Myocardial adrenergic innervation in patients with vasovagal syncope measured with 123I-MIBG uptake

Abstract

Background: Data about biochemical abnormalities (catecholamines) during vasovagal syncope (VVS) are available, but adrenergic myocardial structural damage may be hypothesized as well.

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

Patients and 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.

Conclusion: 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.