptake was severely reduced in the earliest phase of the disease (stage I). Parkinsonian syndromes other than PD did not demonstrate significant reduction in MIBG uptake in any organs except for the lower legs in MSA. In patients with PD without autonomic failure, reduction in MIBG uptake occurs selectively in the heart; this is considered to be a specific finding for PD and useful for the differential diagnosis of the parkinsonian syndromes.
Sympathetic neuronal damage measured by (123)I-MIBG SPECT is larger than infarct size and is closely related to risk area, suggesting high sensitivity of neuronal structures to ischemia compared with myocardial cells.
After early reperfusion for myocardial infarction, viable but denervated myocardium is frequent and correlates with slow depolarisation and repolarisation. However, in patients with small infarct size and preserved left ventricular function, these findings seem to have little influence on outcome.
FDG uptake in PCG and PTL is reduced in AD regardless of whether or not PVE correction is applied, supporting the notion that the reduced FDG uptake in these areas is not the result of atrophy. Furthermore, FDG uptake by grey matter tissue in the MTL, including hippocampal areas, is relatively preserved, suggesting that compensatory mechanisms may play a role in patients with mild AD.
Background—
Although both
123
I-metaiodobenzylguanidine (
123
I-MIBG) imaging and
11
C-hydroxyephedrine (
11
C-HED) positron emission tomography (PET) are used for assessing cardiac sympathetic innervation, their relationship remains unknown. The aims were to determine whether
123
I-MIBG parameters such as heart-to-mediastinum ratio (H/M) are associated with quantitative measures by
11
C-HED PET and to compare image quality, defect size, and location between
123
I-MIBG single-photon emission computed tomography (SPECT) and
11
C-HED PET.
Methods and Results—
Twenty-one patients (mean left ventricular ejection fraction, 39±15%) underwent
123
I-MIBG imaging and
11
C-HED PET. Early (15-minute), late (3-hour) H/M, and washout rate (WR) were calculated for
123
I-MIBG. Myocardial retention and WR was calculated for
11
C-HED. Using a polar map approach, defect was defined as the area with relative activity <60% of the maximum. Both the early (
r
=0.76) and late (
r
=0.84)
123
I-MIBG H/M were correlated with
11
C-HED retention.
123
I-MIBG WR was correlated with
11
C-HED WR (
r
=0.57). Defect size could not be measured in 3 patients because of poor quality
123
I-MIBG SPECT, whereas
11
C-HED defect was measurable in all patients. Although defect size measured by early or late
123
I-MIBG SPECT was closely correlated with that by
11
C-HED PET (early:
r
=0.94; late:
r
=0.88), the late
123
I-MIBG overestimated defect size particularly in the inferior and septal regions.
Conclusions—
123
I-MIBG H/M gives a reliable estimate of cardiac sympathetic innervation as measured by
11
C-HED PET. Furthermore, despite the close correlation in defect size,
11
C-HED PET appears to be more suitable for assessing regional abnormalities than does
123
I-MIBG SPECT.
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