Myocardial adrenergic innervation in patients with vasovagal syncope measured with 123I-MIBG uptake.
BACKGROUND
Data about biochemical abnormalities (catecholamines) during vasovagal syncope (VVS) are available, but adrenergic myocardial structural damage may be hypothesized as well.


OBJECTIVE
To study the global and regional adrenergic myocardial innervations in patients with VVS that was shown by head-up tilt table testing.


METHODS
Fifteen adult patients with VVS were studied. The age of patients was 44+/-18 years (17-73), nine were female and six were male. According to the tilt test results, five patients had cardioinhibition, six patients had vasodepressor syncope and four patients suffered from mixed-type VVS. Ischemic heart diseases were excluded by normal Tc-MIBI rest-stress dipyridamol single-photon emission computed tomography (SPECT) results. A control group was formed from six healthy adult volunteers. To investigate cardiac sympathetic innervations 250-370 MBq iodine-123 meta-iodobenzylguanidine (I-MIBG) was used. Fifteen minutes after the intravenous administration of I-MIBG early, and 2-3 h later, delayed planar myocardial and tomographic (SPECT) scintigraphies were performed. The heart-to-mediastinum count ratio (H/M) was calculated for both early and delayed images, together with the decay-corrected change rates. The regional I-MIBG uptake was visualized on SPECT slices and polar map images. The regional uptake was considered pathological below 50% compared with normal uptake sites.


RESULTS
Delayed H/M ratios significantly depended on group (analysis of variance: P=0.005), whereas early H/M values did not. Although the decay-corrected myocardial MIBG uptake increased in time in controls, less wash-in or even wash-out could be observed in the VVS groups; however, difference from the controls was significant only in the vasodepressor group (Dunnett's t-test: P<0.05). All patients had regional I-MIBG uptake deficit in different regions.


CONCLUSIONS
In our patients with VVS, global I-MIBG deficit was present frequently, and all patients had regional adrenergic nerve function deficit. These alterations may play a role in causing clinical symptoms and have importance in staging and treatment planning.
Lorincz
István
I
Division of Emergency Medicine, First Department of Medicine, University of Debrecen, Hungary. lorincz@internal.med.unideb.hu
Garai
Ildikó
I
Varga
Emma
E
Barta
Kitti
K
Simkó
József
J
Szabó
Zoltán
Z
Galuska
László
L
Varga
József
J
D019797:3-Iodobenzylguanidine / Q000493:pharmacokinetics*; D000293:Adolescent; D000328:Adult; D000368:Aged; D005260:Female; D006321:Heart / Q000000981:diagnostic imaging* / Q000294:innervation*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D011877:Radionuclide Imaging; D019275:Radiopharmaceuticals / Q000493:pharmacokinetics; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D019462:Syncope, Vasovagal / Q000000981:diagnostic imaging* / Q000378:metabolism*; D055815:Young Adult
D019275:Radiopharmaceuticals; D011943:Receptors, Adrenergic, beta; D019797:3-Iodobenzylguanidine